ライフサイエンスコーパス: cGAS

1 cGAS is an intracellular innate immune sensor that detec

2 cGAS promotes inflammatory senescence-associated secreto

3 cGAS synthesizes cyclic GMP-AMP (cGAMP), which binds to

4 cGAS was initially located in the cytosolic compartment

5 cGAS was necessary for the reduced DNA virus replication

6 cGAS was previously thought to not react with self DNA o

7 cGAS-containing cytoplasmic micronuclei are increased in

8 cGAS-mediated inflammation is essential for the antitumo

9 cGAS/DncV-like nucleotidyltransferase (CD-NTase) enzymes

10 igomerizing into the functionally active 2:2 cGAS-dsDNA state.

11 specific peptides, then bind and activate a cGAS/DncV-like nucleotidyltransferase (CD-NTase) to gene

12 nucleus or mitochondria can also serve as a cGAS ligand to activate this pathway and trigger extensi

13 d DNA-dependent protein kinase (DNA-PK) as a cGAS-independent and alternative DNA cytosolic sensor th

14 gonist pUL41 (HSV-1DeltaUL41N) resulted in a cGAS-dependent type I interferon response.

15 IFN-lambda1 production was also induced in a cGAS-independent and DNA-protein kinase (DNA-PK)-depende

16 ed splenic stromal cells produced IFN-I in a cGAS-STING-dependent and MyD88-independent manner, while

17 late cytosolic DNA and produce IFN-beta in a cGAS-STING-dependent manner, which renders dMLH1 tumors

18 ATM increased tumoral T1IFN expression in a cGAS/STING-independent, but TBK1- and SRC-dependent, man

19 bilising small molecule PF-74 also induced a cGAS-dependent IFN response.

20 of a bacterial defense pathway integrating a cGAS-like nucleotidyltransferase with HORMA domain prote

21 Together, T cells are capable to raise a cGAS-dependent cell-intrinsic response to both plasmid D

22 ion, and ectopic STING expression restored a cGAS-dependent DNA response in these cells.

23 In CBASS systems, a cGAS/DncV-like nucleotidyltransferase synthesizes cyclic

24 we show that aspirin can directly acetylate cGAS and efficiently inhibit cGAS-mediated immune respon

25 geting the endothelial Gasdermin D activated cGAS-YAP signaling pathway could serve as a potential st

26 nhibition by cGAMP, the product of activated cGAS.

27 ing cGAS in cGAS-depleted HD cells activates cGAS activity and promotes inflammatory and autophagy re

28 vered that chromosomal instability activates cGAS/STING signaling but strongly suppresses invasivenes

29 ytosolic mitochondrial DNA (mtDNA) activates cGAS-mediated antiviral immune responses, but the mechan

30 and Vpr had complementary activities against cGAS-STING activity.

31 f cGAS that disrupt nucleosome binding alter cGAS-mediated signalling in cells.

32 -1 cells that was dependent on viral DNA and cGAS.

33 , are repurposed or become inaccessible, and cGAS dimerization, another prerequisite for activation,

34 G-I-like receptors, AIM2-like receptors, and cGAS.

35 evidence has shown that self-DNA release and cGAS-STING pathway over-activation can drive lung diseas

36 pendently of type I interferon signaling and cGAS.

37 r the relative contributions of the TLR3 and cGAS-STING signaling pathways to the attenuation of HSV-

38 arily TLR and RLR family members, as well as cGAS-STING signalling, play a critical role in the prese

39 Upon DNA binding, cGAS becomes enzymatically active to generate the second

40 We show that TRIM14 interacts with both cGAS and TBK1 and that macrophages lacking TRIM14 dramat

41 deficiency led to inefficient DNA binding by cGAS and inhibited cGAS-dependent interferon (IFN) produ

42 demonstrate that inhibition of HR repair by cGAS is linked to its ability to self-oligomerize, causi

43 c telomeric DNA fragments that are sensed by cGAS.

44 oplasmic double-stranded (ds) DNA-sensing by cGAS.

45 In mouse T cells, cGAS KO ablated sensing of plasmid DNA, and TREX1 KO ena

46 e mtDNA leakage into the cytosol and chronic cGAS engagement.

47 By contrast, cGAS reactivity against self-DNA in the nucleus is suppr

48 leosomes competitively inhibit DNA-dependent cGAS activation and that the cGAS-STING pathway is not e

49 Depletion of cGAS diminishes cGAS activity and decreases the expression of inflammato

50 Upon binding DNA, cGAS produces cGAMP that binds to and activates the adap

51 On binding to DNA, cGAS is activated to catalyse the synthesis of cyclic GM

52 Here, we demonstrate that endogenous cGAS is predominantly a nuclear protein, regardless of c

53 Moreover, the ability of self-DNA to engage cGAS has emerged as an important mechanism fuelling the

54 ulation of T cell lines provoked an entirely cGAS-dependent type I interferon response, including IRF

55 Upon sensing cytosolic DNA, the enzyme cGAS induces innate immune responses that underpin anti-

56 Activated primary CD4(+) T cells expressed cGAS and responded to plasmid DNA by upregulation of ISG

57 ic immunity, with important implications for cGAS-STING in integrating inflammatory and microbial cue

58 g is independent of the domains required for cGAS activation, and it requires intact nuclear chromati

59 e known cGAS DNA binding sites, required for cGAS activation, are repurposed or become inaccessible,

60 dence, however, points to a complex role for cGAS and STING in cancer.

61 TOP1cc) is both necessary and sufficient for cGAS-mediated cytoplasmic chromatin recognition and SASP

62 of G3BP1 provides a potential treatment for cGAS-related autoimmune diseases.

63 tact capsid physically cloaks viral DNA from cGAS.

64 and reveal the conservation of a functional cGAS-STING pathway in prokaryotic defence against bacter

65 the cGAMP synthase-stimulator of IFN genes (cGAS-STING) pathway, independent of bacterial ligands.

66 ic GMP-AMP synthase/stimulator of IFN genes (cGAS/STING) pathway detects cytosolic DNA to activate in

67 AMP synthase-stimulator of interferon genes (cGAS-STING) in APCs, resulting in more efficient T cell

68 he cyclic GMP-AMP synthase interferon genes (cGAS-STING) innate immune pathway.

69 AMP synthase-stimulator of interferon genes (cGAS-STING) pathway activation, and anti-tumoral immunit

70 AMP synthase-stimulator of interferon genes (cGAS-STING) pathway by using two approaches: the genetic

71 lex serving as a future platform for guiding cGAS inhibitor development at the DNA-bound h-cGAS level

72 1 bound in two alternate alignments to apo h-cGAS(CD), thereby occupying more of the catalytic pocket

73 GAS inhibitor development at the DNA-bound h-cGAS level.

74 Human cGAS (h-cGAS) constitutes an important drug target for control o

75 e also report the crystal structure of the h-cGAS(CD)-DNA complex containing a triple mutant that dis

76 findings provide a structural basis for how cGAS maintains an inhibited state in the nucleus and fur

77 l nucleated cells raises the question of how cGAS is not constitutively activated.

78 Here, we highlight recent advances on how cGAS and STING mediate inflammatory responses and how th

79 However, cGAS binds to DNA irrespective of DNA sequence, therefor

80 Human cGAS (h-cGAS) constitutes an important drug target for c

81 y and selectively inhibiting mouse and human cGAS in cell lines and human primary cells.

82 While inhibitors targeting mouse or human cGAS have been reported, the identification of a small m

83 o-electron microscopy structure of the human cGAS-nucleosome core particle (NCP) complex, two cGAS mo

84 from one scaffold co-crystallize with human cGAS and occupy the ATP- and GTP-binding active site.

85 Here we report the discovery of human-cGAS-specific small-molecule inhibitors by high-throughp

86 cids and, in mammalian cells, include RIG-I, cGAS, and AIM2.

87 Taken together, these results identify cGAS and Cx32 as key factors in ALD pathogenesis and as

88 may attenuate IFI16 expression, reduce IFI16-cGAS cross-talk, and prevent excessive APOL1 expression

89 n epithelial cells, deficient in cGAS and in cGAS and STING expression, respectively.

90 In contrast, reinstating cGAS in cGAS-depleted HD cells activates cGAS activity and promo

91 EK293 T human epithelial cells, deficient in cGAS and in cGAS and STING expression, respectively.

92 Mice genetically deficient in cGAS and IRF3 were protected against ALD.

93 ty, suggesting an ancient role for poxins in cGAS-STING regulation.

94 and MX2 was downregulated and upregulated in cGAS KO and TREX1 KO T cell lines, respectively, compare

95 ge cytosolic surveillance systems, including cGAS and the inflammasome.

96 cute exposure to cisplatin further increases cGAS and STING levels in both 2F8 and 2F8cis cells.

97 erous micronuclei, which are known to induce cGAS, in the cytoplasm of neurons derived from human HD

98 ectly acetylate cGAS and efficiently inhibit cGAS-mediated immune responses.

99 mmune second messenger 2'3'-cGAMP to inhibit cGAS-STING immunity in mammalian cells.

100 nefficient DNA binding by cGAS and inhibited cGAS-dependent interferon (IFN) production.

101 Here we report that acetylation inhibits cGAS activation and that the enforced acetylation of cGA

102 Despite their intact cGAS sensing pathway, human CD4(+) T cells failed to mou

103 ell-based activity will serve as probes into cGAS-dependent innate immune pathways and warrant future

104 In this configuration, all three known cGAS DNA binding sites, required for cGAS activation, ar

105 G N153S mice were crossed to animals lacking cGAS, IRF3/IRF7, IFNAR1, adaptive immunity, alphabeta T

106 of cGAS by promoting the formation of large cGAS complexes.

107 However, during mitotic arrest, low level cGAS-dependent IRF3 phosphorylation slowly accumulates w

108 t DNA into nucleosomes was proposed to limit cGAS autoinduction, but the underlying mechanism was unk

109 Mutating key residues linking cGAS and the acidic patch alleviates nucleosomal inhibit

110 ks double-stranded DNA binding and maintains cGAS in an inactive conformation.

111 ance of linkage specificity beyond mammalian cGAS-STING signaling.

112 Manipulating cGAS or STING may open the door for new therapeutic stra

113 Caspase-mediated cGAS cleavage was enhanced in the presence of dsDNA.

114 Mislocalized cGAS induces potent interferon responses to genotoxic st

115 sm of cGAS in which Mn2+ activates monomeric cGAS without dsDNA.

116 t, given its potency against human and mouse cGAS.

117 hering, we determined the structure of mouse cGAS bound to human nucleosome by cryo-electron microsco

118 cyclic di-GMP synthesized by a neighbouring cGAS/DncV-like nucleotidyltransferase (CD-NTase) enzyme.

119 These novel cGAS inhibitors with cell-based activity will serve as p

120 We show that nuclear cGAS is tethered tightly by a salt-resistant interaction

121 Ablation of cGAS in hepatocytes only phenocopied this hepatoprotecti

122 ivation and that the enforced acetylation of cGAS by aspirin robustly suppresses self-DNA-induced aut

123 Instead, the activation of cGAS and STING results in autophagic cell death.

124 The activation of cGAS-STING signaling induced by various PARPi closely de

125 for DNA sensing and efficient activation of cGAS.

126 ycobacterium tuberculosis is an activator of cGAS-dependent cytosolic DNA sensing, we set out to inve

127 re, we examined expression and activities of cGAS, STING, and PYHINs in human lung epithelial cells.

128 Moreover, the protein levels and activity of cGAS (based on the phosphorylated STING and phosphorylat

129 e demonstrate how the intrinsic allostery of cGAS efficiently yet precisely tunes its activity.

130 To elucidate the molecular basis of cGAS inactivation by nuclear tethering, we determined th

131 G3BP1 enhanced DNA binding of cGAS by promoting the formation of large cGAS complexes.

132 nteracts with cGAS to enhance the binding of cGAS to DNA.

133 Depletion of cGAS diminishes cGAS activity and decreases the expressi

134 Clinically, downregulation of cGAS/STING in human dMMR cancers correlates with poor pr

135 egment of cGAS contributes to enhancement of cGAS enzymatic activity as a result of DNA-induced liqui

136 Accordingly, expression of cGAS and IRF3 in cancer cells makes mouse xenograft tumo

137 tiviral immunity and explain how a family of cGAS-STING evasion enzymes evolved from viral proteases

138 We addressed the functionality of cGAS-mediated DNA sensing in human and murine T cells.

139 small molecule that targets both homologs of cGAS has been challenging.

140 genetic and pharmacological manipulation of cGAS not only attenuated immune signaling, but also prev

141 The canonical activation mechanism of cGAS entails dsDNA-binding and dimerization.

142 report an unexpected activation mechanism of cGAS in which Mn2+ activates monomeric cGAS without dsDN

143 insect viruses suggesting a key mechanism of cGAS-STING evasion may have evolved outside of mammalian

144 Mutations of cGAS that disrupt nucleosome binding alter cGAS-mediated

145 and the expression and ribosome occupancy of cGAS-dependent inflammatory genes (Ccl5 and Cxcl10) are

146 Overexpression of cGAS/STING modifies tumor immunogenicity by upregulating

147 e blood partly, dependent on the presence of cGAS, as was skin inflammatory cell infiltration.

148 inhibitory activity requires the presence of cGAS, but it cannot suppress an immune response in cells

149 ata also indicate that pDC prestimulation of cGAS-STING dampened the TLR9-mediated IFN production.

150 ent formation of micronuclei, recruitment of cGAS, and activation of the cyclic GMP-AMP synthase (cGA

151 ify OASL as a negative-feedback regulator of cGAS.

152 A particular focus is placed on the role of cGAS in the context of sterile inflammatory conditions.

153 l and mechanistic insights into the roles of cGAS and STING in immunity and diseases revealed by thes

154 the positively charged N-terminal segment of cGAS contributes to enhancement of cGAS enzymatic activi

155 explanation for this is the sequestration of cGAS in the cytosol, which is thought to prevent cGAS fr

156 ear tethering maintains the resting state of cGAS and prevents autoreactivity.

157 lution cryo-electron microscopy structure of cGAS in complex with the nucleosome core particle.

158 ure pharmacological studies for treatment of cGAS-dependent inflammatory diseases.

159 Furthermore, triggering of cGAS-STING induced expression of SOCS1 and SOCS3 in pDCs

160 c cisplatin treatment led to upregulation of cGAS and STING proteins in 2F8cis compared to parental 2

161 This review focuses on cGAS-STING signaling in aging, neurodegeneration, and ne

162 uble-stranded DNA (dsDNA)-binding surface on cGAS and sterically prevents cGAS from oligomerizing int

163 volutionarily conserved tethering surface on cGAS and we show that mutation of single amino acids wit

164 r protein, regardless of cell cycle phase or cGAS activation status.

165 R/Cas9 technology of genes encoding STING or cGAS in NIH/3T3 murine fibroblasts and the infection of

166 Accordingly, loss of STING or cGAS in tumor cells decreases tumor infiltration of T ce

167 of PARP1 without eliciting PARP1 trapping or cGAS-STING activation.

168 study, we report that DNA-PK phosphorylates cGAS and suppresses its enzymatic activity.

169 In murine models, CX-6258 induced a potent cGAS-dependent type-I IFN response in tumor cells, incre

170 in the cytosol, which is thought to prevent cGAS from accessing nuclear DNA.

171 ding surface on cGAS and sterically prevents cGAS from oligomerizing into the functionally active 2:2

172 t G3BP1 physically interacts with and primes cGAS for efficient activation.

173 DNA-PK deficiency reduces cGAS phosphorylation and promotes antiviral innate immun

174 In contrast, reinstating cGAS in cGAS-depleted HD cells activates cGAS activity a

175 's disease mice had increased mtDNA release, cGAS activation, and inflammation, all inhibited by exog

176 ngle amino acids within this surface renders cGAS massively and constitutively active against self-DN

177 of the innate immunity cytosolic DNA sensing cGAS-STING pathway.

178 The newly discovered DNA-sensing cGAS-cGAMP-STING pathway mediates type I interferon infl

179 ons, which in turn activated the DNA-sensing cGAS-STING pathway and stimulated production of type I I

180 The cytosolic DNA-sensing cGAS-STING pathway was originally characterized as a key

181 mtDNA was recognized by the DNA sensor cGAS and generated the second messenger cGAMP, which sup

182 The DNA sensor cGAS catalyzes the production of the cyclic dinucleotide

183 e demonstrated that the cytosolic DNA sensor cGAS recognizes baculoviral DNA and that the cGAS-STING

184 IFN-I production mediated by the DNA sensor cGAS.

185 antibody receptor TRIM21 and the DNA sensor cGAS.

186 nction, as a critical regulator of spreading cGAS-driven IRF3 activation through the liver parenchyma

187 mechanism to counteract the IFN-stimulating cGAS-STING pathway.

188 Following genotoxic stress, cGAS can also respond to endogenous DNA, deriving from m

189 nd ISG antagonists, while F17 helps suppress cGAS-mediated responses, we find that a critical functio

190 rus, but not the wild-type virus, suppressed cGAS-dependent innate immune activation.

191 Surprisingly, cGAS-STING activation leads to type I IFN transcription

192 NA-sensing receptor cyclic GMP-AMP synthase (cGAS) and its downstream signalling effector stimulator

193 h the activation of cyclic GMP-AMP synthase (cGAS) and production of the cyclic dinucleotide second m

194 ol is sensed by the cyclic GMP-AMP synthase (cGAS) and stimulator of IFN genes (STING) pathway to ind

195 In these pathways, cGMP-AMP synthase (cGAS) and the pyrin and HIN domain family member (PYHIN)

196 Cyclic GMP-AMP synthase (cGAS) is a critical cytosolic DNA sensor that elicits ro

197 Cyclic GMP-AMP synthase (cGAS) is a double-stranded DNA sensor that catalyses the

198 ion of viral DNA by cyclic GMP-AMP synthase (cGAS) is a first line of defence leading to the producti

199 Cyclic GMP-AMP synthase (cGAS) is a key sensor responsible for cytosolic DNA dete

200 Cyclic cGMP-AMP synthase (cGAS) is a pattern recognition cytosolic DNA sensor that

201 Cyclic GMP-AMP synthase (cGAS) is a sensor of cytoplasmic DNA that activates the

202 Cyclic GMP-AMP synthase (cGAS) is best known as a cytosolic innate immune sensor

203 Cyclic GMP-AMP synthase (cGAS) is the primary sensor for aberrant intracellular d

204 CYCLIC GMP-AMP SYNTHASE (cGAS) is the sensor protein that directly binds dsDNAs.

205 shortening, but by cyclic GMP-AMP synthase (cGAS) recognizing cytosolic chromatin fragments and then

206 The enzyme cyclic GMP-AMP synthase (cGAS) senses cytosolic DNA in infected and malignant cel

207 Here, we report that cGMP-AMP synthase (cGAS), a DNA sensor, is a critical regulator of inflamma

208 solic dsDNA sensor, cyclic GMP-AMP synthase (cGAS), and the stimulator of IFN genes (STING) are requi

209 to DAI/ZBP1, or by cyclic GMP-AMP synthase (cGAS), despite its presence in the cell cytosol.

210 the key DNA sensor cyclic GMP-AMP synthase (cGAS), leads to the synthesis of type I interferon and i

211 ) triggers both the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) and Toll-li

212 d messengers in the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, wh

213 d activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway.

214 r pathways, such as cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING), and propag

215 ation of cyclic GMP-AMP (cGMP-AMP) synthase (cGAS) and generation of the cyclic dinucleotide cGAMP, f

216 hate-adenosine monophosphate (AMP) synthase (cGAS) drives IRF3 activation in both alcohol-injured hep

217 GMP)-adenosine monophosphate (AMP) synthase (cGAS) recognizes cytosolic foreign or damaged DNA to act

218 comprising cyclic GMP-AMP (cGAMP) synthase (cGAS) and stimulator of IFN gene (STING) in human pDCs.

219 Cyclic GMP-AMP (cGAMP) synthase (cGAS) detects infections or tissue damage by binding to

220 Cyclic GMP-AMP (cGAMP) synthase (cGAS) is a major responder to the pathogenic DNA of viru

221 Cyclic-G/AMP (cGAMP) synthase (cGAS) triggers host innate immune responses against cyto

222 nosine monophosphate (AMP) (cGAMP) synthase (cGAS), which produces the second messenger cGAMP.

223 ophosphate-adenosine monophosphate synthase (cGAS) and enhanced interferon signaling mediated by the

224 ophosphate-adenosine monophosphate synthase (cGAS) senses invasion of pathogenic DNA and stimulates i

225 'CDNs) with use of cyclic GMP-AMP synthases (cGAS) from human, mouse, and chicken.

226 rus infection in human epithelial cells than cGAS.

227 Moreover, we documented that cGAS-STING-mediated IFN production is mediated by nuclea

228 Collectively, our results indicate that cGAS is up-regulated in HD and mediates inflammatory and

229 Herein, we report that cGAS is not a cytosolic protein but rather localizes to

230 The structure reveals that cGAS uses two conserved arginines to anchor to the nucle

231 Here we show that cGAS binds to nucleosomes with nanomolar affinity and th

232 13); however, recent studies have shown that cGAS is localized mostly in the nucleus and has low acti

233 The structure shows that cGAS binds to a negatively charged acidic patch formed b

234 ssense mutations of PRKDC, and suggests that cGAS-mediated immune signaling is a potential target for

235 The cGAS-STING pathway has emerged as a major pathway that d

236 The cGAS-STING pathway is a major mechanism that mammalian c

237 The cGAS-STING pathway responds to viral, bacterial, and sel

238 e cytosolic chromatin fragments activate the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interf

239 DNA fragments, which may either activate the cGAS/STING-dependent pathway or-especially in the case o

240 Cytosolic mtDNA activated the cGAS/STING/IRF3 pathway, stimulating inflammatory cytoki

241 f dMMR, it is unknown how dMMR activates the cGAS-STING pathway.

242 , but not virulent Armenia/07, activates the cGAS-STING-IRF3 cascade very early during infection, ind

243 clear DNA into the cytoplasm, activating the cGAS-STING pathway.

244 species, one of the most prominent being the cGAS-STING pathway for DNA and the RLR-MAVS pathway for

245 uted cells with HSV-1 revealed that both the cGAS-STING and the TLR3 signaling pathways are required

246 we demonstrate that, surprisingly, both the cGAS/STING-dependent DNA-sensing pathway and the MAVS-de

247 nhanced interferon signaling mediated by the cGAS-stimulator of interferon genes (STING) pathway in p

248 e (ISG) expression, which is mediated by the cGAS-STING-IRF3 cytosolic DNA-sensing pathway.

249 In contrast, the cGAS-STING pathway is efficiently activated during NH/P6

250 w that virulent Armenia/07 ASFV controls the cGAS-STING pathway, but these mechanisms are not at play

251 HSV-1 that is functionally deficient for the cGAS antagonist pUL41 (HSV-1DeltaUL41N) resulted in a cG

252 critical role of hepatocytes in fueling the cGAS-IRF3 response to alcohol.

253 elopment of inflammation and implicating the cGAS-STING pathway in human inflammatory diseases and ca

254 the mechanism of signal transduction in the cGAS pathway at the atomic resolution.

255 xidation and thus specifically inhibited the cGAS-STING pathway.

256 Armenia/07 inhibits the cGAS-STING pathway by impairing STING activation during

257 a cellular intrinsic mechanism involving the cGAS-mediated cytosolic self-DNA-sensing pathway that in

258 ges (MPhi) in streptococcal infection is the cGAS-STING pathway, whereas conventional dendritic cells

259 ways activated by cisplatin treatment is the cGAS/STING pathway.

260 ch has demonstrated an expanding role of the cGAS-cGAMP-STING pathway in many physiological and patho

261 eported, suggesting an important role of the cGAS-cGAMP-STING pathway in the networking and coordinat

262 Potential interactions of the cGAS-cGAMP-STING pathway with mTORC1 signaling, autophag

263 ctrum of ALD revealed that expression of the cGAS-IRF3 pathway correlated positively with disease sev

264 nstrated increased hepatic expression of the cGAS-IRF3 pathway.

265 gests that the relative contributions of the cGAS-STING and the TLR3 pathways in the attenuation of v

266 hese results indicate that activation of the cGAS-STING pathway induces V-ATPase-dependent LC3B lipid

267 Dysregulation of the cGAS-STING pathway is responsible for a broad array of i

268 MR-induced neoantigens and activation of the cGAS-STING pathway.

269 ow for the first time the involvement of the cGAS-STING-IRF3 route in ASFV infection, where IFN-beta

270 Activation of the cGAS-STING-STAT pathway detected in these cells further

271 Here, we review recent advances on the cGAS-STING pathway governing self-DNA sensing, highlight

272 Particularly, the cGAS-STING pathway resulted in the more relevant product

273 Thus, targeting the cGAS pathway may offer therapeutic benefits in HD.

274 Ribosome profiling revealed that the cGAS mRNA has high ribosome occupancy at exon 1 and codo

275 cGAS recognizes baculoviral DNA and that the cGAS-STING axis is primarily responsible for the attenua

276 Thus, our study indicates that the cGAS-STING pathway exists in parallel to the TLR9-mediat

277 t DNA-dependent cGAS activation and that the cGAS-STING pathway is not effectively activated during n

278 Therefore, we propose that the cGAS-STING pathway senses unnatural cell fusion through

279 ulating innate immune signalling through the cGAS-STING pathway.

280 and IFNbeta via IRF3 activation through the cGAS/IFI16-STING pathway.

281 c DNA is sensed, a signal is relayed via the cGAS-STING pathway: this involves the activation of cycl

282 e innate immune signalling, mediated via the cGAS/STING pathway, causing degeneration of dopaminergic

283 -mediated innate immune modulation where the cGAS-STING pathway might play an important role.IMPORTAN

284 pite this, ablation of ISG responses through cGAS or STING knockout did not rescue defects in late-vi

285 nt quantity, length, and/or accessibility to cGAS.

286 OASL directly and specifically bound to cGAS independently of double-stranded DNA, resulting in

287 The binding of DNA to cGAS activates its enzymatic activity, leading to the sy

288 e we review how endogenous DNA is exposed to cGAS, how signaling is attenuated but activated under pa

289 UVB skin exposure leads to cGAS-activation and both local and systemic IFN-I signat

290 Functionally, the HMGB2-TOP1cc-cGAS axis determines the response of orthotopically tran

291 her, these findings establish a HMGB2-TOP1cc-cGAS axis that enables cytoplasmic chromatin recognition

292 , HIV-1 infection does not appear to trigger cGAS-mediated sensing of viral DNA in T cells, possibly

293 -nucleosome core particle (NCP) complex, two cGAS monomers bridge two NCPs by binding the acidic patc

294 ich are essential for IFN-beta induction via cGAS-STING.

295 of the sensing of cytosolic DNA and RNA via cGAS and RLRs.

296 However, the mechanism by which cGAS recognizes cytoplasmic chromatin is unknown.

297 y establishes a structural framework for why cGAS is silenced on chromatinized self-DNA.

298 e formation of micronuclei colocalizing with cGAS, which is activated by double-stranded DNA.

299 ytoplasmic chromatin and TOP1 interacts with cGAS to enhance the binding of cGAS to DNA.

300 Following the colocalization of ISD with cGAS, the downstream pathway was triggered as STING disa