ライフサイエンスコーパス: cGAS

1 cGAS bound to DNA in the cytoplasm and catalyzed cGAMP s

2 cGAS catalyzes the synthesis of cGAMP, which functions a

3 cGAS homologs and a prokaryotic dinucleotide cyclase for

4 cGAS is activated by chromatin, and consistent with a mi

5 cGAS localized with M. tuberculosis in mouse and human c

6 cGAS signals by synthesis of a second messenger, cyclic

7 nding kinase-interferon regulatory factor 3 (cGAS-STING-TBK1-IRF3) signaling pathway.

8 1 (HSV-1)-triggered antiviral responses in a cGAS-dependent manner.

9 S cells and these cytokines are induced in a cGAS-STING-dependent manner.

10 This study provides evidence of a cGAS-independent mechanism of STING-mediated protection

11 Thus, enveloped RNA viruses stimulate a cGAS-independent STING pathway, which is targeted by IAV

12 unt robust IFN-I responses against CMV via a cGAS/STING/IRF3 pathway.

13 nduction of TRIM14 by type I IFN accelerates cGAS stabilization by recruiting USP14 to cleave the ubi

14 specially since RNA is not known to activate cGAS.

15 Activated cGAS synthesizes 2'3'-cGAMP, which we subsequently can d

16 e presence of DNA in the cytoplasm activates cGAS, while STING is activated by cyclic dinucleotides (

17 lentiviral delivery of enzymatically active cGAS triggers a STING-dependent, IRF3-mediated antiviral

18 e nucleic acid sensor cyclicGMP-AMPsynthase (cGAS) and its adaptorSTINGand is associated with reduced

19 pression of poly(dA:dT)-induced IFN-beta and cGAS transcripts, we have found that induction of IFN-be

20 caspase-4, gasdermin D, interferon-beta, and cGAS levels were elevated in the RPE in human eyes with

21 e identify three sensors, IFI203, DDX41, and cGAS, required for MLV nucleic acid recognition.

22 the cytosolic nucleic acid sensors RIG-I and cGAS, respectively, to induce type I interferons (IFNs)

23 thway dependent on the DNA sensors IFI16 and cGAS as well as the signalling adaptor molecule STING.

24 Our results demonstrate that IFI16 and cGAS cooperate in a novel way to sense nuclear herpesvir

25 e propose that the two DNA sensors IFI16 and cGAS cooperate to prevent the spurious activation of the

26 Deficiency of both MAVS and cGAS, or treatment of MAVS-deficient mice with reverse t

27 oly(dA:dT)-triggered IFN-beta production and cGAS induction.

28 Knockdown of TBK1, STING, and cGAS results in a dramatic reduction in the activation o

29 entiviral vectors targeting TBK1, STING, and cGAS were established in murine MS1 endothelial and RAW

30 Anemone cGAS appears to produce a 3',3' CDN that anemone STING r

31 mong them sensory pathway components such as cGAS, STING, RIG-I, MDA5, and the transcription factor I

32 e report that the direct interaction between cGAS and the Beclin-1 autophagy protein not only suppres

33 lso inhibit cGAS activity and similarly bind cGAS and DNA, suggesting conserved inhibitory mechanisms

34 We show that, upon dsDNA binding, cGAS is activated through conformational transitions, re

35 maherpesviruses encode inhibitors that block cGAS-STING-mediated antiviral immunity, and that modulat

36 DNA sensing in human keratinocytes, as both cGAS and IFI16 are required for the full activation of a

37 activity through a mechanism involving both cGAS binding and DNA binding.

38 following vaccination was dependent on both cGAS and STING.

39 them and present the inhibitor and DNA bound cGAS crystal structures, which will facilitate drug deve

40 cyclic GMP-AMP (cGAMP) synthase (cGAS), but cGAS nevertheless contributes substantially to the overa

41 terferon production in a STING-dependent but cGAS-independent manner.

42 (mtDNA) to drive the production of cGAMP by cGAS.

43 ogen-derived DNA is sensed in the cytosol by cGAS, which produces the cyclic dinucleotide (CDN) secon

44 this pathway, recognition of micronuclei by cGAS may act as a cell-intrinsic immune surveillance mec

45 IFN-? treatment rescued the cross-priming by cGAS or STING-deficient DCs.

46 d by cyclic dinucleotides (cdNs) produced by cGAS or from bacterial origins.

47 features associated with DNA recognition by cGAS and the catalytic mechanisms of cGAMP generation.

48 Although several DNA viruses are sensed by cGAS, viral strategies targeting cGAS are virtually unkn

49 e to the cumulative effect of DNA sensing by cGAS and STING-dependent sensing of c-di-AMP.

50 The cytoplasmic chromatin-cGAS-STING pathway promotes the senescence-associated se

51 o microbial pathogens depends on a conserved cGAS-STING signaling pathway.

52 We created cGAS, Ifi204, and Sting functional knockouts in RAW264.7

53 Here we identify a STING-dependent, cGAS-independent pathway important for full interferon p

54 ll-like receptors and the recently described cGAS-STING pathway.

55 anism of DNA sensing by the newly discovered cGAS-cGAMP-STING pathway and highlight recent progress i

56 Upon sensing cytosolic DNA, cGAS also activates cell-intrinsic antibacterial defense

57 Upon binding to DNA, cGAS is activated to catalyze the synthesis of cGAMP, wh

58 ting the prominent host sensor of viral DNA, cGAS.

59 c escape of mitochondrial DNA, which engages cGAS.

60 The mammalian enzyme cGAS synthesizes a unique cyclic dinucleotide (cGAMP) co

61 These data establish cGAS as the dominant cytosolic DNA sensor responsible fo

62 Furthermore, KSHV infection evokes cGAS-dependent responses that can limit the infection, a

63 cytosolic pathogen DNA to prevent excessive cGAS activation and persistent immune stimulation.

64 at both DNA binding sites are essential for cGAS activation.

65 Here, we show that cells from cGAS-deficient (cGas(-/-)) mice, including fibroblasts,

66 cGAMP signaling by discovery of a functional cGAS-STING pathway in Nematostella vectensis, an anemone

67 ugh which gammaherpesviruses antagonize host cGAS DNA sensing.

68 I interferon response that required the host cGAS/STING/TBK1/IRF3 signaling pathway.

69 However, it is largely unknown how cGAS itself is regulated during pathogen infection and I

70 crystal structures show that DncV and human cGAS generate CDNs in sequential reactions that proceed

71 d test this model by reprogramming the human cGAS active site to produce 3'-5' cGAMP, leading to sele

72 thus curious that a recent study identified cGAS as playing important roles in inhibiting positive-s

73 ed to activate a pathway dependent on IFI16, cGAS and STING.

74 These findings implicate cGAS as a key driver of autoimmune disease and suggest t

75 Collectively, these observations implicate cGAS as an important cytosolic sensor of P. falciparum g

76 tical amino acid residues for DNA binding in cGAS as well as carboxy terminal tail domain for transdu

77 Consistently, mice defective in cGAS or STING are highly susceptible to acute HSE.

78 Mice deficient in cGAS were more susceptible to lethality caused by infect

79 pts were diminished in cells knocked down in cGAS, STING, or TBK1.

80 replication or virus production occurred in cGAS or STING shRNA-targeted cell line pools.

81 pesvirus virions, when these are produced in cGAS-expressing cells.

82 ls via gap junctions to function in trans in cGAS(-)STING(+) cells.

83 and an ORF52 null mutant exhibits increased cGAS signaling.

84 S, poly(I:C), poly(dA:dT), and cGAMP, induce cGAS expression in an IFN-I-dependent manner in both mou

85 antly, dsDNA itself was sufficient to induce cGAS-, STING-, and interferon signaling-dependent ISG15

86 ate that cyclic GMP-AMP produced in infected cGAS(+)STING(-) cells can migrate into adjacent cells vi

87 ogs in other gammaherpesviruses also inhibit cGAS activity and similarly bind cGAS and DNA, suggestin

88 dentify drugs that could potentially inhibit cGAS activity, we performed in silico screening of drug

89 increases during lytic replication, inhibit cGAS to promote the reactivation of the KSHV from latenc

90 anisms utilized by viral proteins to inhibit cGAS and/or STING are also discussed.

91 cytosolic DNA sensing by directly inhibiting cGAS enzymatic activity through a mechanism involving bo

92 n of cGMP-AMP in infected cells, but instead cGAS is partially nuclear in normal human fibroblasts an

93 In invertebrates, cGAS homologs may not act as DNA sensors.

94 study, we show that Trex1 (-/-) mice lacking cGAS are completely protected from lethality, exhibit dr

95 In all responsive cell lines, cGAS/STING short hairpin RNA (shRNA) knockdown resulted

96 Therefore, non-mammalian cGAS may function as a nucleotidyltransferase and could

97 In mice, cGAS/cGAMP amplify both inflammasome and IFN-I to contro

98 es in Y-form DNA as a highly active, minimal cGAS recognition motif that enables detection of HIV-1 s

99 Modern cGAS and STING may have acquired structural features, in

100 nly provides a novel mechanism of modulating cGAS expression, but also adds another layer of regulati

101 Here the authors develop small molecule cGAS inhibitors, functionally characterize them and pres

102 The structure of mouse cGAS bound to an 18 bp dsDNA revealed that cGAS interact

103 The structure of mouse cGAS bound to dsDNA and 2',5' cGAMP provided insight int

104 In vivo, genetic ablation of murine cGAS reveals its requirement in the antiviral response t

105 urthermore, we determined that STING but not cGAS is critical for host protection against Brucella in

106 Disruption of STING, but not cGAS or IRF3, attenuated cell death, suggesting that STI

107 Wild-type, but not cGAS-deficient, mice exhibited slower growth of B16 mela

108 cognition receptor and adaptor STING but not cGAS.

109 Furthermore, we observed cGAS localized in punctate regions on the cytosolic side

110 hanistic rationale for the unique ability of cGAS to produce 2'-5' cGAMP.

111 romothripsis, leads to rapid accumulation of cGAS, providing a mechanism by which self-DNA becomes ex

112 Activation of cGAS occurs with viruses that infect through different h

113 cifically enhanced the enzymatic activity of cGAS.

114 Phylogenetic analysis of cGAS and STING families showed that their origins could

115 nzyme assays and IFN-beta reporter assays of cGAS mutants demonstrated that interactions at both DNA

116 ting USP14 to cleave the ubiquitin chains of cGAS at lysine (K) 414.

117 xpression of IFI16 amplifies the function of cGAS.

118 we have provided evidence that induction of cGAS by IFN-I meditates the subsequent positive feedback

119 oter region of cGAS mediate the induction of cGAS by IFN-I.

120 A-triggered IFN-I production by induction of cGAS.

121 eII(-/-) mice and suggest that inhibition of cGAS may lead to prevention and treatment of some human

122 KSHV) ORF52 (also known as KSHV inhibitor of cGAS [KicGAS]) has been detected in purified virions, th

123 Knockout or knockdown of cGAS in mouse or human cell lines blocked cytokine induc

124 Knockdown of cGAS inhibited IRF3 activation and interferon-beta induc

125 Knockdown or knockout of cGAS in human or mouse macrophages blocked cytokine prod

126 findings reveal a positive feedback loop of cGAS signaling generated by TRIM14-USP14 and provide ins

127 ided insight into the catalytic mechanism of cGAS.

128 Mutants of cGAS dsDNA-binding or catalytic pocket residues exhibit

129 r, the evolutionary functions and origins of cGAS and STING remain largely elusive.

130 One outcome of cGAS-STING signaling is the activation of the absent in

131 Overexpression of cGAS activated the transcription factor IRF3 and induced

132 e elements (ISREs) in the promoter region of cGAS mediate the induction of cGAS by IFN-I.

133 However, post-translational regulation of cGAS remains largely unknown.

134 ion, expand the immune-sensing repertoire of cGAS and caspase-4 to noninfectious human disease, and i

135 , these data highlight an unexpected role of cGAS in responding to mobile-element transcripts, reveal

136 unctioned by inhibiting dsDNA stimulation of cGAS.

137 We report that K48-linked ubiquitination of cGAS is a recognition signal for p62-depdendent selectiv

138 and that this accumulation was dependent on cGAS.

139 ors, RIG-I-like receptors, inflammasomes, or cGAS, each with its own cellular localization, ligand sp

140 though infected cells deficient for STING or cGAS alone failed to induce IFN-beta, coculture of cells

141 ulture of cells depleted for either STING or cGAS rescued IFN-beta expression.

142 canonical autophagy pathway (Atg14, Ulk1, or cGAS).

143 e pathogenicity factor DncV is a prokaryotic cGAS-like enzyme whose activity provides a mechanistic r

144 Recently, cGAS and STING have been identified as intracellular sen

145 onding to mobile-element transcripts, reveal cGAS-driven interferon signaling as a conduit for mitoch

146 ymes control the signaling activity of RLRs, cGAS, and IFI16 as well as their proximal adaptor protei

147 cribe an unexpected role for the DNA sensing cGAS-STING pathway in the mechanism of action of the Th1

148 es the innate immunity cytosolic DNA-sensing cGAS-STING (cyclic GMP-AMP synthase linked to stimulator

149 the cytosol, where it engages the DNA sensor cGAS (also known as MB21D1) and promotes STING (also kno

150 on of F. novicida detected by the DNA sensor cGAS and its adaptor STING induced type I interferon-dep

151 cells following activation of the DNA sensor cGAS and its downstream effector STING.

152 chitosan required the cytoplasmic DNA sensor cGAS and STING, implicating this pathway in dendritic ce

153 n Nature reveal how the cytosolic DNA sensor cGAS gains access to the cargo within micronuclei to dri

154 ed the type I interferon-inducing DNA sensor cGAS in a sequence-dependent manner.

155 ced activation of the cytoplasmic DNA sensor cGAS influences the outcome of infections, autoinflammat

156 TING in a manner dependent on the DNA sensor cGAS.

157 ted cells, where it activates the DNA sensor cGAS.

158 ere, we have shown that nucleic acid sensors cGAS-, STING-, MDA5-, MAVS-, or transcription factor IRF

159 on by stimulator of interferon genes (STING)-cGAS impaired interferon signalling.

160 that a cationic polymer can engage the STING-cGAS pathway to trigger innate and adaptive immune respo

161 DNA-sensing cyclic guanine adenine synthase (cGAS) was severely compromised for the pUL25 mutant.

162 mal compartment and cyclic GMP-AMP synthase (cGAS) and absent in melanoma 2 (AIM2) in the cytoplasm.

163 osolic DNA sensors, cyclic GMP-AMP synthase (cGAS) and Ifi204, are both required for the STING-depend

164 rough activation of cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING).

165 sm by targeting the cyclic GMP-AMP synthase (cGAS) and the stimulator of interferon (IFN) genes (STIN

166 ined that STING and cyclic GMP-AMP synthase (cGAS) are important to engage the type I IFN pathway, bu

167 ssenger produced by cyclic GMP-AMP synthase (cGAS) as well as RNA ligands and viruses.

168 Cyclic GMP-AMP synthase (cGAS) detects cytosolic DNA during virus infection and i

169 gets the DNA sensor cyclic GMP-AMP synthase (cGAS) for lysosomal degradation to avoid the detection o

170 The DNA sensor cyclic GMP-AMP synthase (cGAS) has been shown to bind cytosolic DNA to generate c

171 le protein 16 (IFI16) and cGMP-AMP synthase (cGAS) have both been proposed to detect herpesviral DNA

172 e antiviral protein cyclic GMP-AMP synthase (cGAS) in neuronal SH-SY5Y cells, which is the first demo

173 aled a key role for cyclic GMP-AMP synthase (cGAS) in STING activation.

174 A was recognized by cyclic-GMP-AMP synthase (cGAS) in the DC cytosol, contributing to type I interfer

175 Cyclic GMP-AMP synthase (cGAS) is a cytosolic DNA sensor mediating innate antimic

176 cGMP-AMP synthase (cGAS) is a key DNA sensor that produces the cyclic dinuc

177 Cyclic GMP-AMP synthase (cGAS) is an essential DNA virus sensor that triggers typ

178 es.Upon DNA binding cyclic GMP-AMP synthase (cGAS) produces a cyclic dinucleotide, which leads to the

179 nvolving the enzyme cyclic GMP-AMP synthase (cGAS) was described and potentially linked to Aicardi-Go

180 nity; despite this, cyclic GMP-AMP synthase (cGAS), a cytosolic sensor of double-stranded DNA, is act

181 Cyclic GMP-AMP synthase (cGAS), a DNA sensor that produces a cyclic guanine-adeni

182 tion and MS, we found the cGMP-AMP synthase (cGAS), an innate immune DNA sensor, to be a cellular int

183 tosolic DNA sensor, cyclic GMP-AMP synthase (cGAS), is activated by DNA-induced dimerization.

184 tosolic DNA sensor, cyclic GMP-AMP synthase (cGAS), is required for activating IFN production via the

185 ically deficient in cyclic GMP-AMP synthase (cGAS), its adaptor STING, IRF3, or the type I IFN recept

186 are dependent upon cyclic GMP-AMP synthase (cGAS), STING, and interferon regulatory factor 3 (IRF3)

187 ll-derived DNA, via cyclic-GMP-AMP synthase (cGAS), STING, and interferon regulatory factor 3 (IRF3).

188 DNA (dsDNA) sensor cyclic GMP-AMP synthase (cGAS), the innate immune adaptor STING, and interferon s

189 osolic DNA receptor cyclic GMP-AMP synthase (cGAS), which produces the second messenger cyclic GMP-AM

190 ase-1, and requires cyclic GMP-AMP synthase (cGAS)-dependent interferon-beta production and gasdermin

191 pathway, including cyclic GMP-AMP synthase (cGAS).

192 binds and activates cyclic GMP-AMP synthase (cGAS).

193 ecognition receptor cyclic GMP-AMP synthase (cGAS).

194 ytosolic DNA sensor cyclic GMP-AMP synthase (cGAS, also known as MB21D1) as a gene whose expression a

195 G is activated downstream of cGAMP synthase (cGAS) to induce type I interferon.

196 pectrometry, we identified a cGAMP synthase (cGAS), which belongs to the nucleotidyltransferase famil

197 by cytoplasmic dsDNA sensor cGAMP synthase (cGAS).

198 DNA sensors cyclic GMP-AMP (cGAMP) synthase (cGAS) and interferon gamma (IFNgamma)-inducible protein

199 te-adenosine monophosphate (cGAMP) synthase (cGAS) as a cytosolic DNA sensor that triggers innate imm

200 te-adenosine monophosphate (cGAMP) synthase (cGAS) binds to DNA and produces cGAMP, which in turn bin

201 te-adenosine monophosphate (cGAMP) synthase (cGAS) in macrophages to produce cGAMP, a second messenge

202 Cyclic GMP-AMP (cGAMP) synthase (cGAS) is a cytosolic DNA sensor that activates innate im

203 cGMP-AMP (cGAMP) synthase (cGAS) is a cytosolic DNA sensor that activates innate im

204 Cyclic GMP-AMP (cGAMP) synthase (cGAS) is a cytosolic DNA sensor that activates the IFN p

205 Cyclic GMP-AMP (cGAMP) synthase (cGAS) is recently identified as a cytosolic DNA sensor a

206 DNA sensor cyclic GMP-AMP (cGAMP) synthase (cGAS) mediated sensing of irradiated-tumor cells in DCs.

207 trated that cyclic GMP-AMP (cGAMP) synthase (cGAS) plays an important role in sensing cytosolic DNA a

208 te-adenosine monophosphate (cGAMP) synthase (cGAS) to produce cGAMP, which binds to and activates the

209 of dsDNA by cyclic GMP-AMP (cGAMP) synthase (cGAS) triggers formation of the metazoan second messenge

210 id receptor cyclic GMP-AMP (cGAMP) synthase (cGAS), but cGAS nevertheless contributes substantially t

211 DNA sensor, cyclic GMP-AMP (cGAMP) synthase (cGAS), resulting in production of the second messenger c

212 DNA sensor cyclic-GMP-AMP (cGAMP) synthase (cGAS), which catalyzes the production of cGAMP that in t

213 ophosphate-adenosine monophosphate synthase (cGAS) detects intracellular DNA and signals through the

214 ted by CDNs generated by the cGAMP synthase, cGAS.

215 ly discovered cyclic dinucleotide synthetase cGAS and the cyclic dinucleotide receptor STING.

216 Cyclic GMP-AMP synthetase (cGAS) is a DNA-specific cytosolic sensor, which detects

217 NA sensor cyclic GMP-AMP (cGAMP) synthetase (cGAS) produces the second messenger cGAMP to initiate th

218 e sensed by cGAS, viral strategies targeting cGAS are virtually unknown.

219 d that induction of IFN-beta is earlier than cGAS.

220 n activates the cGAS-STING pathway, and that cGAS and STING also play an important role in regulating

221 These results demonstrate that cGAS activation causes the autoimmune diseases in Trex1(

222 These results demonstrate that cGAS is a vital innate immune sensor of M. tuberculosis

223 n RAW264.7 macrophages and demonstrated that cGAS and Ifi204 cooperate to sense dsDNA and activate th

224 These results demonstrated that cGAS is activated by dsDNA-induced oligomerization.

225 We determined that cGAS is required for IFN-beta expression during chlamydi

226 These novel findings provide evidence that cGAS-mediated DNA sensing directs IFN-beta expression du

227 We found that cGAS shows low production of cGMP-AMP in infected cells,

228 Collectively, our studies indicate that cGAS and Ifi204 cooperate to sense cytosolic dsDNA and F

229 These results indicate that cGAS is a cytosolic DNA sensor that induces interferons

230 These results indicate that cGAS is an innate immune sensor of HIV and other retrovi

231 Further experiments indicated that cGAS is an IFN-stimulated gene (ISG), and two adjacent I

232 Here, we report that cGAS localizes to micronuclei arising from genome instab

233 e cGAS bound to an 18 bp dsDNA revealed that cGAS interacts with dsDNA through two binding sites, for

234 Importantly, we show that cGAS binds M. tuberculosis DNA during infection, providi

235 Here we show that cGAS is indispensable for the antitumor effect of immune

236 river of autoimmune disease and suggest that cGAS inhibitors may be useful therapeutics for Aicardi-G

237 The cGAS-cGAMP-STING-IRF3 pathway of cytosolic DNA sensing p

238 The cGAS-STING pathway not only mediates protective immune d

239 The cGAS/STING DNA sensing complex has recently been establi

240 The cGAS/STING/TBK1/IRF3 cascade was not a direct target of

241 We report that KSHV infection activates the cGAS-STING pathway, and that cGAS and STING also play an

242 of TBK1 and IRF3 and thereby antagonize the cGAS-mediated restriction of KSHV lytic replication.

243 Instead, detection of cytosolic DNA by the cGAS-STING axis induces a cell death program initiating

244 HIV-1 evades immune detection by the cGAS-STING cytosolic DNA-sensing pathway during acute in

245 Here we review how viruses are sensed by the cGAS-STING signaling pathway as well as how viruses modu

246 This is recognized by the cGAS/STING-dependent DNA sensing pathway, which initiate

247 r results demonstrate a pivotal role for the cGAS-STING pathway in the initial detection of CMV infec

248 In humans, the cGAS-STING immunity pathway signals in response to cytos

249 Importantly, the cGAS-STING-NLRP3 pathway constitutes the default inflamm

250 undant, tissue-specific or integrated in the cGAS-cGAMP pathway is unclear.

251 Here, we show that IFI16 functions in the cGAS-STING pathway on two distinct levels.

252 glein-2 (Ad7) viral receptors all induce the cGAS/STING/TBK1/IRF3 cascade.

253 ncoded by a human DNA virus that inhibit the cGAS-STING DNA sensing pathway.

254 icularly, a cytoplasmic isoform, inhibit the cGAS-STING-dependent phosphorylation of TBK1 and IRF3 an

255 Furthermore, activation of the cGAS cascade occurred in a cell-specific manner.

256 However, aberrant activation of the cGAS pathway by self DNA can also lead to autoimmune and

257 hese results indicate that activation of the cGAS pathway is important for intrinsic antitumor immuni

258 ng pathway and highlights the breadth of the cGAS-induced antiviral response.

259 ial mechanism that dampens activation of the cGAS-STING axis.

260 s virus-host stand-off in the context of the cGAS-STING innate immune pathway.

261 tly become clear that core components of the cGAS-STING pathway evolved more than 600 million years a

262 ther, assembling signaling components of the cGAS-STING pathway onto the eukaryotic evolutionary map

263 er DNA viruses can prevent activation of the cGAS-STING pathway remains largely unknown.

264 e we discuss the evolutionary origins of the cGAS-STING pathway, and consider the possibility that th

265 the recent advances in understanding of the cGAS-STING pathway, focusing on the regulatory mechanism

266 us, as potent and specific inhibitors of the cGAS-STING pathway.

267 t comprehensive evolutionary analyses of the cGAS-STING pathway.

268 us induced efficient early activation of the cGAS/STING cascade in a cell-specific manner.

269 ovirus, we have modeled the influence of the cGAS/STING cascade in permissive human cell lines (A549,

270 and desmoglein-2), and the magnitude of the cGAS/STING DNA response cascade is influenced by serotyp

271 found no evidence that Ad stimulation of the cGAS/STING DNA response had an impact on viral replicati

272 itochondrial DNA-dependent activation of the cGAS/STING pathway and results in the establishment of a

273 parum genomic DNA and reveal the role of the cGAS/STING pathway in the induction of type I IFN in res

274 Activation of the cGAS/STING response did not impact viral replication, an

275 interferon-stimulated genes dependent on the cGAS-STING signaling pathway.

276 oncogenes in human tumor cells restores the cGAS-STING pathway.

277 immune evasion strategies did not target the cGAS/STING/TBK1/IRF3 cascade.

278 We conclude that targeting the cGAS-STING-LCD-NLRP3 pathway will ameliorate pathology i

279 This study shows for the first time that the cGAS DNA sensor directs a dominant IRF3/IFN/ISG antivira

280 nfection in the CNS by microglia through the cGAS-STING pathway orchestrates an antiviral program tha

281 -1 inhibits type I IFN induction through the cGAS-STING-TBK1 pathway in human macrophages, in a manne

282 stimulates type I IFN expression through the cGAS-STING-TBK1 signaling axis.

283 Thus, the cGAS pathway must be properly regulated.

284 Thus, the cGAS-Beclin-1 interaction shapes innate immune responses

285 However, their relation to the cGAS-STING pathway is not clear.

286 ermissive cell lines that do not trigger the cGAS/STING cascade following infection.

287 or reverse-transcribed and detected via the cGAS-cGAMP-STING pathway, triggering a second, sustained

288 e of cytosolic DNA recognition, in which the cGAS-STING axis triggers antiviral immunity, whereas AIM

289 Ds) that were predicted to interact with the cGAS/dsDNA complex.

290 N-beta production almost exclusively through cGAS-STING-dependent recognition of bacterial DNA.

291 By directly binding to cGAS, LANA, and particularly, a cytoplasmic isoform, inh

292 diseases associated with type I IFNs due to cGAS activation.

293 The nucleotidyl transferase cGAS, its second-messenger product cGAMP, and the cGAMP

294 cell-intrinsic dsDNA sensing dependent upon cGAS-STING.IMPORTANCE By antagonizing type I interferon

295 Our data demonstrate a mechanism by which cGAS senses cellular damage upon DENV infection.

296 inducible protein 16 (IFI16) cooperates with cGAS during DNA sensing in human keratinocytes, as both