Citation: Ling Wang, Shunbin Ning. “Toll-free” pathways for production of type I interferons[J]. AIMS Allergy and Immunology, 2017, 1(3): 143-163. doi: 10.3934/Allergy.2017.3.143
[1] | François Baccelli, Augustin Chaintreau, Danny De Vleeschauwer, David R. McDonald . HTTP turbulence. Networks and Heterogeneous Media, 2006, 1(1): 1-40. doi: 10.3934/nhm.2006.1.1 |
[2] | D. Alderson, H. Chang, M. Roughan, S. Uhlig, W. Willinger . The many facets of internet topology and traffic. Networks and Heterogeneous Media, 2006, 1(4): 569-600. doi: 10.3934/nhm.2006.1.569 |
[3] | Paola Goatin, Chiara Daini, Maria Laura Delle Monache, Antonella Ferrara . Interacting moving bottlenecks in traffic flow. Networks and Heterogeneous Media, 2023, 18(2): 930-945. doi: 10.3934/nhm.2023040 |
[4] | Divya Pandey, Vandana Kushwaha . The use of Analytical Hierarchy Process in sensor-based networks for security-aware congestion control. Networks and Heterogeneous Media, 2023, 18(1): 244-274. doi: 10.3934/nhm.2023009 |
[5] | Olli-Pekka Tossavainen, Daniel B. Work . Markov Chain Monte Carlo based inverse modeling of traffic flows using GPS data. Networks and Heterogeneous Media, 2013, 8(3): 803-824. doi: 10.3934/nhm.2013.8.803 |
[6] | Yuri B. Gaididei, Carlos Gorria, Rainer Berkemer, Peter L. Christiansen, Atsushi Kawamoto, Mads P. Sørensen, Jens Starke . Stochastic control of traffic patterns. Networks and Heterogeneous Media, 2013, 8(1): 261-273. doi: 10.3934/nhm.2013.8.261 |
[7] | Leah Anderson, Thomas Pumir, Dimitrios Triantafyllos, Alexandre M. Bayen . Stability and implementation of a cycle-based max pressure controller for signalized traffic networks. Networks and Heterogeneous Media, 2018, 13(2): 241-260. doi: 10.3934/nhm.2018011 |
[8] | Maya Briani, Rosanna Manzo, Benedetto Piccoli, Luigi Rarità . Estimation of NOx and O3 reduction by dissipating traffic waves. Networks and Heterogeneous Media, 2024, 19(2): 822-841. doi: 10.3934/nhm.2024037 |
[9] | Michael Herty, S. Moutari, M. Rascle . Optimization criteria for modelling intersections of vehicular traffic flow. Networks and Heterogeneous Media, 2006, 1(2): 275-294. doi: 10.3934/nhm.2006.1.275 |
[10] | Cécile Appert-Rolland, Pierre Degond, Sébastien Motsch . Two-way multi-lane traffic model for pedestrians in corridors. Networks and Heterogeneous Media, 2011, 6(3): 351-381. doi: 10.3934/nhm.2011.6.351 |
In this article, we investigate the following Kirchhoff-Schrödinger-Poisson type systems on the Heisenberg group:
{−(a+b∫Ω|∇Hu|pdξ)ΔH,pu−μϕ|u|p−2u=λ|u|q−2u+|u|Q∗−2uin Ω,−ΔHϕ=|u|pin Ω,u=ϕ=0on ∂Ω, | (1.1) |
where a,b are positive real numbers, Ω⊂HN is a bounded region with smooth boundary, 1<p<Q, Q=2N+2 is the homogeneous dimension of the Heisenberg group HN, Q∗=pQQ−p, q∈(2p,Q∗), ΔH,pu=div(|∇Hu|p−2∇Hu) is known as the p-horizontal Laplacian, and μ and λ are some positive real parameters.
In recent years, geometrical analysis of the Heisenberg group has found significant applications in quantum mechanics, partial differential equations and other fields, which has attracted the attention of many scholars who tried to establish the existence and multiplicity of solutions of partial differential equations on the Heisenberg group. For instance, in the subcase of problem (1.1), when p=2 and b=μ=0, the existence of solutions for some nonlinear elliptic problems in bounded domains has been established. Tyagi [1] studied a class of singular boundary value problem on the Heisenberg group:
{−ΔHu=μg(ξ)u(|z|4+t2)12+λf(ξ,t),ξ∈Ω,u|∂Ω=0, | (1.2) |
and under appropriate conditions, obtained some existence results using Bonanno's three critical point theorem. Goel and Sreenadh [2] dealt with a class of Choquard type equation on the Heisenberg group, and they established regularity of solutions and nonexistence of solutions invoking the mountain pass theorem, the linking theorem and iteration techniques and boot-strap method.
In the case b≠0 and μ=0, problem (1.1) becomes the Kirchhoff problem, which has also been widely studied. For example, Sun et al. [3] dealt with the following Choquard-Kirchhoff problem with critical growth:
M(‖u‖2)(−ΔHu+u)=∫HN|u(η)|Q∗λ|η−1ξ|λdη|u|Q∗λ−2u+μf(ξ,u), |
where f is a Carathéodory function, M is the Kirchhoff function, ΔH is the Kohn Laplacian on the Heisenberg group HN, μ>0 is a parameter and Q∗λ=2Q−λQ−2 is the critical exponent. In their paper, a new version of the concentration-compactness principle on the Heisenberg group was established for the first time. Moreover, the existence of nontrivial solutions was obtained even under nondegenerate and degenerate conditions. Zhou et al. [4] proved the existence of solutions of Kirchhoff type nonlocal integral-differential operators with homogeneous Dirichlet boundary conditions on the Heisenberg group using the variational method and the mountain pass theorem. Deng and Xian [5] obtained the existence of solutions for Kirchhoff type systems involving the Q-Laplacian operator on the Heisenberg group with the help of the Trudinger-Moser inequality and the mountain pass theorem. For more related results, see [6,7,8,9,10,11,12,13].
When b=0, p=2 and μ≠0, problem (1.1) becomes the Schrödinger-Poisson system. This is a very interesting subject and has recently witnessed very profound results. For example, An and Liu [14] dealt with the following forms of Schrödinger-Poisson type system on the Heisenberg group:
{−ΔHu+μϕu=λ|u|q−2u+|u|2uin Ω,−ΔHϕ=u2in Ω,u=ϕ=0on ∂Ω, |
where μ∈R and λ>0 are some real parameters and 1<q<2. By applying the concentration compactness and the critical point theory, they found at least two positive solutions and a positive ground state solution.
Liang and Pucci [15] studied the following critical Kirchhoff-Poisson system on the Heisenberg group:
{−M(∫Ω|∇Hu|2dξ)ΔHu+ϕ|u|q−2u=h(ξ,u)+λ|u|2uin Ω,−ΔHϕ=|u|qin Ω,u=ϕ=0on ∂Ω, |
where Ω⊂H1 is a smooth bounded domain, ΔH is the Kohn-Laplacian on the first Heisenberg group H1 and 1<q<2. By applying the symmetric mountain pass lemma, they obtained the multiplicity of solutions with λ sufficiently small.
The Kirchhoff-Poisson system on the Heisenberg group with logarithmic and critical nonlinearity was considered by Pucci and Ye [13]:
{−M(∫Ω|∇Hu|2dξ)ΔHu+ϕu=|u|2u+λ|u|q−2uln|u|2in Ω,−ΔHϕ=|u|2in Ω,u=ϕ=0on ∂Ω. |
Under suitable assumptions on the Kirchhoff function M covering the degenerate case, they showed that for a sufficiently large λ>0, there exists a nontrivial solution to the above problem.
When p≠2 and μ≠0, as far as we know, for Kirchhoff-Schrodinger-Poisson systems (1.1) with critical nonlinearities on the Heisenberg group, existence and multiplicity results are not yet available. In the Euclidean case, Du et al. [16] first studied the existence results for the Kirchhoff-Poisson systems with p-Laplacian under the subcritical case using the mountain pass theorem. Later, Du et al. [17] studied quasilinear Schrödinger-Poisson systems. For the critical case, Du et al. [18] also obtained the existence of ground state solutions with the variational approach.
Inspired by the above achievements, we aim to establish some results on the existence and multiplicity of nontrivial solutions of the Kirchhoff-Schrödinger-Poisson systems (1.1). The major difficulties in dealing with problem (1.1) are the presence of a nonlocal term and critical nonlinearities making the study of this problem very challenging.
Before presenting the main results of this article, we first present some concepts of the Heisenberg group. The Heisenberg group is represented by HN. If ξ=(x,y,t)∈HN, then the definition of this group operation is
τξ(ξ′)=ξ∘ξ′=(x+x′,y+y′,t+t′+2(x′y−y′x)), for every ξ,ξ′∈HN, |
ξ−1=−ξ is the inverse, and therefore (ξ′)−1∘ξ−1=(ξ∘ξ′)−1.
The definition of a natural group of dilations on HN is δs(ξ)=(sx,sy,s2t), for every s>0. Hence, δs(ξ0∘ξ)=δs(ξ0)∘δs(ξ). It can be easily proved that the Jacobian determinant of dilatations δs:HN→HN is constant and equal to sQ, for every ξ=(x,y,t)∈HN. The critical exponent is Q∗:=pQQ−p, where the natural number Q=2N+2 is called the homogeneous dimension of HN. We define the Korányi norm as follows
|ξ|H=[(x2+y2)2+t2]14, for every ξ∈HN, |
and we derive this norm from the Heisenberg group's anisotropic dilation. Hence, the homogeneous degree of the Korányi norm is equal to 1, in terms of dilations
δs:(x,y,t)↦(sx,sy,s2t), for every s>0. |
The set
BH(ξ0,r)={ξ∈HN:dH(ξ0,ξ)<r}, |
denotes the Korányi open ball of radius r centered at ξ0. For the sake of simplicity, we shall denote Br=Br(O), where O=(0,0) is the natural origin of HN.
The following vector fields
T=∂∂t, Xj=∂∂xj+2yj∂∂t, Yj=∂∂yj−2xj∂∂t, |
generate the real Lie algebra of left invariant vector fields for j=1,⋯,n, which forms a basis satisfying the Heisenberg regular commutation relation on HN. This means that
[Xj,Yj]=−4δjkT, [Yj,Yk]=[Xj,Xk]=[Yj,T]=[Xj,T]=0. |
The so-called horizontal vector field is just a vector field with the span of [Xj,Yj]nj=1.
The Heisenberg gradient on HN is
∇H=(X1,X2,⋯,Xn,Y1,Y2,⋯,Yn), |
and the Kohn Laplacian on HN is given by
ΔH=N∑j=1X2j+Y2j=N∑j=1[∂2∂x2j+∂2∂y2j+4yj∂2∂xj∂t−4xj∂2∂xj∂t+4(x2j+y2j)∂2∂t2]. |
The Haar measure is invariant under the left translations of the Heisenberg group and is Q-homogeneous in terms of dilations. More precisely, it is consistent with the (2n+1)-dimensional Lebesgue measure. Hence, as shown Leonardi and Masnou [19], the topological dimension 2N+1 of HN is strictly less than its Hausdorff dimension Q=2N+2. Next, |Ω| denotes the (2N + 1)-dimensional Lebesgue measure of any measurable set Ω⊆HN. Hence,
|δs(Ω)|=sQ|Ω|, d(δsξ)=sQdξ and |BH(ξ0,r)|=αQrQ, where αQ=|BH(0,1)|. |
Now, we can state the main result of the paper.
Theorem 1.1. Let q∈(2p,Q∗). Then there exist positive constants μ1 and λ1 such that for every μ∈(0,μ1) and λ∈(λ1,+∞), the following assertions hold:
(I) Problem (1.1) has a nontrivial weak solution;
(II) Problem (1.1) has infinitely many nontrivial weak solutions if parameter a is large enough.
We can give the following example for problem (1.1) with p=3 and Ω⊂H1:
{−(a+∫Ω|∇Hu|2dξ)ΔHu+μϕu=λ|u|6u+|u|10uin Ω,−ΔHϕ=|u|3in Ω,u=ϕ=0on ∂Ω. |
In this case, N=1, p=3 and q=8, then Q=2N+2=4, Q∗=12. If positive parameters μ small enough and λ large enough, by Theorem 1.1, we know that problem (1.1) has a nontrivial weak solution. Moreover, if in addition the parameter a is large enough, problem (1.1) has infinitely many nontrivial weak solutions. It should be noted that the methods in An and Liu [14] and Liang and Pucci [15] do not seem to apply to problem (1.1).
Remark 1.1. Compared with previous results, this paper has the following key new features:
1) The presence of the nonlocal term ϕ|u|p−2u;
2) The lack of compactness caused by critical index;
3) The presence of the p-Laplacian makes this problem more complex and interesting.
It is worth stressing that the nonlocal term and the critical exponent lead to the lack of compactness condition, and we use the concentration-compactness principle to overcome this difficulty. Moreover, we shall use some more refined estimates to overcome the presence of the p-Laplacian.
We need to emphasize here that despite the similarity of some properties between the classical Laplacian Δ and Kohn Laplacian ΔH, similarities can be misleading (see Garofalo and Lanconelli [20]), so there are still many properties that deserve further study. Moreover, for the case p≠2, it is difficult to prove the boundedness of Palais-Smale sequences. In order to overcome these difficulties, we use some more accurate estimates of relevant expression. Additionally, we use the concentration-compactness principle on the Heisenberg group to prove the compactness condition.
The paper is organized as follows. In Section 2, we introduce some notations and known facts. Moreover, we introduce some key estimates. In addition, we define the corresponding energy functional Iλ and its derivative at u, that is, I′λ(u). In Section 3, we prove Theorem 1.1.
First of all, we collected some known facts, useful in the sequel. For additional background material, readers are advised to refer to Papageorgiou et al. [21].
Let
‖u‖ss=∫Ω|u|sdξ, for every u∈Ls(Ω), |
represent the usual Ls-norm.
Following Folland and Stein [22], we define the space ˚S21(Ω) as the closure of C∞0(Ω) in S21(HN). Then ˚S21(Ω) is a Hilbert space with the norm
‖u‖2˚S21(Ω)=∫Ω|∇Hu|2dξ. |
We define the Folland-Stein space S1,p(Ω) as the closure of C∞0(Ω) with the norm
‖u‖=(∫Ω|∇Hu|pdξ)1p. |
Then the embedding
S1,p(Ω)↪Ls(Ω), for every s∈(1,Q∗), |
is compact. However, if s=Q∗, the embedding is only continuous (see Vassiliev [23]).
Additionally, we say that (u,ϕ)∈S1,p(Ω)×S1,p(Ω) is a solution of problem (1.1) if and only if
a∫Ω|∇Hu|p−2∇Hu∇Hvdξ+b‖u‖p∫Ω|∇Hu|p−2∇Hu∇Hvdξ −μ∫Ωϕ|u|p−2uvdξ−λ∫Ω|u|q−2uvdξ−∫Ω|u|Q∗−2uvdξ=0 |
and
∫Ω∇Hϕ∇Hωdξ−∫Ω|u|pωdξ=0, |
for every v,ω∈S1,p(Ω)×S1,p(Ω). Moreover, (u,ϕ)∈S1,p(Ω)×S1,p(Ω) is a positive solution of problem (1.1) if u and ϕ are both positive. Therefore, in order to apply the critical point theory, we need to define the functional J(u,ϕ):S1,p(Ω)×S1,p(Ω)→R as follows
J(u,ϕ)=ap‖u‖p+b2p‖u‖2p+μ2p∫Ω|∇Hϕ|2dξ−μp∫Ωϕ|u|pdξ−λq∫Ω|u|qdξ−1Q∗∫Ω|u|Q∗dξ, |
for every (u,ϕ)∈S1,p(Ω)×S1,p(Ω). Then J is C1 on S1,p(Ω)×S1,p(Ω) and its critical points are the solutions of problem (1.1). Indeed, the partial derivatives of J at (u,ϕ) are denoted by J′u(u,ϕ), J′ϕ(u,ϕ), namely for every v,ω∈S1,p(Ω)×S1,p(Ω),
J′u(u,ϕ)[v]=a∫Ω|∇Hu|p−2∇Hu∇Hvdξ+b‖u‖p∫Ω|∇Hu|p−2∇Hu∇Hvdξ −μ∫Ωϕ|u|p−2uvdξ−λ∫Ω|u|q−2uvdξ−∫Ω|u|Q∗−2uvdξ=0 |
and
J′ϕ(u,ϕ)=μp∫Ω∇Hϕ∇Hωdξ−μp∫Ω|u|pωdξ. |
Standard computations show that J′u (respectively J′ϕ) continuously maps S1,p(Ω)×S1,p(Ω) into the dual of S1,p(Ω). Moreover, the functional J is C1 on S1,p(Ω)×S1,p(Ω) and
J′u(u,ϕ)=J′ϕ(u,ϕ)=0 |
if and only if (u,ϕ) is a solution of problem (1.1).
Lemma 2.1. Let u∈S1,p(Ω). Then there is a unique nonnegative function ϕu∈˚S21(Ω) such that
{−ΔHϕ=|u|pin Ω,ϕ=0on ∂Ω. | (2.1) |
Furthermore, ϕu≥0 and ϕu>0 if u≠0. Also,
(i) ϕtu=tpϕu, for every t>0;
(ii) ‖ϕu‖˚S21(Ω)≤ˆC‖u‖p, where ˆC>0;
(iii) Let un⇀u in S1,p(Ω). Then, ϕun⇀ϕu in ˚S21(Ω), and
∫Ωϕun|un|p−2unvdξ→∫Ωϕu|u|p−2uvdξ, forevery v∈S1,p(Ω). | (2.2) |
Proof. For any u∈˚S21(Ω), we define W:˚S21(Ω)→R,
W(v)=∫Ωv|u|pdξ, for every v∈˚S21(Ω). |
Let vn→v∈˚S21(Ω), as n→∞. It follows by the Hölder inequality that
|W(vn)−W(v)|≤∫Ω(vn−v)|u|pdξ≤(∫Ω|vn−v|Q∗dξ)1Q∗(∫Ω|u|pQ∗Q∗−1dξ)Q∗−1Q∗≤S−1p‖vn−v‖|u|ppQ∗Q∗−1→0, as n→∞, |
where
S=infu∈S1,p(Ω)∖{0}∫Ω|∇Hu|pdξ(∫Ω|u|Q∗dξ)pQ∗ | (2.3) |
is the best Sobolev constant. This implies that W is a continuous linear functional. Using the Lax-Milgram theorem, we see that there is a unique ϕu∈˚S21(Ω) satisfying
∫Ω∇Hϕu∇Hvdξ=∫Ωv|u|pdξ, for every v∈S1,p(Ω). | (2.4) |
Thus, ϕu∈˚S21(Ω) is the unique solution of problem (2.1). Moreover, applying the maximum principle, one has ϕu≥0 and ϕu>0 if u≠0. Indeed, for every t>0, one has
−ΔHϕtu=tpup=tp(−ΔHϕu)=−ΔH(tpϕu). |
Hence ϕtu=tpϕu due to the uniqueness of ϕu.
Furthermore, since ϕu∈S1,p(Ω), we can view it as a text function in problem (2.1). Then by (2.4), the Sobolev inequality and the Hölder inequality, we have (henceforth C0, C1, C2 will denote positive constants)
∫Ω|∇Hϕu|2dξ=∫Ωϕu|u|pdξ≤|ϕu|L2(Ω)|u|pL2p(Ω)≤C1‖ϕu‖˚S21(Ω)‖u‖p. |
Therefore, we get ‖ϕu‖˚S21(Ω)≤C1‖u‖p.
Since un⇀u in S1,p(Ω), we can conclude that un→u a.e. in Ω and {|un|p} is bounded in L2(Ω). Moreover, we have |un|p⇀|u|p in L2(Ω). Then for every v∈˚S21(Ω), it follows that
∫Ωv|un|pdξ→∫Ωv|u|pdξ, as n→∞. |
Therefore, ϕun⇀ϕu in ˚S21(Ω). By the Hölder inequality, the Sobolev inequality and (ⅱ), one has
∫Ω|ϕun|un|p−2un|2p2p−1dξ≤|ϕun|2p2p−1L2(Ω)(∫Ω|un|2pdξ)p−12p−1≤C0‖ϕun‖2p2p−1˚S21(Ω)(∫Ω|un|2pdξ)p−12p−1≤C2‖ϕun‖2p22p−1(∫Ω|un|2pdξ)p−12p−1. |
Hence, {ϕun|un|p−2un} is bounded in L2p2p−1(Ω). Since
ϕun|un|p−2un→ϕu|u|p−2u, a.e. in Ω, |
we get
∫Ωϕun|un|p−2unvdξ→∫Ωϕu|u|p−2uvdξ, for every v∈S1,p(Ω). |
The proof of Lemma 2.1 is complete.
By similar arguments as in An and Liu [14], we can get the following result.
Lemma 2.2. Let Ψ(u)=ϕu for every u∈S1,p(Ω), where ϕu is as in Lemma 2.1, and let
Υ={(u,ϕ)∈S1,p(Ω)×S1,p(Ω):J′ϕ(u,ϕ)=0}. |
Then Ψ is C1 and Υ is the graph of Ψ.
We define the corresponding energy functional Iλ(u)=J(u,ϕu) of problem (1.1) by
Iλ(u)=ap‖u‖p+b2p‖u‖2p−μ2p∫Ωϕu|u|pdξ−λq∫Ω|u|qdξ−1Q∗∫Ω|u|Q∗dξ, for every u∈S1,p(Ω). | (2.5) |
Based on the definition of J and Lemma 2.2, we can conclude that Iλ is of C1.
Lemma 2.3. (see An and Liu [14]) Let (u,ϕ)∈S1,p(Ω)×S1,p(Ω). Then (u,ϕ) is a critical point of J if and only if u is a critical point of Iλ and ϕ=Ψ(u), where Ψ was defined in Lemma 2.2.
According to Lemma 2.3, we know that a solution (u,ϕu) of problem (1.1) corresponds to a critical point u of the functional Iλ with ϕ=Ψ(u) and
⟨I′λ(u),v⟩=a∫Ω|∇Hu|p−2∇Hu∇Hvdξ+b‖u‖p∫Ω|∇Hu|p−2∇Hu∇Hvdξ −μ∫Ωϕu|u|p−2uvdξ−λ∫Ω|u|q−2uvdξ−∫Ω|u|Q∗−2uvdξ, for every v∈S1,p(Ω). | (2.6) |
Therefore, based on the above arguments, we shall strive to use critical point theory and some analytical techniques to prove the existence of critical points of functional Iλ.
In this subsection, our main focus will be on proving that the functional Iλ satisfies the Palais-Smale condition.
Lemma 2.4. Let q∈(2p,Q∗). Then there exists μ1>0 such that for any μ<μ1, the energy functional Iλ satisfies (PS)c condition, where
c∈(0, (1q−1Q∗)(aS)Qp) | (2.7) |
and S is the best Sobolev constant given by (2.3).
Proof. Let us assume that {un}n⊂S1,p(Ω) is a (PS)c sequence related to the functional Iλ, that is,
Iλ(un)→c and I′λ(un)→0,as n→∞. | (2.8) |
It follows that
c+o(1)‖un‖=Iλ(un)−1qI′λ(un)un≥a(1p−1q)‖un‖p+b(12p−1q)‖un‖2p−μ(12p−1q)∫Ωϕun|un|pdξ+(1q−1Q∗)∫Ω|un|Q∗dξ≥a(1p−1q)‖un‖p+(b−μˆC)(12p−1q)‖un‖2p, | (2.9) |
where ˆC is a positive constant given by Lemma 2.1(ⅱ). Let μ1=bˆC. By (2.9), we know that (PS)c sequence {un}n⊂S1,p(Ω) is bounded for every μ<μ1. Thus, we may assume that un⇀u weakly in S1,p(Ω), and un→u in Ls(Ω) with 1<s<Q∗. Furthermore, since Iλ(un)=Iλ(|un|), we may also assume that un≥0 and u≥0. Therefore, invoking the concentration compactness principle on the Heisenberg group (see Vassiliev [23, Lemma 3.5]), we obtain
|∇Hun|pdξ⇀dω≥|∇Hu|pdξ+Σj∈Λωjδxj,|un|Q∗dξ⇀dν=|u|Q∗dξ+Σj∈Λνjδxj, | (2.10) |
where {xj}j∈Λ⊂Ω is the most a countable set of distinct points, ω and ν in HN are two positive Radon measures, and {ωj}j∈Λ, {νj}j∈Λ are nonnegative numbers. Moreover, we have
ωj≥SνpQ∗j. | (2.11) |
Next, we shall show that Λ=∅. Indeed, assume that the hypothesis ωj≠0 holds for some j∈Λ. Then when ε>0 is sufficiently small, we can find 0≤ψε,j≤1 satisfying the following
{ψε,j=1in BH(ξj,ε2),ψε,j=0in Ω∖BH(ξj,ε),|∇Hψε,j|≤2ε, | (2.12) |
where ψε,j∈C∞0(BH(ξj,ε)) is a cut-off function. Clearly, (unψε,j)n is bounded in S1,p(Ω). It follows from (2.8) and the boundedness of (unψε,j)n that
⟨I′λ(un),unψε,j⟩→0, as n→∞, |
that is,
a(∫Ω|∇Hun|pψε,j+∫Ωun|∇Hun|p−2∇Hun∇Hψε,jdξ)+b‖un‖p(∫Ω|∇Hun|pψε,j+∫Ωun|∇Hun|p−2∇Hun∇Hψε,jdξ)−μ∫Ωϕun|un|pψε,jdξ=λ∫Ωuqnψε,jdξ+∫ΩuQ∗nψε,jdξ+o(1). | (2.13) |
It follows from the dominated convergence theorem that
∫BH(ξj,ε)|un|qψε,jdξ→∫BH(ξj,ε)|u|qψε,jdξ, as n→∞. |
Hence, letting ε→0, we get
limε→0limn→∞∫BH(ξj,ε)|un|qψε,jdξ=0. | (2.14) |
By Lemma 2.1,
limn→∞∫Ωϕun|un|p−2unudξ=∫Ωϕu|u|pdξ, | (2.15) |
and since un→u in Ls(Ω) with 1<s<Q∗, one has
∫Ω(ϕun|un|p−ϕun|un|p−1u)dξ≤∫Ω|ϕun||un|p−1|un−u|dξ≤(∫Ω|ϕun|un|p−1|pp−1dξ)p−1p|un−u|p→0. | (2.16) |
Combining (2.15) with (2.16), we obtain that
limn→∞∫Ωϕun|un|pdξ=∫Ωϕu|u|pdξ, |
thus
limε→0limn→∞∫BH(ξj,ε)ϕun|un|pψε,jdξ=limε→0∫BH(ξj,ε)ϕu|u|pψε,jdξ=0. | (2.17) |
Since
∫BH(ξj,ε)dξ=∫BH(0,ε)dξ=|BH(0,1)|εQ, |
applying the Hölder inequality, we obtain
limε→0limn→∞∫Ωun|∇Hun|p−1∇Hψε,jdξ≤limε→0limn→∞(∫BH(ξj,ε)|∇Hun|pdξ)p−1p(∫BH(ξj,ε)|un∇Hψε,j|pdξ)1p≤Climε→0(∫BH(ξj,ε)|un|p|∇Hψε,j|pdξ)1p≤Climε→0(∫BH(ξj,ε)|un|Q∗dξ)1Q∗(∫BH(ξj,ε)|∇Hψε,j|Qdξ)1Q=0. |
By (2.10), we have
limε→0limn→∞∫Ω|∇Hun|pψε,jdξ≥limε→0(ωj+∫BH(ξj,ε)|∇Hu|pψε,jdξ)=ωj | (2.18) |
and
limε→0limn→∞∫ΩuQ∗nψε,jdξ=limε→0(νj+∫BH(ξj,ε)uQ∗nψε,jdξ)=νj. | (2.19) |
Therefore, by (2.13)–(2.19), one gets νj≥aωj. It follows from (2.11) that
νj=0orνj≥(aS)Qp. |
In fact, if νj≥(aS)Qp holds, therefore by (2.8) and (2.10), for every μ<μ1, we have
c=limn→∞{Iλ(un)−1qI′λ(un)un}≥limn→∞(1q−1Q∗)∫Ω|un|Q∗dξ≥(1q−1Q∗)νj≥(1q−1Q∗)(aS)Qp, | (2.20) |
which contradicts (2.7). Thus, Λ=∅. By (2.10) and Λ=∅, we have
∫Ω|un|Q∗dξ→∫Ω|u|Q∗dξ. | (2.21) |
Let
limn→∞‖un‖p=A. |
If A=0, then un→0 in S1,p(Ω). So assume now that A>0. By (2.8), we get
a∫Ω|∇Hun|p−2∇Hun∇Hvdξ+bA∫Ω|∇Hun|p−2∇Hun∇Hvdξ −μ∫Ωϕun|un|p−2unvdξ−λ∫Ω|un|q−2unvdξ−∫Ω|un|Q∗−2unvdξ=o(1). | (2.22) |
Let v=u in (2.22). Then
a‖u‖p+bA‖u‖p−μ∫Ωϕu|u|pdξ−λ∫Ω|u|qdξ−∫Ω|u|Q∗dξ=0. | (2.23) |
By (2.8), (2.10), (2.21) and Lemma 2.1, one also has
limn→∞a‖un‖p+bA‖un‖p−μ∫Ωϕu|u|pdξ−λ∫Ω|u|qdξ−∫Ω|u|Q∗dξ=0. | (2.24) |
Thus, combining (2.23) and (2.24), we get limn→∞‖un‖p=‖u‖p. Thus, we see that un→u in S1,p(Ω) by the uniform convexity of S1,p(Ω). This completes the proof of Lemma 2.4.
We need the following auxiliary lemmas to prove our main result.
Lemma 3.1. Let q∈(2p,Q∗) and μ∈(0,μ1). Then functional Iλ satisfies the mountain pass geometry, that is,
(i) There exist constants ρ,α>0 satisfying Iλ(u)|∂Bρ≥α, for every u∈S1,p(Ω);
(ii) There exists e∈S1,p(Ω)∖¯Bρ satisfying Iλ(e)<0.
Proof. First, applying the Hölder inequality, we get
Iλ(u)=ap‖u‖p+b2p‖u‖2p−μ2p∫Ωϕu|u|pdξ−λq∫Ω|u|qdξ−1Q∗∫Ω|u|Q∗dξ≥ap‖u‖p+b−μˆC2p‖u‖2p−λq∫Ω|u|qdξ−1Q∗∫Ω|u|Q∗dξ≥ap‖u‖p−λqS−qp|Ω|Q∗−qQ∗‖u‖q−1Q∗S−Q∗p‖u‖Q∗=‖u‖p{ap−λqS−qp|Ω|Q∗−qQ∗‖u‖q−p−1Q∗S−Q∗p‖u‖Q∗−p}. | (3.1) |
Let
f(t)=ap−λqS−qp|Ω|Q∗−qQ∗tq−p−1Q∗S−Q∗ptQ∗−p, for every t≥0. |
We now show that there exists a constant ρ>0 satisfying f(ρ)≥ap. We see that f is a continuous function on [0,+∞) and limt→0+f(t)=ap. Hence there exists ρ such that f(t)≥ap−ε1, for every 0≤t≤ρ, where ρ is small enough such that ‖u‖=ρ. If we choose ε1=a2p, we have f(t)≥a2p, for every 0≤t≤ρ. In particular, f(ρ)≥a2p and we obtain Iλ(u)≥a2pρp=α for ‖u‖=ρ. Hence assertion (i) of Lemma 3.1 holds.
Next, we shall show that assertion (ⅱ) of Lemma 3.1 also holds:
Iλ(su)=aspp‖u‖p+bs2p2p‖u‖2p−μs2p2p∫Ωϕu|u|pdξ−λsqq∫Ω|u|qdξ−sQ∗Q∗∫Ω|u|Q∗dξ≤aspp‖u‖p+bs2p2p‖u‖2p−sQ∗Q∗∫Ω|u|Q∗dξ→−∞ as s→+∞. | (3.2) |
Thus, we can deduce that Iλ(s0u)<0 and s0‖u‖>ρ, for every s0 large enough. Let e=s0u. Then e is the desired function and the proof of (ⅱ) of Lemma 3.1 is complete.
Proof of Theorem 1.1(I). We claim that
0<cλ=infh∈Γmax0≤s≤1Iλ(h(s))<(1q−1Q∗)(aS)Qp, | (3.3) |
where
Γ={h∈C([0,1],S1,p(Ω)):h(0)=1,h(1)=e}. |
Indeed, we can choose v1∈S1,p(Ω)∖{0} with ‖v1‖=1. From (3.2), we have lims→+∞Iλ(sv1)=−∞. Then
sups≥0Iλ(sv1)=Iλ(sλv1), for some sλ>0. |
So sλ satisfies
aspλ‖v1‖p+bs2pλ‖v1‖2p=μs2pλ∫Ωϕv1|v1|pdξ+λsqλ∫Ω|v1|qdξ+sQ∗λ∫Ω|v1|Q∗dξ. | (3.4) |
Next, we shall prove that {sλ}μ>0 is bounded. In fact, suppose that the following hypothesis sλ≥1 is satisfied for every λ>0. Then it follows from (3.4) that
(a+b)s2pλ≥aspλ‖v1‖p+bs2pλ‖v1‖2p=μs2pλ∫Ωϕv1|v1|pdξ+λsqλ∫Ω|v1|qdξ+sQ∗λ∫Ω|v1|Q∗dξ≥sQ∗λ∫Ω|v1|Q∗dξ. | (3.5) |
Since 2p<q<Q∗, we can deduce that {sλ}λ>0 is bounded.
Next, we shall demonstrate that sλ→0, as λ→∞. Suppose to the contrary, that there exist sλ>0 and a sequence (λn)n with λn→∞, as n→∞, satisfying sλn→sλ, as n→∞. Invoking the Lebesgue dominated convergence theorem, we see that
∫Ω|sλnv1|qdξ→∫Ω|sλv1|qdξ, as n→∞. |
It now follows that
λn∫Ω|sλv1|qdξ→∞, as n→∞. |
Thus, invoking (3.4), we can show that this cannot happen. Therefore, sλ→0, as λ→∞.
Furthermore, (3.4) implies that
limλ→∞λ∫Ω|sλv1|qdξ=0 |
and
limλ→∞∫Ω|sλv1|Q∗dξ=0. |
Hence based on the definition of Iλ and sλ→0, as λ→∞, we get that
limλ→∞(sups≥0Iλ(sv1))=limλ→∞Iλ(sλv1)=0. |
So, there is λ1>0, satisfying for every λ>λ1,
sups≥0Iλ(sv1)<(1q−1Q∗)(aS)Qp. |
Letting e=t1v1 with t1 large enough for Iλ(e)<0, we get
0<cλ≤max0≤s≤1Iλ(h(s)), where h(s)=st1v1. |
Therefore
0<cλ≤sups≥0Iλ(sv1)<(1q−1Q∗)(aS)Qp, |
for λ large enough. This completes the proof of Theorem 1.1(Ⅰ).
In this subsection, we shall use the Krasnoselskii genus theory to prove Theorem 1.1(Ⅱ). To this end, let E be a Banach space and denote by Λ the class of all closed subsets A⊂E∖{0} that are symmetric with respect to the origin, that is, u∈E implies −u∈E. Moreover, suppose that X is k-dimensional and X=span{z1,⋯,zk}. For every n≥k, inductively select zn+1∉Xn=span{z1,⋯,zn}. Let Rn=R(Zn) and Υn=BRn⋂Zn. Define
Wn={φ∈C(Υn,E):φ|∂BRn⋂Zn=id and φ is odd} |
and
Γi={φ(¯Υn∖V):φ∈Wn,n≥i,V∈Λ,Λ is closed,γ(V)≤n−i}, |
where γ(V) is the Krasnoselskii genus of V.
Theorem 3.1. (see Rabinowitz [24, Theorem 9.12]) Let I∈C1(E,R) be even with I(0)=0 and let E be an infinite-dimensional Banach space. Assume that X is a finite-dimensional space, E=X⊕Y and that I satisfies the following properties:
(i) There exists θ>0 such that I satisfies (PS)c condition, for every c∈(0,θ);
(ii) There exist ρ,α>0 satifying I(u)≥α, for every u∈∂Bρ⋂Y;
(iii) For every finite-dimensional subspace ˜E⊂E, there exists R=R(˜E)>ρ such that I(u)≤0 on ˜E∖BR.
For every i∈N, let ci=infX∈Γimaxu∈ZI(u), hence, 0≤ci≤ci+1 and ci<θ, for every i>k. Then every ci is a critical value of I. Moreover, if ci=ci+1=⋯=ci+p=c<θ for i>k, then γ(Kc)≥p+1, where
Kc={u∈E:I(u)=c and I′(u)=0}. |
Lemma 3.2. There is a nondecreasing sequence {sn} of positive real numbers, independent of λ, such that for every λ>0, we have
cλn=infW∈Γnmaxu∈WIλ(u)<sn, |
where Γn was defined in Theorem 3.1.
Proof. By the definition of Γn, one has
cλn≤infW∈Γnmaxu∈W{ap‖un‖p+b2p‖un‖2p−μ2p∫Ωϕunupndξ−1Q∗∫Ω|un|Q∗dξ}=sn, |
therefore sn<∞ and sn≤sn+1.
Proof of Theorem 1.1(II). We note that Iλ satisfies Iλ(0)=0 and Iλ(−u)=Iλ(u). In the sequel, we shall divide the proof into the following three steps:
Step 1. We shall prove that Iλ satisfies hypothesis (ⅱ) of Theorem 3.1. Indeed, similar to the proof of (ⅰ) in Lemma 3.1, we can easily prove that the energy functional Iλ satisfies the hypothesis (ii) of Theorem 3.1.
Step 2. We shall prove that Iλ satisfies hypothesis (ⅲ) of Theorem 3.1. Indeed, let Y be a finite-dimensional subspace of S1,p(Ω). Since all norms in finite-dimensional space are equivalent, it follows that for every u∈Y, we have
Iλ(u)≤ap‖u‖p+b2p‖u‖2p−1Q∗∫Ω|u|Q∗dξ≤ap‖u‖p+b2p‖u‖2p−1Q∗C‖u‖Q∗, | (3.6) |
for some positive constant C>0. Also, because of 2p<Q∗, we can choose a large R>0 such that Iλ(u)≤0 on S1,p(Ω)∖BR. This fact implies that the energy functional Iλ satisfies the hypothesis (iii) of Theorem 3.1.
Step 3. We shall prove that problem (1.1) has infinitely many nontrivial weak solutions. Indeed, applying the argument in Wei and Wu [25], we can choose a1 large enough so that for every a>a1,
supsn<(1q−1Q∗)(aS)Qp, |
that is,
cλn<sn<(1q−1Q∗)(aS)Qp. |
Thus, one has
0<cλ1≤cλ2≤⋯≤cλn<sn<(1q−1Q∗)(aS)Qp. |
From Lemma 2.4, we know that Iλ satisfies (PS)cλi(i=1,2,⋯,n) condition. This fact implies that the levels cλ1≤cλ2≤⋯≤cλn are critical values of Iλ, which be guaranteed by an application of the Rabinowitz result [24, Proposition 9.30].
If cλi=cλi+1 where i=1,2,⋯,k−1, then applying the Ambrosetti and Rabinowitz result [26, Remark 2.12 and Theorem 4.2], we see that the set Kcλi consists of infinite number of different points, so problem (1.1) has infinite number of weak solutions. Hence, problem (1.1) has at least k pairs of solutions. Since k is arbitrary, we can conclude that problem (1.1) has infinitely many solutions. This completes the proof of Theorem 1.1(Ⅱ).
The authors declare they have not used Artificial Intelligence (AI) tools in the creation of this article.
Song was supported by the National Natural Science Foundation of China (No. 12001061), the Science and Technology Development Plan Project of Jilin Province, China (No. 20230101287JC) and Innovation and Entrepreneurship Talent Funding Project of Jilin Province (No. 2023QN21). Repovš was supported by the Slovenian Research Agency program No. P1-0292 and grants Nos. J1-4031, J1-4001, N1-0278, N1-0114 and N1-0083.
The authors declare there is no conflict of interest.
[1] |
Takaoka A, Wang Z, Choi MK, et al. (2007) DAI (DLM-1/ZBP1) is a cytosolic DNA sensor and an activator of innate immune response. Nature 448: 501–505. doi: 10.1038/nature06013
![]() |
[2] |
Kim T, Pazhoor S, Bao M, et al. (2010) Aspartate-glutamate-alanine-histidine box motif (DEAH)/RNA helicase A helicases sense microbial DNA in human plasmacytoid dendritic cells. Proc Natl Acad Sci USA 107: 15181–15186. doi: 10.1073/pnas.1006539107
![]() |
[3] |
Parvatiyar K, Zhang Z, Teles RM, et al. (2012) The helicase DDX41 recognizes the bacterial secondary messengers cyclic di-GMP and cyclic di-AMP to activate a type I interferon immune response. Nat Immunol 13: 1155–1161. doi: 10.1038/ni.2460
![]() |
[4] |
Zhang Z, Yuan B, Bao M, et al. (2011) The helicase DDX41 senses intracellular DNA mediated by the adaptor STING in dendritic cells. Nat Immunol 12: 959–965. doi: 10.1038/ni.2091
![]() |
[5] |
Chiu YH, MacMillan JB, Chen ZJ (2009) RNA polymerase III detects cytosolic DNA and induces type I interferons through the RIG-I pathway. Cell 138: 576–591. doi: 10.1016/j.cell.2009.06.015
![]() |
[6] |
Zhang X, Brann TW, Zhou M, et al. (2011) Ku70 is a novel cytosolic DNA sensor that induces type-III rather than type-I IFN. J Immunol 186: 4541–4545. doi: 10.4049/jimmunol.1003389
![]() |
[7] |
Kondo T, Kobayashi J, Saitoh T, et al. (2013) DNA damage sensor MRE11 recognizes cytosolic double-stranded DNA and induces type I interferon by regulating STING trafficking. Proc Natl Acad Sci USA 110: 2969–2974. doi: 10.1073/pnas.1222694110
![]() |
[8] |
Xia P, Wang S, Ye B, et al. (2015) Sox2 functions as a sequence-specific DNA sensor in neutrophils to initiate innate immunity against microbial infection. Nat Immunol 16: 366–375. doi: 10.1038/ni.3117
![]() |
[9] |
Yang P, An H, Liu X, et al. (2010) The cytosolic nucleic acid sensor LRRFIP1 mediates the production of type I interferon via a beta-catenin-dependent pathway. Nat Immunol 11: 487–494. doi: 10.1038/ni.1876
![]() |
[10] | Pichlmair A, Lassnig C, Eberle CA, et al. (2011) IFIT1 is an antiviral protein that recognizes 5'-triphosphate RNA. Nat Immunol 12: 624–630. |
[11] |
Hornung V, Hartmann R, Ablasser A, et al. (2014) OAS proteins and cGAS: unifying concepts in sensing and responding to cytosolic nucleic acids. Nat Rev Immunol 14: 521–528. doi: 10.1038/nri3719
![]() |
[12] |
Ori D, Murase M, Kawai T (2017) Cytosolic nucleic acid sensors and innate immune regulation. Int Rev Immunol 36: 74–88. doi: 10.1080/08830185.2017.1298749
![]() |
[13] |
Xia P, Wang S, Gao P, et al. (2016) DNA sensor cGAS-mediated immune recognition. Protein Cell 7: 777–791. doi: 10.1007/s13238-016-0320-3
![]() |
[14] |
Schlee M, Hartmann G (2016) Discriminating self from non-self in nucleic acid sensing. Nat Rev Immunol 16: 566–580. doi: 10.1038/nri.2016.78
![]() |
[15] |
Ning S, Pagano J, Barber G (2011) IRF7: activation, regulation, modification, and function. Genes Immun 12: 399–414. doi: 10.1038/gene.2011.21
![]() |
[16] |
Chen Q, Sun L, Chen ZJ (2016) Regulation and function of the cGAS-STING pathway of cytosolic DNA sensing. Nat Immunol 17: 1142–1149. doi: 10.1038/ni.3558
![]() |
[17] |
Wilson EB, Yamada DH, Elsaesser H, et al. (2013) Blockade of chronic type I interferon signaling to control persistent LCMV infection. Science 340: 202–207. doi: 10.1126/science.1235208
![]() |
[18] |
Teijaro JR, Ng C, Lee AM, et al. (2013) Persistent LCMV infection is controlled by blockade of type I interferon signaling. Science 340: 207–211. doi: 10.1126/science.1235214
![]() |
[19] |
Cha L, Berry CM, Nolan D, et al. (2014) Interferon-alpha, immune activation and immune dysfunction in treated HIV infection. Clin Trans Immunol 3: e10. doi: 10.1038/cti.2014.1
![]() |
[20] |
Catalfamo M, Wilhelm C, Tcheung L, et al. (2011) CD4 and CD8 T cell immune activation during chronic HIV infection: roles of homeostasis, HIV, type I IFN, and IL-7. J Immunol 186: 2106–2116. doi: 10.4049/jimmunol.1002000
![]() |
[21] |
Crouse J, Kalinke U, Oxenius A (2015) Regulation of antiviral T cell responses by type I interferons. Nat Rev Immunol 15: 231–242. doi: 10.1038/nri3806
![]() |
[22] |
Bosque A, Planelles V (2009) Induction of HIV-1 latency and reactivation in primary memory CD4+ T cells. Blood 113: 58–65. doi: 10.1182/blood-2008-07-168393
![]() |
[23] |
Härtlova A, Erttmann SF, Raffi FAM, et al. (2015) DNA damage primes the type i interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity. Immunity 42: 332–343. doi: 10.1016/j.immuni.2015.01.012
![]() |
[24] |
White MJ, McArthur K, Metcalf D, et al. (2014) Apoptotic caspases suppress mtDNA-induced STING-mediated type I IFN production. Cell 159: 1549–1562. doi: 10.1016/j.cell.2014.11.036
![]() |
[25] |
Vilenchik MM, Knudson AG (2003) Endogenous DNA double-strand breaks: production, fidelity of repair, and induction of cancer. Proc Natl Acad Sci USA 100: 12871–12876. doi: 10.1073/pnas.2135498100
![]() |
[26] |
de Galarreta MR, Lujambio A (2017) DNA sensing in senescence. Nat Cell Biol 19: 1008–1009. doi: 10.1038/ncb3603
![]() |
[27] | Gluck S, Guey B, Gulen MF, et al. (2017) Innate immune sensing of cytosolic chromatin fragments through cGAS promotes senescence. Nat Cell Biol 19: In press. |
[28] | Ng KW, Marshall EA, Bell JC, et al. (2017) cGAS-STING and cancer: dichotomous roles in tumor immunity and development. Trends Immunol: In press. |
[29] |
Yang H, Wang H, Ren J, et al. (2017) cGAS is essential for cellular senescence. Proc Natl Acad Sci USA 114: E4612–E4620. doi: 10.1073/pnas.1705499114
![]() |
[30] |
Baccala R, Hoebe K, Kono DH, et al. (2007) TLR-dependent and TLR-independent pathways of type I interferon induction in systemic autoimmunity. Nat Med 13: 543–551. doi: 10.1038/nm1590
![]() |
[31] |
Shibutani ST, Saitoh T, Nowag H, et al. (2015) Autophagy and autophagy-related proteins in the immune system. Nat Immunol 16: 1014–1024. doi: 10.1038/ni.3273
![]() |
[32] |
Agod Z, Fekete T, Budai MM, et al. (2017) Regulation of type I interferon responses by mitochondria-derived reactive oxygen species in plasmacytoid dendritic cells. Redox Biol 13: 633–645. doi: 10.1016/j.redox.2017.07.016
![]() |
[33] |
McNab F, Mayer-Barber K, Sher A, et al. (2015) Type I interferons in infectious disease. Nat Rev Immunol 15: 87–103. doi: 10.1038/nri3787
![]() |
[34] |
Forster S (2012) Interferon signatures in immune disorders and disease. Immunol Cell Biol 90: 520–527. doi: 10.1038/icb.2012.12
![]() |
[35] |
Elkon KB, Wiedeman A (2012) Type I IFN system in the development and manifestations of SLE. Curr Opin Rheumatol 24: 499–505. doi: 10.1097/BOR.0b013e3283562c3e
![]() |
[36] |
Sandler NG, Bosinger SE, Estes JD, et al. (2014) Type I interferon responses in rhesus macaques prevent SIV infection and slow disease progression. Nature 511: 601–605. doi: 10.1038/nature13554
![]() |
[37] |
Mogensen T, Melchjorsen J, Larsen C, et al. (2010) Innate immune recognition and activation during HIV infection. Retrovirology 7: 54. doi: 10.1186/1742-4690-7-54
![]() |
[38] |
Tough DF (2012) Modulation of T-cell function by type I interferon. Immunol Cell Biol 90: 492–497. doi: 10.1038/icb.2012.7
![]() |
[39] |
Zitvogel L, Galluzzi L, Kepp O, et al. (2015) Type I interferons in anticancer immunity. Nat Rev Immunol 15: 405–414. doi: 10.1038/nri3845
![]() |
[40] |
Gajewski TF, Corrales L (2015) New perspectives on type I IFNs in cancer. Cytokine Growth F R 26: 175–178. doi: 10.1016/j.cytogfr.2015.01.001
![]() |
[41] | Dominguez-Villar M, Gautron AS, de Marcken M, et al. (2015) TLR7 induces anergy in human CD4+ T cells. Nat Immunol 16: 118–128. |
[42] | Andreeva L, Hiller B, Kostrewa D, et al. (2017) cGAS senses long and HMGB/TFAM-bound U-turn DNA by forming protein-DNA ladders. Nature: In press. |
[43] |
Cordaux R, Batzer MA (2009) The impact of retrotransposons on human genome evolution. Nat Rev Genet 10: 691–703. doi: 10.1038/nrg2640
![]() |
[44] | Liu S, Cai X, Wu J, et al. (2015) Phosphorylation of innate immune adaptor proteins MAVS, STING, and TRIF induces IRF3 activation. Science 347. |
[45] |
Wang Q, Liu X, Cui Y, et al. (2014) The E3 ubiquitin ligase AMFR and INSIG1 bridge the activation of TBK1 kinase by modifying the adaptor STING. Immunity 41: 919–933. doi: 10.1016/j.immuni.2014.11.011
![]() |
[46] |
Man SM, Karki R, Kanneganti TD (2016) AIM2 inflammasome in infection, cancer, and autoimmunity: role in DNA sensing, inflammation, and innate immunity. Eur J Immunol 46: 269–280. doi: 10.1002/eji.201545839
![]() |
[47] |
Diner BA, Lum KK, Cristea IM (2015) The emerging role of nuclear viral DNA sensors. J Biol Chem 290: 26412–26421. doi: 10.1074/jbc.R115.652289
![]() |
[48] |
West AP, Khoury-Hanold W, Staron M, et al. (2015) Mitochondrial DNA stress primes the antiviral innate immune response. Nature 520: 553–557. doi: 10.1038/nature14156
![]() |
[49] |
Ansari MA, Singh VV, Dutta S, et al. (2013) Constitutive interferon-inducible protein 16-inflammasome activation during Epstein-Barr virus latency I, II, and III in B and epithelial cells. J Virol 87: 8606–8623. doi: 10.1128/JVI.00805-13
![]() |
[50] |
Christensen MH, Paludan SR (2017) Viral evasion of DNA-stimulated innate immune responses. Cell Mol Immunol 14: 4–13. doi: 10.1038/cmi.2016.06
![]() |
[51] |
Zevini A, Olagnier D, Hiscott J (2017) Crosstalk between cytoplasmic RIG-I and STING sensing pathways. Trends Immunol 38: 194–205. doi: 10.1016/j.it.2016.12.004
![]() |
[52] |
Satoh T, Kato H, Kumagai Y, et al. (2010) LGP2 is a positive regulator of RIG-I- and MDA5-mediated antiviral responses. Proc Natl Acad Sci USA 107: 1512–1517. doi: 10.1073/pnas.0912986107
![]() |
[53] |
Kato K, Omura H, Ishitani R, et al. (2017) Cyclic GMP-AMP as an endogenous second messenger in innate immune signaling by cytosolic DNA. Annu Rev Biochem 86: 541–566. doi: 10.1146/annurev-biochem-061516-044813
![]() |
[54] |
Wu JJ, Li W, Shao Y, et al. (2015) Inhibition of cGAS DNA sensing by a herpesvirus virion protein. Cell Host Microbe 18: 333–344. doi: 10.1016/j.chom.2015.07.015
![]() |
[55] |
Li W, Avey D, Fu B, et al. (2016) Kaposi's sarcoma-associated herpesvirus inhibitor of cGAS (KicGAS), encoded by orf52, is an abundant tegument protein and is required for production of infectious progeny viruses. J Virol 90: 5329–5342. doi: 10.1128/JVI.02675-15
![]() |
[56] |
Ma Z, Jacobs SR, West JA, et al. (2015) Modulation of the cGAS-STING DNA sensing pathway by gammaherpesviruses. Proc Natl Acad Sci USA 112: E4306–E4315. doi: 10.1073/pnas.1503831112
![]() |
[57] |
Hwang SW, Kim D, Jung JU, et al. (2017) KSHV-encoded viral interferon regulatory factor 4 (vIRF4) interacts with IRF7 and inhibits interferon alpha production. Biochem Bioph Res Co 486: 700–705. doi: 10.1016/j.bbrc.2017.03.101
![]() |
[58] |
Lau L, Gray EE, Brunette RL, et al. (2015) DNA tumor virus oncogenes antagonize the cGAS-STING DNA-sensing pathway. Science 350: 568–571. doi: 10.1126/science.aab3291
![]() |
[59] | de Souza RF, Iyer LM, Aravind L (2010) Diversity and evolution of chromatin proteins encoded by DNA viruses. BBA-Gene Regul Mech 1799: 302–318. |
[60] |
Towers GJ, Noursadeghi M (2014) Interactions between HIV-1 and the cell-autonomous innate immune system. Cell Host Microbe 16: 10–18. doi: 10.1016/j.chom.2014.06.009
![]() |
[61] | Sandstrom TS, Ranganath N, Angel JB (2017) Impairment of the type I interferon response by HIV-1: potential targets for HIV eradication. Cytokine Growth F R: In press. |
[62] |
Rongvaux A, Jackson R, Harman CCD, et al. (2014) Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA. Cell 159: 1563–1577. doi: 10.1016/j.cell.2014.11.037
![]() |
[63] |
Zheng Q, Hou J, Zhou Y, et al. (2017) The RNA helicase DDX46 inhibits innate immunity by entrapping m6A-demethylated antiviral transcripts in the nucleus. Nat Immunol 18: 1094–1103. doi: 10.1038/ni.3830
![]() |
[64] | Boss IW, Renne R (2011) Viral miRNAs and immune evasion. BBA-Gene Regul Mech 1809: 708–714. |
[65] |
Cullen BR (2013) MicroRNAs as mediators of viral evasion of the immune system. Nat Immunol 14: 205–210. doi: 10.1038/ni.2537
![]() |
[66] |
Wang L, Li G, Yao ZQ, et al. (2015) MicroRNA regulation of viral immunity, latency, and carcinogenesis of selected tumor viruses and HIV. Rev Med Virol 25: 320–341. doi: 10.1002/rmv.1850
![]() |
[67] |
Ding L, Huang XF, Dong GJ, et al. (2015) Activated STING enhances Tregs infiltration in the HPV-related carcinogenesis of tongue squamous cells via the c-jun/CCL22 signal. BBA-Mol Basis Dis 1852: 2494–2503. doi: 10.1016/j.bbadis.2015.08.011
![]() |
[68] |
Yarbrough ML, Zhang K, Sakthivel R, et al. (2014) Primate-specific miR-576-3p sets host defense signaling threshold. Nat Commun 5: 4963–4963. doi: 10.1038/ncomms5963
![]() |
[69] |
Wu MZ, Cheng WC, Chen SF, et al. (2017) miR-25/93 mediates hypoxia-induced immunosuppression by repressing cGAS. Nat Cell Biol 19: 1286–1296. doi: 10.1038/ncb3615
![]() |
[70] |
Yuan F, Dutta T, Wang L, et al. (2015) Human DNA exonuclease TREX1 is also an exoribonuclease that acts on single-stranded RNA. J Biol Chem 290: 13344–13353. doi: 10.1074/jbc.M115.653915
![]() |
[71] |
Samuel CE (2011) Adenosine deaminases acting on RNA (ADARs) are both antiviral and proviral dependent upon the virus. Virology 411: 180–193. doi: 10.1016/j.virol.2010.12.004
![]() |
[72] |
Liddicoat BJ, Piskol R, Chalk AM, et al. (2015) RNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonself. Science 349: 1115–1120. doi: 10.1126/science.aac7049
![]() |
[73] |
Yang S, Deng P, Zhu Z, et al. (2014) ADAR1 Limits RIG-I RNA detection and suppresses IFN production responding to viral and endogenous RNAs. J Immunol 193: 3436–3445. doi: 10.4049/jimmunol.1401136
![]() |
[74] |
Wang Q, Li X, Qi R, et al. (2017) RNA Editing, ADAR1, and the innate immune response. Genes 8: 41. doi: 10.3390/genes8010041
![]() |
[75] |
Gandy SZ, Linnstaedt SD, Muralidhar S, et al. (2007) RNA editing of the human herpesvirus 8 kaposin transcript eliminates its transforming activity and is induced during lytic replication. J Virol 81: 13544–13551. doi: 10.1128/JVI.01521-07
![]() |
[76] |
Iizasa H, Wulff BE, Alla NR, et al. (2010) Editing of Epstein-Barr virus-encoded BART6 microRNAs controls their dicer targeting and consequently affects viral latency. J Biol Chem 285: 33358–33370. doi: 10.1074/jbc.M110.138362
![]() |
[77] |
Rebhandl S, Huemer M, Greil R, et al. (2015) AID/APOBEC deaminases and cancer. Oncoscience 2: 320–333. doi: 10.18632/oncoscience.155
![]() |
[78] |
Konno H, Konno K, Barber GN (2013) Cyclic dinucleotides trigger ULK1 (ATG1) phosphorylation of STING to prevent sustained innate immune signaling. Cell 155: 688–698. doi: 10.1016/j.cell.2013.09.049
![]() |
[79] |
Seo GJ, Yang A, Tan B, et al. (2015) Akt kinase-mediated checkpoint of cGAS DNA sensing pathway. Cell Rep 13: 440–449. doi: 10.1016/j.celrep.2015.09.007
![]() |
[80] | Li S, Zhu M, Pan R, et al. (2016) The tumor suppressor PTEN has a critical role in antiviral innate immunity. Nat Immunol 17: 241–249. |
[81] | Nekhai S, Jerebtsova M, Jackson A, et al. (2007) Regulation of HIV-1 transcription by protein phosphatase 1. Curr Hiv Res 5: 3–9. |
[82] |
Wies E, Wang MK, Maharaj NP, et al. (2013) Dephosphorylation of the RNA sensors RIG-I and MDA5 by the phosphatase PP1 is essential for innate immune signaling. Immunity 38: 437–449. doi: 10.1016/j.immuni.2012.11.018
![]() |
[83] |
Davis ME, Wang MK, Rennick LJ, et al. (2014) Antagonism of the phosphatase PP1 by the measles virus V protein is required for innate immune escape of MDA5. Cell Host Microbe 16: 19–30. doi: 10.1016/j.chom.2014.06.007
![]() |
[84] |
Opaluch AM, Schneider M, Chiang CY, et al. (2014) Positive regulation of TRAF6-dependent innate immune responses by protein phosphatase PP1-gamma. Plos One 9: e89284. doi: 10.1371/journal.pone.0089284
![]() |
[85] |
Ilinykh PA, Tigabu B, Ivanov A, et al. (2014) Role of protein phosphatase 1 in dephosphorylation of Ebola virus VP30 protein and its targeting for the inhibition of viral transcription. J Biol Chem 289: 22723–22738. doi: 10.1074/jbc.M114.575050
![]() |
[86] | Cougot D, Allemand E, Rivière L, et al. (2012) Inhibition of PP1 phosphatase activity by HBx: a mechanism for the activation of hepatitis B virus transcription. Sci Signal 5: ra1. |
[87] | Gu M, Zhang T, Lin W, et al. (2014) Protein phosphatase PP1 negatively regulates the Toll-like receptor- and RIG-I-like receptor-triggered production of type I interferon by inhibiting IRF3 phosphorylation at serines 396 and 385 in macrophage. Sci Signal: In press. |
[88] |
Gu M, Ouyang C, Lin W, et al. (2014) Phosphatase holoenzyme PP1/GADD34 negatively regulates TLR response by inhibiting TAK1 serine 412 phosphorylation. J Immunol 192: 2846–2856. doi: 10.4049/jimmunol.1302537
![]() |
[89] | Clavarino G, Claudio N, Dalet A, et al. (2012) Protein phosphatase 1 subunit Ppp1r15a/GADD34 regulates cytokine production in polyinosinic: polycytidylic acid-stimulated dendritic cells. Proc Natl Acad Sci USA: In press. |
[90] |
Peng D, Wang Z, Huang A, et al. (2017) A novel function of F-Box protein FBXO17 in negative regulation of type I IFN signaling by recruiting PP2A for IFN regulatory factor 3 deactivation. J Immunol 198: 808–819. doi: 10.4049/jimmunol.1601009
![]() |
[91] |
Shanker V, Trincucci G, Heim HM, et al. (2013) Protein phosphatase 2A impairs IFNα-induced antiviral activity against the hepatitis C virus through the inhibition of STAT1 tyrosine phosphorylation. J Viral Hepatitis 20: 612–621. doi: 10.1111/jvh.12083
![]() |
[92] |
Wang L, Zhao J, Ren J, et al. (2016) Protein phosphatase 1 abrogates IRF7-mediated type I IFN response in antiviral immunity. Eur J Immunol 46: 2409–2419. doi: 10.1002/eji.201646491
![]() |
[93] | Davis ME, Gack MU (2015) Ubiquitination in the antiviral immune response. Virology 479–480: 52–65. |
[94] |
Lin D, Zhong B (2015) Regulation of cellular innate antiviral signaling by ubiquitin modification. Acta Biochim Biophys Sin (Shanghai) 47: 149–155. doi: 10.1093/abbs/gmu133
![]() |
[95] |
Heaton SM, Borg NA, Dixit VM (2016) Ubiquitin in the activation and attenuation of innate antiviral immunity. J Exp Med 213: 1–13. doi: 10.1084/jem.20151531
![]() |
[96] |
Zhou Y, He C, Lin W, et al. (2017) Post-translational regulation of antiviral innate signaling. Eur J Immunol 47: 1414–1426. doi: 10.1002/eji.201746959
![]() |
[97] |
van Tol S, Hage A, Giraldo M, et al. (2017) The TRIMendous role of TRIMs in virus-host interactions. Vaccines 5: 23. doi: 10.3390/vaccines5030023
![]() |
[98] |
Damgaard RB, Nachbur U, Yabal M, et al. (2012) The ubiquitin ligase XIAP recruits LUBAC for NOD2 signaling in inflammation and innate immunity. Mol Cell 46: 746–758. doi: 10.1016/j.molcel.2012.04.014
![]() |
[99] |
Keusekotten K, Elliott PR, Glockner L, et al. (2013) OTULIN antagonizes LUBAC signaling by specifically hydrolyzing Met1-linked polyubiquitin. Cell 153: 1312–1326. doi: 10.1016/j.cell.2013.05.014
![]() |
[100] |
Rivkin E, Almeida SM, Ceccarelli DF, et al. (2013) The linear ubiquitin-specific deubiquitinase gumby regulates angiogenesis. Nature 498: 318–324. doi: 10.1038/nature12296
![]() |
[101] |
Takiuchi T, Nakagawa T, Tamiya H, et al. (2014) Suppression of LUBAC-mediated linear ubiquitination by a specific interaction between LUBAC and the deubiquitinases CYLD and OTULIN. Genes Cells 19: 254–272. doi: 10.1111/gtc.12128
![]() |
[102] |
Tokunaga F, Nishimasu H, Ishitani R, et al. (2012) Specific recognition of linear polyubiquitin by A20 zinc finger 7 is involved in NFκB regulation. Embo J 31: 3856–3870. doi: 10.1038/emboj.2012.241
![]() |
[103] |
Hrdinka M, Fiil BK, Zucca M, et al. (2016) CYLD Limits Lys63- and Met1-Linked Ubiquitin at receptor complexes to regulate innate immune signaling. Cell Rep 14: 2846–2858. doi: 10.1016/j.celrep.2016.02.062
![]() |
[104] |
Damgaard RB, Walker JA, Marco-Casanova P, et al. (2016) The deubiquitinase OTULIN is an essential negative regulator of inflammation and autoimmunity. Cell 166: 1215–1230. doi: 10.1016/j.cell.2016.07.019
![]() |
[105] |
Wang Q, Huang L, Hong Z, et al. (2017) The E3 ubiquitin ligase RNF185 facilitates the cGAS-mediated innate immune response. Plos Pathog 13: e1006264. doi: 10.1371/journal.ppat.1006264
![]() |
[106] | Ni G, Konno H, Barber GN (2017) Ubiquitination of STING at lysine 224 controls IRF3 activation. Sci Immunol 2: In Press. |
[107] |
Zhang J, Hu MM, Wang YY, et al. (2012) TRIM32 protein modulates type I interferon induction and cellular antiviral response by targeting MITA/STING protein for K63-linked ubiquitination. J Biol Chem 287: 28646–28655. doi: 10.1074/jbc.M112.362608
![]() |
[108] |
Tsuchida T, Zou J, Saitoh T, et al. (2010) The ubiquitin ligase TRIM56 regulates innate immune responses to intracellular double-stranded DNA. Immunity 33: 765–776. doi: 10.1016/j.immuni.2010.10.013
![]() |
[109] |
Wang J, Yang S, Liu L, et al. (2017) HTLV-1 Tax impairs K63-linked ubiquitination of STING to evade host innate immunity. Virus Res 232: 13–21. doi: 10.1016/j.virusres.2017.01.016
![]() |
[110] |
Liu Y, Li J, Chen J, et al. (2015) Hepatitis B virus polymerase disrupts K63-linked ubiquitination of STING to block innate cytosolic DNA-sensing pathways. J Virol 89: 2287–2300. doi: 10.1128/JVI.02760-14
![]() |
[111] |
Zhong B, Zhang L, Lei C, et al. (2009) The ubiquitin ligase RNF5 regulates antiviral responses by mediating degradation of the adaptor protein MITA. Immunity 30: 397–407. doi: 10.1016/j.immuni.2009.01.008
![]() |
[112] |
Wang Y, Lian Q, Yang B, et al. (2015) TRIM30α is a negative-feedback regulator of the intracellular DNA and DNA virus-triggered response by targeting STING. Plos Pathog 11: e1005012. doi: 10.1371/journal.ppat.1005012
![]() |
[113] |
Qin Y, Zhou MT, Hu MM, et al. (2014) RNF26 temporally regulates virus-triggered type I interferon induction by two distinct mechanisms. Plos Pathog 10: e1004358. doi: 10.1371/journal.ppat.1004358
![]() |
[114] |
Chen Y, Wang L, Jin J, et al. (2017) p38 inhibition provides anti-DNA virus immunity by regulation of USP21 phosphorylation and STING activation. J Exp Med 214: 991–1010. doi: 10.1084/jem.20161387
![]() |
[115] |
Lang X, Tang T, Jin T, et al. (2017) TRIM65-catalized ubiquitination is essential for MDA5-mediated antiviral innate immunity. J Exp Med 214: 459–473. doi: 10.1084/jem.20160592
![]() |
[116] | Liu B, Zhang M, Chu H, et al. (2017) The ubiquitin E3 ligase TRIM31 promotes aggregation and activation of the signaling adaptor MAVS through Lys63-linked polyubiquitination. Nat Immunol 18: 214–224. |
[117] |
Narayan K, Waggoner L, Pham ST, et al. (2014) TRIM13 is a negative regulator of MDA5-mediated type I interferon production. J Virol 88: 10748–10757. doi: 10.1128/JVI.02593-13
![]() |
[118] |
Gao D, Yang YK, Wang RP, et al. (2009) REUL is a novel E3 ubiquitin ligase and stimulator of retinoic-acid-inducible gene-I. Plos One 4: e5760. doi: 10.1371/journal.pone.0005760
![]() |
[119] |
Oshiumi H, Matsumoto M, Hatakeyama S, et al. (2009) Riplet/RNF135, a RING-finger protein, ubiquitinates RIG-I to promote interferon-beta induction during the early phase of viral infection. J Biol Chem 284: 807–817. doi: 10.1074/jbc.M804259200
![]() |
[120] |
Gack MU, Shin YC, Joo CH, et al. (2007) TRIM25 RING-finger E3 ubiquitin ligase is essential for RIG-I-mediated antiviral activity. Nature 446: 916–920. doi: 10.1038/nature05732
![]() |
[121] |
Jiang J, Li J, Fan W, et al. (2016) Robust Lys63-linked ubiquitination of RIG-I promotes cytokine eruption in early influenza B virus infection. J Virol 90: 6263–6275. doi: 10.1128/JVI.00549-16
![]() |
[122] |
Yan J, Li Q, Mao AP, et al. (2014) TRIM4 modulates type I interferon induction and cellular antiviral response by targeting RIG-I for K63-linked ubiquitination. J Mol Cell Biol 6: 154–163. doi: 10.1093/jmcb/mju005
![]() |
[123] |
Wang W, Jiang M, Liu S, et al. (2016) RNF122 suppresses antiviral type I interferon production by targeting RIG-I CARDs to mediate RIG-I degradation. Proc Natl Acad Sci USA 113: 9581–9586. doi: 10.1073/pnas.1604277113
![]() |
[124] |
Arimoto K, Takahashi H, Hishiki T, et al. (2007) Negative regulation of the RIG-I signaling by the ubiquitin ligase RNF125. Proc Natl Acad Sci USA 104: 7500–7505. doi: 10.1073/pnas.0611551104
![]() |
[125] |
Ning S, Campos AD, Darnay B, et al. (2008) TRAF6 and the three C-terminal lysine sites on IRF7 are required for its ubiquitination-mediated activation by the tumor necrosis factor receptor family member latent membrane protein 1. Mol Cell Biol 28: 6536–6546. doi: 10.1128/MCB.00785-08
![]() |
[126] |
Ning S, Pagano J (2010) The A20 deubiquitinase activity negatively regulates LMP1 activation of IRF7. J Virol 84: 6130–6138. doi: 10.1128/JVI.00364-10
![]() |
[127] |
Iwai K, Fujita H, Sasaki Y (2014) Linear ubiquitin chains: NF-kappaB signalling, cell death and beyond. Nat Rev Mol Cell Bio 15: 503–508. doi: 10.1038/nrm3836
![]() |
[128] |
Rieser E, Cordier SM, Walczak H (2013) Linear ubiquitination: a newly discovered regulator of cell signalling. Trends Biochem Sci 38: 94–102. doi: 10.1016/j.tibs.2012.11.007
![]() |
[129] |
Tokunaga F (2013) Linear ubiquitination-mediated NF-kappaB regulation and its related disorders. J Biochem 154: 313–323. doi: 10.1093/jb/mvt079
![]() |
[130] |
Tokunaga F, Iwai K (2012) Linear ubiquitination: a novel NF-kappaB regulatory mechanism for inflammatory and immune responses by the LUBAC ubiquitin ligase complex. Endocr J 59: 641–652. doi: 10.1507/endocrj.EJ12-0148
![]() |
[131] |
Shimizu Y, Taraborrelli L, Walczak H (2015) Linear ubiquitination in immunity. Immunol Rev 266: 190–207. doi: 10.1111/imr.12309
![]() |
[132] |
Ikeda F (2015) Linear ubiquitination signals in adaptive immune responses. Immunol Rev 266: 222–236. doi: 10.1111/imr.12300
![]() |
[133] |
Ikeda F, Deribe YL, Skanland SS, et al. (2011) SHARPIN forms a linear ubiquitin ligase complex regulating NF-kappaB activity and apoptosis. Nature 471: 637–641. doi: 10.1038/nature09814
![]() |
[134] |
Tokunaga F, Nakagawa T, Nakahara M, et al. (2011) SHARPIN is a component of the NF-kappaB-activating linear ubiquitin chain assembly complex. Nature 471: 633–636. doi: 10.1038/nature09815
![]() |
[135] |
Tian Y, Zhang Y, Zhong B, et al. (2007) RBCK1 negatively regulates tumor necrosis factor- and interleukin-1-triggered NF-kappaB activation by targeting TAB2/3 for degradation. J Biol Chem 282: 16776–16782. doi: 10.1074/jbc.M701913200
![]() |
[136] |
Niu J, Shi Y, Iwai K, et al. (2011) LUBAC regulates NF-kappaB activation upon genotoxic stress by promoting linear ubiquitination of NEMO. EMBO J 30: 3741–3753. doi: 10.1038/emboj.2011.264
![]() |
[137] |
Hostager BS, Kashiwada M, Colgan JD, et al. (2011) HOIL-1L interacting protein (HOIP) is essential for CD40 signaling. Plos One 6: e23061. doi: 10.1371/journal.pone.0023061
![]() |
[138] |
Zak DE, Schmitz F, Gold ES, et al. (2011) Systems analysis identifies an essential role for SHANK-associated RH domain-interacting protein (SHARPIN) in macrophage Toll-like receptor 2 (TLR2) responses. Proc Natl Acad Sci USA 108: 11536–11541. doi: 10.1073/pnas.1107577108
![]() |
[139] |
Rodgers MA, Bowman JW, Fujita H, et al. (2014) The linear ubiquitin assembly complex (LUBAC) is essential for NLRP3 inflammasome activation. J Exp Med 211: 1333–1347. doi: 10.1084/jem.20132486
![]() |
[140] |
Kirisako T, Kamei K, Murata S, et al. (2006) A ubiquitin ligase complex assembles linear polyubiquitin chains. EMBO J 25: 4877–4887. doi: 10.1038/sj.emboj.7601360
![]() |
[141] |
Emmerich CH, Schmukle AC, Walczak H (2011) The emerging role of linear ubiquitination in cell signaling. Sci Signal 4: re5. doi: 10.1126/scisignal.2001798
![]() |
[142] |
Tokunaga F, Sakata Si, Saeki Y, et al. (2009) Involvement of linear polyubiquitylation of NEMO in NF-kappa B activation. Nat Cell Biol 11: 123–132. doi: 10.1038/ncb1821
![]() |
[143] |
Inn KS, Gack MU, Tokunaga F, et al. (2011) Linear ubiquitin assembly complex negatively regulates RIG-I- and TRIM25-mediated type I interferon induction. Mol Cell 41: 354–365. doi: 10.1016/j.molcel.2010.12.029
![]() |
[144] |
Zhang M, Tian Y, Wang RP, et al. (2008) Negative feedback regulation of cellular antiviral signaling by RBCK1-mediated degradation of IRF3. Cell Res 18: 1096–1104. doi: 10.1038/cr.2008.277
![]() |
[145] |
Belgnaoui SM, Paz S, Samuel S, et al. (2012) Linear ubiquitination of NEMO negatively regulates the interferon antiviral response through disruption of the MAVS-TRAF3 complex. Cell Host Microbe 12: 211–222. doi: 10.1016/j.chom.2012.06.009
![]() |
[146] | Wang L, Wang Y, Zhao J, et al. (2017) LUBAC modulates LMP1 activation of NFκB and IRF7. J Virol 91: e1138–e1116. |
[147] |
Orzalli MH, DeLuca NA, Knipe DM (2012) Nuclear IFI16 induction of IRF-3 signaling during herpesviral infection and degradation of IFI16 by the viral ICP0 protein. Proc Natl Acad Sci USA 109: E3008–E3017. doi: 10.1073/pnas.1211302109
![]() |
[148] |
Li T, Chen J, Cristea IM (2013) Human cytomegalovirus tegument protein pUL83 inhibits IFI16-mediated DNA sensing for immune evasion. Cell Host Microbe 14: 591–599. doi: 10.1016/j.chom.2013.10.007
![]() |
[149] |
Yu Y, Wang SE, Hayward GS (2005) The KSHV immediate-early transcription factor RTA encodes ubiquitin E3 ligase activity that targets IRF7 for proteosome-mediated degradation. Immunity 22: 59–70. doi: 10.1016/j.immuni.2004.11.011
![]() |
[150] |
van Gent M, Braem SGE, de Jong A, et al. (2014) Epstein-Barr virus large tegument protein BPLF1 contributes to innate immune evasion through interference with Toll-like receptor signaling. Plos Pathog 10: e1003960. doi: 10.1371/journal.ppat.1003960
![]() |
[151] |
Hu MM, Yang Q, Xie XQ, et al. (2016) Sumoylation promotes the stability of the DNA sensor cGAS and the adaptor STING to regulate the kinetics of response to DNA virus. Immunity 45: 555–569. doi: 10.1016/j.immuni.2016.08.014
![]() |
[152] |
Liang Q, Deng H, Li X, et al. (2011) Tripartite motif-containing protein 28 is a small ubiquitin-related modifier E3 ligase and negative regulator of IFN Regulatory Factor 7. J Immunol 187: 4754–4763. doi: 10.4049/jimmunol.1101704
![]() |
[153] |
Yang WL, Zhang X, Lin HK (2010) Emerging role of Lys-63 ubiquitination in protein kinase and phosphatase activation and cancer development. Oncogene 29: 4493–4503. doi: 10.1038/onc.2010.190
![]() |
[154] |
Yang Y, Kelly P, Schmitz R, et al. (2016) Targeting non-proteolytic protein ubiquitination for the treatment of diffuse large B cell lymphoma. Cancer Cell 29: 494–507. doi: 10.1016/j.ccell.2016.03.006
![]() |
1. | Rena Bakhshi, Lucia Cloth, Wan Fokkink, Boudewijn Haverkort, 2009, Mean-Field Analysis for the Evaluation of Gossip Protocols, 978-0-7695-3808-2, 247, 10.1109/QEST.2009.38 | |
2. | Rena Bakhshi, Lucia Cloth, Wan Fokkink, Boudewijn R. Haverkort, Mean-field framework for performance evaluation of push–pull gossip protocols, 2011, 68, 01665316, 157, 10.1016/j.peva.2010.08.025 | |
3. | Luca Bortolussi, Jane Hillston, Diego Latella, Mieke Massink, Continuous approximation of collective system behaviour: A tutorial, 2013, 70, 01665316, 317, 10.1016/j.peva.2013.01.001 | |
4. | Ciro D'Apice, Rosanna Manzo, Benedetto Piccoli, A Fluid Dynamic Model for Telecommunication Networks with Sources and Destinations, 2008, 68, 0036-1399, 981, 10.1137/060674132 | |
5. | Rena Bakhshi, Lucia Cloth, Wan Fokkink, Boudewijn R. Haverkort, MeanField analysis for the evaluation of gossip protocols, 2008, 36, 0163-5999, 31, 10.1145/1481506.1481513 | |
6. | JAVIER GÓMEZ-SERRANO, CARL GRAHAM, JEAN-YVES LE BOUDEC, THE BOUNDED CONFIDENCE MODEL OF OPINION DYNAMICS, 2012, 22, 0218-2025, 1150007, 10.1142/S0218202511500072 | |
7. | Ciro D'Apice, Rosanna Manzo, Benedetto Piccoli, On the Validity of Fluid-dynamic Models for Data Networks, 2012, 7, 1796-2056, 10.4304/jnw.7.6.980-990 |