ライフサイエンスコーパス: gasdermin

1 gous to all three mouse gasdermins and human gasdermin.

2 involved in proteolytic processing of other gasdermins.

3 e we show that both mice harbor mutations in gasdermin 3 (Gsdm3), a gene of unknown function.

4 post-GPI attachment to proteins 3, GSDMB, or gasdermin A (3.1 x 10(-9) <P < 1.8 x 10(-4)).

5 s protease Staphopain A (ScpA) cleaves inert Gasdermin A (GSDMA).

6 21 (zona pellucida binding protein 2 [ZPBP2]-gasdermin A [GSDMA]).

7 Gasdermins, a family of five pore-forming proteins (GSDM

8 of the structure and function of the murine gasdermin A3 (mGSDMA3), the molecular mechanisms of GSDM

9 Gasdermins abundant in other tissues may have similar fu

10 highlight the mechanistic insights into the gasdermin activation and regulation that are provided.

11 asdermins, the molecular pathways regulating gasdermin activity in fungi remain largely unknown.

12 Efforts to develop drugs to modulate gasdermin activity to reduce inflammation or activate mo

13 orting the evolutionary relationship between gasdermin and rcd-1 This report documents an ancient tra

14 peptide highly homologous to all three mouse gasdermins and human gasdermin.

15 Gasdermins are a family of pore-forming proteins control

16 The gasdermins are a family of pore-forming proteins recentl

17 Gasdermins are a family of structurally related proteins

18 Characterized mammalian gasdermins are activated through proteolytic cleavage by

19 Gasdermins are canonically associated with plasma membra

20 Immunohistochemical analysis revealed that gasdermins are expressed specifically in cells at advanc

21 Gasdermins are proteins that can self-assemble into memb

22 f pyroptosis with an emphasis on the role of gasdermins as executioners of pyroptosis and potential m

23 specifically induced proteolytic cleavage of gasdermin B (GSDMB) (50 kDa), evident by the appearance

24 ona pellucida binding protein 2 (ZPBP2), and gasdermin B (GSDMB) and is correlated with high IgE leve

25 Multiple SNPs in gasdermin B (GSDMB) associated with asthma severity (odd

26 Gasdermin B (GSDMB) belongs to a family of structurally

27 Gasdermin B (GSDMB) belongs to a large family of pore-fo

28 Gasdermin B (GSDMB) is currently the least studied, and

29 Gasdermin B (GSDMB) on chromosome 17q21 demonstrates a s

30 e located at 17q11.2-q12, and rs8069176 near gasdermin B (GSDMB; P = 1.88 x 10(-8)) at 17q12-q21.

31 consistently implicated the ORM1-like 3 and gasdermin B (ORMDL3-GSDMB), IL33, IL-1 receptor-like 1 a

32 between asthma risk allele, rs7216389-T and Gasdermin-B (GSDMB) in placenta (r2=27%) versus lung (r2

33 The exact function of human gasdermin-B (GSDMB), which regulates differentiation and

34 as related to alternative splicing of GSDMB (gasdermin-B) transcripts.

35 Here, we characterize a gasdermin-based cell death reaction controlled by the he

36 location, enhancing the transcription of the gasdermin C (GSDMC) gene.

37 Gasdermin C (GsdmC), predominantly expressed in intestin

38 Epithelial organoids deficient in Gasdermin C develop normally and show no alterations in

39 Gasdermin C genes are upregulated by type 2 immunity, ye

40 Here, we tested the functional role of Gasdermin C in intestinal homeostasis, inflammation and

41 Furthermore, evidence for the role of Gasdermin C in the intestine is scarce and partly contro

42 Gasdermin C is one of the least studied members of the g

43 Gasdermin C-deficient mice show no changes in tissue arc

44 leading to inflammatory caspase activation, gasdermin cleavage, and cytokine release.

45 When activated, they cleave mouse and human gasdermin D (GSDMD) after Asp276 and Asp275, respectivel

46 se 1 (RIPK1)-dependent caspase-8 cleavage of gasdermin D (GSDMD) and inflammatory cell death (pyropto

47 ntly, mIL-1beta secretion was independent of gasdermin D (GSDMD) and pyroptosis but relied on IFN-ind

48 tosis field, beginning with the discovery of Gasdermin D (GSDMD) as a substrate of caspase-1 and casp

49 to cells or endogenous fumarate reacts with gasdermin D (GSDMD) at critical cysteine residues to for

50 The recognition and cleavage of gasdermin D (GSDMD) by inflammatory caspases-1, 4, 5, an

51 masome activation results in the cleavage of gasdermin D (GSDMD) by pro-inflammatory caspases.

52 e determined if the dual site recognition of gasdermin D (GSDMD) by the inflammatory caspases is empl

53 y discovered exosite-mediated recognition of gasdermin D (GSDMD) by the inflammatory caspases to deve

54 pendent increase in cytosolic calcium drives Gasdermin D (GSDMD) cleavage and activation, which trigg

55 Gasdermin D (GSDMD) cleavage by caspase-1 or caspase-11

56 Canonically, gasdermin D (GSDMD) cleavage by caspase-1 through inflam

57 demonstrated that caspase-8 (CASP8)-mediated gasdermin D (GSDMD) cleavage drives pyroptotic cell deat

58 Conversely, NLRP3 and microglial gasdermin D (GSDMD) deficiency markedly attenuates lipop

59 inflammasome-activated, pore-forming protein gasdermin D (GSDMD) during infection.

60 ), peptidyl arginine deiminase 4 (PAD4), and gasdermin D (GSDMD) for NET formation in vivo following

61 Gasdermin D (GSDMD) has emerged as a key executor of inf

62 Gasdermin D (GSDMD) has recently been identified as a cy

63 Gasdermin D (GSDMD) induces pyroptosis via the pore-form

64 Gasdermin D (GSDMD) is a protein that, when cleaved, for

65 Gasdermin D (GSDMD) is a protein which belongs to the ga

66 we demonstrate that the pore-forming protein gasdermin D (GSDMD) is active in neutrophils from septic

67 Gasdermin D (GSDMD) is an effector molecule for pyroptos

68 Gasdermin D (GSDMD) is an important downstream effector

69 The pyroptotic cell death effector gasdermin D (GSDMD) is required for murine models of her

70 Gasdermin D (GSDMD) is the common effector for cytokine

71 ed that the "apoptotic" caspase-8 can cleave gasdermin D (GSDMD) leading to pyroptosis-like cell deat

72 nts or the downstream cell death executioner gasdermin D (GSDMD) led to an initial reduction in cell

73 causes pyroptotic cell death facilitated by gasdermin D (GSDMD) pore formation.

74 ulation, through triggering the formation of gasdermin D (GSDMD) pores and subsequent phosphatidylser

75 ed DC expression of the pore-forming protein gasdermin D (Gsdmd) results in reduced expression of cGA

76 MWCNTs induced the cleavage of gasdermin D (GSDMD) to form the 31 kDa N-terminal fragme

77 Caspase-1 activates gasdermin D (GSDMD) under inflammatory conditions, where

78 ein, we report that the pyroptosis regulator gasdermin D (GSDMD) was necessary for IL-1beta secretion

79 , we report that EV71 induces degradation of gasdermin D (GSDMD), an essential component of pyroptosi

80 in 3 (NLRP3), absent in melanoma 2 (AIM2) or gasdermin D (GSDMD), an inflammasome-induced executor of

81 lopment, reducing albumin leakage, IL-1beta, gasdermin D (GSDMD), and NETs formation.

82 n requires cleavage of the caspase substrate gasdermin D (GSDMD), and the release of the GSDMD N-term

83 n requires cleavage of the caspase substrate gasdermin D (GSDMD), and the release of the GSDMD N-term

84 One of these proteins, gasdermin D (GSDMD), has been identified as the executio

85 Gasdermin D (GSDMD), the pore-forming caspase-1 substrat

86 Knockdown of caspase-4 or gasdermin D (GSDMD), translocation of NleF, which blocks

87 put screen for compounds that could activate gasdermin D (GSDMD), which is expressed widely in tumors

88 (IL-1beta) and IL-18, as well as cleavage of gasdermin D (GSDMD), which promotes a lytic form of cell

89 Gasdermin D (GSDMD)-activated inflammatory cell death (p

90 inflammasome activation induces a caspase-1/gasdermin D (Gsdmd)-dependent lytic cell death called py

91 n in intestinal epithelial cells (IECs) in a Gasdermin D (GSDMD)-dependent manner.

92 Gasdermin D (GSDMD)-dependent PCD was further targeted u

93 ctivate the NLRC4 inflammasome, resulting in Gasdermin D (GSDMD)-dependent, but GSDME independent IL-

94 ecules block NLRP3 inflammasome assembly and gasdermin D (GSDMD)-induced pyroptosis.

95 te the maturation of interleukin (Il)-18 and gasdermin D (Gsdmd)-induced pyroptosis.

96 apoptosis, while the NLRP3 inflammasome and gasdermin D (GSDMD)-mediated pyroptosis are activated.

97 d by activating inflammasomes and consequent gasdermin D (GSDMD)-mediated pyroptosis, coupled to sign

98 he formation of large transmembrane pores by gasdermin D (GSDMD).

99 s also inactivate the pyroptosis executioner Gasdermin D (GSDMD).

100 and other inflammatory caspases that cleave gasdermin D (GSDMD).

101 to the cleavage of the pore-forming protein gasdermin D (GSDMD).

102 caspases to process cytokines (IL-1beta) and gasdermin D (GSDMD).

103 sdermins, the best characterized of which is gasdermin D (GSDMD).

104 e-11 interaction, leading to the cleavage of gasdermin D (GSDMD).

105 caspase-3 [CASP-3] cleavage) and pyroptosis (gasdermin D [GSDMD] cleavage) in livers, and CVC prevent

106 sults suggest that targeting the endothelial Gasdermin D activated cGAS-YAP signaling pathway could s

107 inactivation increased NF-kappaB, NLRP3 and gasdermin D activation in vivo, worsening experimental a

108 n-canonical caspase-11, canonical caspase-1, gasdermin D and cognate genes is induced in nervous tiss

109 cytokines (IL-1alpha, IL-1beta, IL-18), and gasdermin D and E (GSDMD/E) cleavage with parallel loss

110 nflammasome, where it is activated to cleave gasdermin D and induce pyroptosis.

111 ages as well as astrocytes but caspase-1 and gasdermin D are restricted to reactive microglia/macroph

112 Our data identify gasdermin D as a critical target of caspase-11 and a key

113 , and recruited four GBPs plus caspase-4 and Gasdermin D as a cytokine and cell death immune signalin

114 in D pores, consistent with our data showing gasdermin D associates with mitochondria and contributes

115 D, which contributes to our understanding of gasdermin D autoinhibition and activation and will infor

116 ivation of the pore-forming effector protein gasdermin D by inflammatory caspases.

117 in-3 also promotes caspase-11 activation and gasdermin D cleavage in macrophages treated with outer m

118 ells, characterized by NF-kappaB activation, gasdermin D cleavage, and increased secretion of proinfl

119 stantially reduced caspase-11 activation and gasdermin D cleavage, which are required for NLRP3 infla

120 caspase-11 to levels comparable with that of gasdermin D cleavage.

121 spase 11 dimerization and subsequent massive gasdermin D cleavage.

122 Finally, cathepsin inhibition reduced gasdermin D expression, thus revealing an unexpected rol

123 MAC by increasing NLRP3, pro-caspase 1, and gasdermin D expression.

124 Gasdermin D forms large, ~21 nm diameter pores in the pl

125 activation, polymorphisms that cause loss of gasdermin D function convert inflammatory pyroptotic cel

126 sttranslational modifications did not affect gasdermin D function or pyroptosis, polymorphisms disrup

127 be structurally important dramatically alter gasdermin D function.

128 ining a CARD (ASC), and pore-forming protein gasdermin D in TCI-TNBC neoplastic cells.

129 Knocking out pyrin, caspase-1, or gasdermin D inhibited the secretion of these S100 alarmi

130 Gasdermin D is an executioner of inflammatory cell death

131 Here we show that gasdermin D is essential for caspase-11-dependent pyropt

132 s confirmed that caspase-11 prefers cleaving gasdermin D over the pro-ILs.

133 Furthermore, introducing the gasdermin D P1'-P4' region into pro-IL18 enhanced cataly

134 rs through caspase-1 and caspase-11-mediated gasdermin D pore formation.

135 Gasdermin D pores allow for the secretion of active IL-1

136 Mechanistically, caspase-7 counteracts gasdermin D pores and preserves cell integrity by cleavi

137 utrophils secrete IL-1B through formation of gasdermin D pores and promote granulopoiesis.

138 ophils secrete IL-1beta through formation of gasdermin D pores and promote granulopoiesis.

139 in pyroptosis, with its release dependent on gasdermin D pores opened during pyroptosis.

140 Caspase-1 activates gasdermin D pores to lyse the cell; however, caspase-1 a

141 ptotic cells serve as carriers of functional gasdermin D pores to propagate pyroptosis to bystander c

142 er-membrane discontinuities the same size as gasdermin D pores, consistent with our data showing gasd

143 and pro-IL-18 and triggers the formation of gasdermin D pores.

144 e circulatory release of Ox-mtDNA by opening gasdermin D pores.

145 on adjacent to the cleavage site, influences gasdermin D recognition by caspase-11.

146 tides indicated that P1'-P4', the C-terminal gasdermin D region adjacent to the cleavage site, influe

147 Inflammasome processed pro-IL-1beta, and gasdermin D results in IL-1beta secretion that increases

148 maturation of caspase 1, IL-1beta, IL-18 and gasdermin D to drive inflammation and cell death, the ot

149 -18 secretion, cell death, and processing of gasdermin D were detected, indicating that pyroptosis wa

150 ta to generate mature bioactive cytokine and gasdermin D which facilitates IL-1 release and pyroptoti

151 During pyroptosis, GSDMD (gasdermin D), the pore-forming effector protein, is clea

152 tivates caspase-1 inflammasome and increases Gasdermin D, an effector of pyroptosis.

153 ge of the proinflammatory markers caspase-1, gasdermin D, and prointerleukin-1beta.

154 iated by the P1'-P4' region in its substrate gasdermin D, and similar experiments confirmed that the

155 n, including the activation of caspase-8 and gasdermin D, and the recruitment of NLRP3 and ASC into a

156 Mechanistically, caspase-11 cleaves gasdermin D, and the resulting amino-terminal fragment p

157 ses activate the pyroptosis effector protein gasdermin D, but caspase-1 mostly activates the inflamma

158 mbrane rupture through NINJ1, independent of gasdermin D, gasdermin E, and MLKL.

159 of other pore-forming executioner proteins, gasdermin D, gasdermin E, and MLKL.

160 is-associated speck-like protein, caspase-1, Gasdermin D, IL-1beta, IL-18, and tissue factor, in mono

161 Moreover, caspase-4, gasdermin D, interferon-beta, and cGAS levels were eleva

162 e 1 and 11, or of the pyroptosis executioner gasdermin D, reversed these adverse changes.

163 variation by investigating polymorphisms in gasdermin D, the key pyroptotic effector protein.

164 al structures of full-length human and mouse gasdermin D, which contributes to our understanding of g

165 ide (LPS) activated the pore-forming protein Gasdermin D, which formed mitochondrial pores and induce

166 -1beta and IL-18 and a pore-forming protein, gasdermin D, which triggers pyroptosis, an inflammatory

167 these cells die by an NLRP3, caspase-1, and gasdermin D-dependent induction of pyroptosis.

168 AS)-dependent interferon-beta production and gasdermin D-dependent interleukin-18 secretion.

169 We find that lipopolysaccharide elicits gasdermin D-dependent pyroptosis to enable passive SQSTM

170 ess in caspase cross talk and caspase-driven gasdermin D-induced pyroptosis.

171 litating caspase-1 activation and subsequent gasdermin D-mediated cell death and IL-1B and IL-18 cyto

172 litating caspase-1 activation and subsequent gasdermin D-mediated cell death and IL-1beta and IL-18 c

173 pendent membrane repair can delay or prevent gasdermin D-mediated cell death.

174 It is a lytic process driven by gasdermin D-mediated cellular permeabilization and presu

175 w how M. tuberculosis causes caspase-1/NLRP3/gasdermin D-mediated pyroptosis of human monocytes and m

176 cytokines IL-1beta and IL-18, as well as to gasdermin D-mediated pyroptotic cell death.

177 Like GSDME-N, inflammasome-generated gasdermin D-N (GSDMD-N), can also permeabilize the mitoc

178 including NLRP3-inflammasome, caspase-1, and gasdermin D.

179 ent in IL-1B, ASC, caspase-1, caspase-11, or gasdermin D.

180 tivate NF-kappaB, the NLRP3 inflammasome and gasdermin D.

181 NLRP3 and AIM2 inflammasomes, caspase-1 and gasdermin D.

182 future development of therapeutics targeting gasdermin D.

183 but did not absolutely require Caspase-1 or Gasdermin D.

184 the inflammatory cell death, pyroptosis, via gasdermin D.

185 CARD (ASC) speck; cleavage of caspase-1 and gasdermin D; release of IL-1beta, IL-18, caspase-1, and

186 deficiencies of caspases-8/1/11 or caspase-8/gasdermin-D (GSDM-D) renders mice impaired to produce bo

187 Gasdermin-D (GSDMD) in inflammasome-activated macrophage

188 Gasdermin-D (GsdmD) is a critical mediator of innate imm

189 In this context, gasdermin-D (GsdmD) is a cytoplasmic protein that is act

190 Gasdermin-D (GSDMD) is cleaved by caspase-1, caspase-4,

191 Gasdermin-D (GSDMD) is the ultimate effector of pyroptos

192 During pyroptosis, the formation of gasdermin-D (GSDMD) pores on the plasma membrane leads t

193 Since a new gasdermin-D (GSDMD) protein was identified in 2015, vari

194 a release is gasdermin-D dependent, and that gasdermin-D and caspase-1/11 deficient mice show deficit

195 uman caspase-4 (murine caspase-11) to cleave gasdermin-D and induce pyroptotic cell death.

196 f IL-1beta and IL-18, as well as cleavage of Gasdermin-d and pyroptotic cell death.

197 f pro-interleukin (IL)-1beta, pro-IL-18, and gasdermin-D by activated caspase-1 resulted in the cellu

198 y, we show that ex vivo IL-1alpha release is gasdermin-D dependent, and that gasdermin-D and caspase-

199 Increased active Caspase-1 and Gasdermin-D expression was observed in human and rat cir

200 omain-like protein (MLKL) in necroptosis and gasdermin-D in pyroptosis] were recently discovered, bri

201 Inflammatory caspases cleave gasdermin-D in the interdomain linker but not GSDMB.

202 ecretion of bioactive IL-1beta and IL-18 via gasdermin-D pores in the plasma membrane.

203 tasis specifically through its regulation of gasdermin-D, and not via its involvement in the producti

204 ere we report that inflammasomes trigger the Gasdermin-D- and calcium-dependent eruption of filopodia

205 ough the GBP platform is essential to induce gasdermin-D-dependent pyroptosis and processing of inter

206 long with continuous NLRP3-inflammasome- and Gasdermin-D-dependent pyroptotic cell death.

207 ers the production of cytokines as well as a gasdermin-D-mediated form of cell death known as pyropto

208 n 2, and reducing cleavage of caspase 11 and gasdermin-D.

209 phipathic alpha-helices, as shown for murine gasdermin-D.

210 f the recently described pyroptotic effector gasdermin-D.

211 ing and release of IL-1beta independently of gasdermin-D.

212 Here we identify Gasdermin E (GSDME) as a master switch for neutrophil ly

213 , while tumor cells treated with HLA display Gasdermin E (GSDME) cleavage and a cellular phenotype re

214 ort that the related gasdermin family member gasdermin E (GSDME) is activated upon detection of YopJ

215 cell death was observed through a caspase-3/gasdermin E (GSDME) pathway, achieving notable antitumor

216 nd death receptor-mediated apoptosis promote gasdermin E (GSDME)-dependent calcium mobilization and m

217 Gasdermin E (GSDME, also known as DFNA5)-mutated in fami

218 Gasdermin E (GSDME/DFNA5) cleavage by caspase-3 liberate

219 Generation of gasdermin E KO and ATG7 KO THP-1 cells revealed that the

220 the release of IL-1beta was not dependent on gasdermin E or ATG7.

221 e through NINJ1, independent of gasdermin D, gasdermin E, and MLKL.

222 e-forming executioner proteins, gasdermin D, gasdermin E, and MLKL.

223 sed NRAS mutant xenograft growth and induced gasdermin E-associated pyroptosis.

224 pid-binding motif to match that of the other gasdermins enhanced GsdmC oligomerization and increased

225 Members of the gasdermin family contain positively charged N-terminal d

226 Here, we report that the related gasdermin family member gasdermin E (GSDME) is activated

227 d for lytic cell death is dependent on which gasdermin family member is activated.

228 caspases to develop a system that activates gasdermin family members in an efficient and equivalent

229 Determination of the propensity of various gasdermin family members to cause pyroptosis has been ha

230 and common features of autoinhibition among gasdermin family members utilizing their beta1-beta2 loo

231 n contrast to the canonical function of most gasdermin family members, GSDMB does not inhibit Shigell

232 shares this pore-forming ability with other gasdermin family members, which induce pyroptosis during

233 thin the NTDs is known to inactivate several gasdermin family members.

234 C is one of the least studied members of the gasdermin family of proteins, known for their critical i

235 identifying a previously unknown function of gasdermin family proteins.

236 Here, we review the broader gasdermin family, focusing on recent discoveries in inve

237 in, a peroxisome-associated protein from the gasdermin family, has been shown to protect against this

238 Additionally, we comprehensively examine the Gasdermin family, renowned for their role as executioner

239 a comprehensive evolutionary analysis of the gasdermin family.

240 we review current knowledge of the family of gasdermins, focusing on their mechanisms of action and r

241 To investigate the role of the gasdermin gene family an antiserum was raised to a pepti

242 , we uncovered that the vast majority of the gasdermin genes are clustered with protease-encoding gen

243 discuss the implications for the rest of the gasdermin (GSDM) family, which are emerging as mediators

244 Gasdermin (GSDM) proteins are a family of pore-forming e

245 Gasdermin (GSDM) proteins are executioner pore-forming m

246 In response to pathogen infection, gasdermin (GSDM) proteins form membrane pores that induc

247 Gasdermins (GSDMs) are a family of pore-forming effector

248 Gasdermins (GSDMs) are a family of pore-forming proteins

249 Gasdermins (GSDMs) are mediators of cell death that trig

250 Gasdermins (GSDMs) are pore-forming proteins that play c

251 ily of structurally related proteins [(i.e., gasdermins (GSDMs)].

252 have been identified, how GSDMA-the dominant gasdermin in the skin-is activated, remains unknown.

253 This expression pattern suggests a role for gasdermins in differentiation of the epidermis and its a

254 asdermins share many features with mammalian gasdermins including their mode of activation through pr

255 an monocytes, caspase-8 functions in a novel gasdermin-independent mechanism controlling IL-1beta rel

256 icity for cargo-release and how cells repair gasdermin-induced damage to the plasma membrane.

257 verses the SASP, and mitigates ROS and NLRP3/Gasdermin/interleukin (IL)-1beta-driven pyroptotic epith

258 ow that the cytotoxic activity of the HET-Q1 gasdermin is controlled by proteolysis.

259 Gasdermin-mediated inflammatory cell death (pyroptosis)

260 Differences in gasdermin-mediated pyroptosis between cell types, stimul

261 At its most simple, gasdermin-mediated pyroptosis in bacterial infection wou

262 Gasdermin-mediated pyroptosis is a newly discovered mech

263 Gasdermin-mediated pyroptosis is a typical inflammatory

264 iew we cover recent advances in the field of gasdermin-mediated pyroptosis with a focus on bacterial

265 Additionally, we discuss how pyroptosis and gasdermins might contribute to the dysfunction of epithe

266 f microbial and endogenous agents, including gasdermin, MLKL and the MLKL-like action of coronavirus

267 Gasdermins oligomerize to form pores in the cell membran

268 Caspase-1 repeatedly changes its target gasdermin over evolutionary time at speciation junctures

269 Here we discuss how gasdermin pore formation is regulated to induce membrane

270 Gasdermin pore formation is triggered by caspase-mediate

271 ecular and cellular mechanisms that regulate gasdermin pore formation.

272 However, gasdermin pore forming activities must be tightly regula

273 activate caspases, which, in turn, activate gasdermin pore-forming proteins to induce pyroptotic cel

274 duce membrane permeabilization or lysis, how gasdermin pores achieve specificity for cargo-release an

275 g, and electrophysiology to demonstrate that gasdermin pores display phosphoinositide-dependent dynam

276 tosis by repairing and subsequently removing gasdermin pores.

277 ich are permeabilized in a process requiring gasdermin pores.

278 The N- and C-terminal domains of all gasdermins possess lipid-binding and regulatory activiti

279 and knocking out Mst1/2 causes dysregulated gasdermin protein cleavage for pyroptotic death.

280 D (GSDMD) is a protein which belongs to the gasdermin protein family and plays a role in inflammator

281 akin gene, which encodes a new member of the gasdermin protein family.

282 Most gasdermin proteins are believed to have pore-forming cap

283 Gasdermin proteins form large membrane pores in human ce

284 Collectively, our results point to a role of gasdermin proteins in targeting the mitochondria to prom

285 t few years to investigate the mechanisms of gasdermin proteins in the activation and pore formation.

286 Cleavage of the gasdermin proteins to produce pore-forming amino-termina

287 In this review, we discuss the gasdermin proteins with particular emphasis on GSDMD and

288 Similar to gasdermin, RCD-1 binds acidic phospholipids in vitro, no

289 Different features of gasdermin sequence, structure, expression characteristic

290 Fungal and bacterial gasdermins share many features with mammalian gasdermins

291 osites in diverse proteases engage different gasdermin substrates.

292 It is the only gasdermin that lacks a mouse ortholog, making in vivo me

293 Mammals encode five gasdermins that can trigger pyroptosis: GSDMA, B, C, D,

294 log of the N-terminal pore-forming domain of gasdermin, the executioner protein of a highly inflammat

295 ied family of pore-forming proteins known as gasdermins, the best characterized of which is gasdermin

296 een established between mammalian and fungal gasdermins, the molecular pathways regulating gasdermin

297 icles (LNPs) encoding only the N-terminus of gasdermin to trigger pyroptosis, eliciting robust antitu

298 Bacterial gasdermins were activated by dedicated caspase-like prot

299 Gasdermins were recently identified as the mediators of

300 ptosis occurs when activated caspases cleave gasdermins, which can then form pores in the plasma memb