ライフサイエンスコーパス: ATG5

1 ly deficient in an autophagy-essential gene (ATG5).

2 nd requires the protein autophagy related 5 (ATG5).

3 mediated silencing of the autophagy mediator ATG5.

4 h promotes lipidation upon its attachment to ATG5.

5 agy inhibitors and short interfering RNA for ATG5.

6 presynaptic autophagy in part by scaffolding Atg5.

7 eins GBP1 or GBP2 and the autophagic protein ATG5.

8 oxygen production by the NADPH oxidase, and ATG5.

9 hox and p67phox, NOS2, and autophagy through ATG5.

10 ear PRKN or MSR1, and exonic duplications of ATG5.

11 roglial cells is abrogated in the absence of ATG5.

12 niques, we showed that RACK1 interacted with ATG5.

13 flux and defects in conjugation of ATG12 to ATG5.

14 es a physical association of AMPK with ATG16-ATG5-12 and an AMPK-dependent recruitment of the VPS34 a

15 231M mutant of WIPI2b to ATG16L1 (as well as ATG5-12) is significantly reduced in GFP pull-down exper

16 Atg5/7-deficient TM cells showed changes in transcript l

17 but grew normally in macrophages that lacked ATG5, a component of the autophagy LC3 conjugation syste

18 The induction of autophagy depended upon ATG5, a critical autophagy regulator, but the inhibition

19 The activation involves Atg5, a key component of autophagy, but not the mTOR pat

20 p5-Cre) allows us to specifically inactivate Atg5, a protein necessary for autophagy, in salivary aci

21 Atg5 (A5;Kras) or heterozygous disruption of Atg5 (A5(+/-);Kras), and compared them with mice with on

22 ncer cells and have homozygous disruption of Atg5 (A5;Kras) or heterozygous disruption of Atg5 (A5(+/

23 ladenine or overexpressing dominant-negative ATG5 abolished the deficiency of the p38alpha MAPK-induc

24 s deficient for the essential autophagy gene ATG5 Accordingly, inhibition of PLA2 significantly decre

25 berculosis infection, reveal new outcomes of ATG5 activity, and shed light on early events in innate

26 iated TFEB relocalization required Atg9A and Atg5 activity.

27 se was significantly reduced by knockdown of ATG5 Additionally, trehalose downregulated the expressio

28 has been confirmed at the mRNA level: PRDM1, ATG5, AIM1, and HACE1.

29 Accordingly, shRNA-mediated suppression of Atg5, an E3 ubiquitin ligase essential for autophagosome

30 stically, Bassoon was found to interact with Atg5, an E3-like ligase essential for autophagy, and to

31 Cells lacking ATG5, an essential component of the LC3 lipidation machi

32 3-kinase (PI3-kinase) prevented induction of ATG5 and activation of LC3-II and blocked autophagosome

33 -5-16L1-positive puncta, and interacted with Atg5 and also with Atg12-5 conjugate.

34 ion of these microRNAs reduced the levels of ATG5 and ATG16L1 and inhibited autophagy, leading to inc

35 terocytes blocked AIEC-induced inhibition of ATG5 and ATG16L1 expression and restored functional auto

36 en levels of MIR30C and MIR130A and those of ATG5 and ATG16L1, supporting in vitro findings.

37 f these same microRNAs and reduced levels of ATG5 and ATG16L1.

38 the autophagosome membrane extension, Atg4, Atg5 and Atg3.

39 by deletion of two essential autophagy genes ATG5 and ATG7 leads to failure of CHK1 activation by 20A

40 of AGR2 level in cells genetic depletion of Atg5 and Atg7, or by autophagy inhibitors.

41 h silenced expression of the autophagy genes Atg5 and Atg7.

42 is not essential for synthesizing the ATG12-ATG5 and ATG8-phosphatidylethanolamine adducts that are

43 in expression levels of ATG4 family members, ATG5 and BECLIN-1 are significantly increased in CD34(+)

44 This signalling is dependent on ATG5 and Beclin1 but not on ATG13, suggesting ARE belong

45 ression analysis revealed elevated levels of ATG5 and BNIP3 in acid-conditioned cells, suggesting cel

46 Caspase-8 forms a complex with Atg5 and colocalizes with LC3 and p62.

47 tory paradigm, HuD-null mice displayed lower ATG5 and LC3 levels in pancreatic beta cells.

48 ver, t-TUCB restored hepatic levels of Atg12-Atg5 and LC3-II conjugates and reduced p62 expression, i

49 ns in protein levels of autophagy regulators Atg5 and phospho-mTOR, and suppression of biochemical fe

50 studies have identified polymorphisms in the Atg5 and possibly Atg7 genes, involved in both canonical

51 pancreatic cells, heterozygous disruption of Atg5 and reduced protein levels promotes tumor developme

52 The protein ATG5 and the kinase ULK1 are involved in classical autop

53 deed, with dual blockade of both pathways by Atg5(-/-) and dominant-negative rab5, ER cholesterol fai

54 tial autophagy proteins autophagy related 5 (ATG5) and beclin1 increased NVP-BEZ235-mediated radiosen

55 Mutations and methylation in PRDM1, ATG5, and AIM1 have been reported in NKTCL cell lines.

56 her autophagy genes including Atg14, Fip200, Atg5, and Atg7 in myeloid cells also led to elevated bas

57 sion of three autophagy-related genes, Atg3, Atg5, and Atg7 were identified to be inhibited by MPA tr

58 y and autophagy-initiation proteins Atg3 and Atg5, and it is abrogated by chelating cytoplasmic calci

59 ompanied by increased expression of beclin1, ATG5, and LC3-II and autophagosome formation marked by t

60 with changes in lung expression of LC3B-II, ATG5, and p62, consistent with increased autophagy, and

61 ess markers CHOP, GADD45, EDEM, ATF4, Hsp90, ATG5, and phospho-eIF2alpha.

62 e concerted interactions among TECPR1, Atg12-Atg5, and PtdIns(3)P provide the fusion specificity betw

63 hagy requires the core pathway kinases Atg1, Atg5, and Vps34, and other components of the phosphatidy

64 cles that are mobilized to the vacuole in an ATG5- and ATG7-dependent manner.

65 In human PDAC samples, lower levels of ATG5 associated with tumor metastasis and shorter surviv

66 at 3p14, the SCHIP1-IL12A locus at 3q25, and ATG5 at 6q21, as well as a suggested association of the

67 s on the role ubiquitin-like proteins (UBLs)-Atg5, Atg12, and Atg8-play in the formation of the doubl

68 rculosis co-localizes with autophagy factors ATG5, ATG12, ATG16L1, p62, NDP52, BECN1 and LC3, stimula

69 pression of key autophagy effectors (such as ATG5, ATG12, LC3B and LAMP1) and AMPK-dependent activati

70 TUFM interacted with Atg5-Atg12 and Atg16L1 and has similar functions as NLRX

71 g Atg7 or Atg5 or blocking LC3 lipidation or ATG5-ATG12 conjugation decreases ERK phosphorylation.

72 and DFCP1 to autophagic precursors, reduced ATG5-ATG12 conjugation, and compromised autophagosome fo

73 IFNgamma against MNV in macrophages required Atg5-Atg12, Atg7, and Atg16L1, but not induction of auto

74 functions of the autophagy-related proteins Atg5-Atg12, but NLRX1 did not associate with Atg5-Atg12.

75 Atg5-Atg12, but NLRX1 did not associate with Atg5-Atg12.

76 Thus, the Atg5-Atg12/Atg16L1 complex performs a pivotal, nondegrad

77 We show that the Atg5-Atg12/Atg16L1 protein complex, whose prior known fu

78 ed autophagy by competing with ATG16 to bind ATG5/ATG12 and preventing ATG16/ATG5/ATG12 formation.

79 TG16 to bind ATG5/ATG12 and preventing ATG16/ATG5/ATG12 formation.

80 at escape senescence express a high level of ATG5/ATG12.

81 Increased expression of Atg5, Atg16, Irgm1, Tlr4, and Lyz genes was observed in

82 The interaction of the Atg12~Atg5-Atg16 complex and Atg8 with Atg19 is mutually exclu

83 The interaction of Atg19 with the Atg12~Atg5-Atg16 complex is mediated by its Atg8-interacting m

84 ATG5 is a key component of an E3-like ATG12-ATG5-ATG16 protein complex that catalyzes conjugation of

85 tg3, the E1 Atg7, and the composite E3 Atg12-Atg5-Atg16 with pathologies including cancers, infection

86 ptors interact with the E3-like enzyme Atg12~Atg5-Atg16, which stimulates Atg8 conjugation.

87 not of other essential autophagy components ATG5, ATG16L1 or ATG7-in mediating quiescence of tissue-

88 Levels of ATG5, ATG16L1, and SQSTM1 (also called p62) were knocked

89 pendent of the autophagy-elongation proteins ATG5, ATG16L1, ATG4B, ATG7, and LC3B.

90 roteins to phagophore membranes by the ATG12-ATG5-ATG16L1 (E3) complex are two critical steps in auto

91 olamine, including Atg7, Atg3, and the Atg12-Atg5-Atg16L1 complex play crucial roles in the control o

92 12 is a component of the ATG12 approximately ATG5-ATG16L1 E3 complex that promotes lipid conjugation

93 The Atg12-Atg5/Atg16L1 complex is recruited by WIPI2b to the site

94 diated knockdown of pro-autophagic proteins (ATG5, ATG7 and Beclin-1) also restores Delta133p53alpha

95 We identified Atg5, Atg7, Bax, Bid, Bik, and Noxa as potential therape

96 me key autophagy-related proteins, including Atg5, Atg7, Beclin-1 and LC3A/B-II, seen in HFD-fed cont

97 ssing LAP components (Nox2, Rubicon, Beclin, Atg5, Atg7, or Atg16L1) but not in macrophages defective

98 tophagy in vitro by RNA interference against ATG5 (autophagy-related 5) decreased the phagocytosis of

99 n cells depleted of the autophagic mediators ATG5, Beclin1, and p62.

100 mportantly, Atg5 LOF as well as targeting an Atg5-binding peptide derived from Bassoon inhibited pres

101 evelopment, whereas homozygous disruption of Atg5 blocks tumorigenesis.

102 ugh a pathway that is dependent on WIPI2 and ATG5 but independent of the ULK and VPS34-beclin kinase

103 ATG5 but not ULK1 cooperated with ELMO1 in LC3 accumulat

104 formed immortalized Baby Mouse Kidney (iBMK) ATG5(+/+) but not in autophagy-deficient ATG5(-/-) cells

105 We further found that adoptive transfer of Atg5(-/-), but not wild-type, bone marrow-derived dendri

106 ar response to oncogenic RAS, overexpressing ATG5, but not autophagy-deficient ATG5 mutant K130R, byp

107 tophagy-related proteins Beclin 1, PI3K, and ATG5, but not on the upstream autophagy-initiating prote

108 G5(-/-) fibroblasts to a greater extent than ATG5(+/+) cells.

109 Decreased ERK phosphorylation in Atg5(-)/(-) cells does not occur from overactive phospha

110 MK) ATG5(+/+) but not in autophagy-deficient ATG5(-/-) cells.

111 y increased calpain activation, beclin 1 and ATG5 cleavage, and intestinal epithelial cell (IEC) deat

112 lin1 from Bcl-2 by activating JNK and blocks Atg5 cleavage, both of which are critical for the induct

113 n 3 (LC3) form II (LC3-II) and LC3 puncta in Atg5-competent BMMs but not in Atg5-deficient BMMs, whil

114 ere we report that TECPR1 binds to the Atg12-Atg5 conjugate and phosphatidylinositol 3-phosphate (Ptd

115 mutually exclusive complexes with the Atg12-Atg5 conjugate, and TECPR1 binds PtdIns(3)P upon associa

116 s PtdIns(3)P upon association with the Atg12-Atg5 conjugate.

117 utophagy by knockdown of the autophagic gene ATG5 consistently reduced melanoma cell survival in low

118 in an autophagy-deficient Arabidopsis mutant atg5 correlated with N-BODIPY labeling.

119 r proliferation levels in salivary glands of Atg5/Cre mice from each genotype.

120 Salivary flow rates and amylase contents of Atg5/Cre mice indicated that acinar-specific inactivatio

121 Atg5 deficiency did not alter reactivation from B cells,

122 high concentrations of Rapamycin in LC3B and ATG5 deficient bone marrow derived macrophages, suggesti

123 LC3 puncta in Atg5-competent BMMs but not in Atg5-deficient BMMs, while no p62 turnover was observed.

124 Elimination of autophagy using Atg5-deficient fibroblasts or siRNA-mediated impairment

125 elanin-deficient A. fumigatus is restored in Atg5-deficient macrophages and in mice upon conditional

126 Pancreata from ATG5-deficient mice had signs of inflammation, necrosis,

127 ed on transcriptome and metabolome analyses, ATG5-deficient mice produced higher levels of reactive o

128 ATG5-deficient mice were placed on diets containing 25%

129 atitis (CP) and compared with pancreata from ATG5-deficient mice.

130 d many histologic similarities to those from ATG5-deficient mice.

131 ce of this process was verified in mice with Atg5-deficient RPE cells that showed evidence of disrupt

132 ably, compared with kidneys of control mice, Atg5(Delta) (flox/) (Delta) (flox) kidneys showed more c

133 f autophagy in proximal tubular S3 segments (Atg5(Delta) (flox/) (Delta) (flox)) presented with signi

134 However, the canonical ATG5-dependent autophagy pathway is not required for IFI

135 pergillus fumigatus germination activates an Atg5-dependent autophagy pathway termed LC3-associated p

136 Deficiency of ATG5-dependent autophagy reduced T-cell proliferation an

137 Our findings demonstrate that ATG5-dependent autophagy uncouples T-cell proliferation

138 ian cells with LAT led to enhanced mTOR- and Atg5-dependent autophagy.

139 tes mammalian target of rapamycin (mTOR) and Atg5-dependent autophagy.

140 In several in vivo models of allo-HSCT, ATG5-dependent dissociation of T-cell functions contribu

141 ane phagosomes containing engulfed POS in an Atg5-dependent manner that required Beclin1, but not the

142 degradation and amyloid beta clearance in an Atg5-dependent manner.

143 Mice with pancreas-specific disruption of Atg5 develop a form of CP similar to that of humans.

144 Mice with pancreas-specific disruption of Atg5 developed atrophic CP, independent of beta-cell fun

145 dicated that acinar-specific inactivation of ATG5 did not alter carbachol-evoked saliva and amylase s

146 c and proapoptotic functions of beclin 1 and ATG5 during inflammation.

147 dings shift our understanding of the role of ATG5 during M. tuberculosis infection, reveal new outcom

148 RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished SAHA's car

149 ch Atg5 is substituted with the mutant human ATG5 exhibit severe movement disorder, in contrast to fl

150 ntiation into TH9 cells relative to Atg3- or Atg5-expressing control cells.

151 Our results reveal HuD to be an inducer of ATG5 expression and hence a critical regulator of autoph

152 his study, we investigated the regulation of ATG5 expression by HuD.

153 is known about the mechanisms that regulate ATG5 expression levels.

154 Both in vivo and in vitro, Atg5(f/f)/Cre(+) acinar cells had reduced intracellular

155 orms, were infrequently observed in infected Atg5(f/f)/Cre(+) cells.

156 Compared to Cre(-) littermates, Atg5(f/f)/Cre(+) mice had an approximately 2,000-fold lo

157 We generated Atg5(f/f)/Cre(+) mice, in which the essential autophagy

158 Additionally, administration of IGF-1 to Atg5(f/f);Aqp5-Cre mice did not preserve physiological f

159 In this study, we utilized Atg5(f/f);Aqp5-Cre mice which harbor a conditional knock

160 Collectively, Atg5(f/f);Aqp5-Cre mice would be a useful tool to enhanc

161 ted secretory granules in salivary glands of Atg5(f/f);Aqp5-Cre mice.

162 y for autophagy, in salivary acinar cells of Atg5(f/f);Aqp5-Cre mice.

163 activated T cells lacking the autophagy gene Atg5 fail to upregulate Foxp3 to the same extent as wild

164 Taken together, our results demonstrate that Atg5 favors R. australis infection in mouse macrophages

165 P-BEZ235 radiosensitized autophagy-deficient ATG5(-/-) fibroblasts to a greater extent than ATG5(+/+)

166 M. tuberculosis infection of Atg5(fl/fl) LysM-Cre(+) mice relative to autophagy-profi

167 The greater concentration of R. australis in Atg5(flox/flox) bone marrow-derived macrophages (BMMs) t

168 ne marrow-derived macrophages (BMMs) than in Atg5(flox/flox) Lyz-Cre BMMs in vitro was abolished by e

169 (flox/flox) mice than in the counterparts of Atg5(flox/flox) Lyz-Cre mice, in association with a redu

170 significantly greater in infected tissues of Atg5(flox/flox) mice than in the counterparts of Atg5(fl

171 conditional deletion of autophagy-related 5 (Atg5) for selective ablation of autophagy in proximal tu

172 otecting the autophagy proteins beclin 1 and ATG5 from calpain-mediated cleavage during inflammation.

173 ds verified that HMGB1 protects beclin 1 and ATG5 from calpain-mediated cleavage events that generate

174 Mice with a conditionally knocked out ATG5 gene in myeloid cells showed increased susceptibili

175 he first time, we found that deletion of the Atg5 gene specifically in CD11c(+) cells, which leads to

176 vivo and autophagy-independent functions of ATG5 have been described.

177 CD4 T cells lacking Atg3 or Atg5 have increased interleukin-9 (IL-9) expression upon

178 o, and mice with T cell-specific deletion of Atg5 have reduced tumour outgrowth in an IL-9-dependent

179 In HCC patients, the expression of low-Atg5, high-miR-224, and low-Smad4 showed significant cor

180 Through its effect on ATG5, HuD contributed to the lipidation of LC3 and the f

181 The absence of ATG5 in allo-stimulated T cells enhanced their ability t

182 mice that lack the autophagy-related protein Atg5 in cardiomyocytes.

183 A (siRNA) knockdown of the autophagy protein Atg5 in CCCP-treated cells.

184 deletion of the essential autophagy protein ATG5 in classical dendritic cells (DCs), which are prese

185 Knockdown of ATG5 in HCT-116 cells increased 11G5-induced senescence,

186 Knockdown of ATG5 in HCT-116 cells increased numbers of intracellular

187 and in mice upon conditional inactivation of Atg5 in hematopoietic cells.

188 hibition of autophagy or genetic deletion of Atg5 in hepatocytes did not protect against TNF-alpha/Ac

189 These data highlight the contribution of Atg5 in macrophages to the pathogenesis of rickettsial d

190 By contrast, mice lacking ATG5 in monocyte-derived cells and neutrophils (polymorp

191 lacking the essential autophagy gene Atg7 or Atg5 in myeloid cells.

192 Knockdown of Atg5 in pancreatic cancer cell lines increased their mig

193 es during M. tuberculosis infection, loss of Atg5 in PMNs can sensitize mice to M. tuberculosis.

194 alphav and the autophagy components LC3 and atg5 in regulating TLR signalling and B-cell immunity.

195 ated' in the sentence starting: 'Deletion of Atg5 in the host similarly regulated circulating arginin

196 utation, changing a conserved amino acid, in ATG5 in two siblings with congenital ataxia, mental reta

197 p whereby knocking down the autophagy factor ATG5 in Wnt5A(high) cells decreased Wnt5A and increased

198 owed a key role for the autophagy related 5 (Atg5) in resistance to Toxoplasma gondii.

199 mice which harbor a conditional knockout of Atg5, in salivary acinar cells.

200 0, beclin 1, Atg14, Atg16l1, Atg7, Atg3, and Atg5, in the myeloid compartment, inhibited MHV68 reacti

201 erefore, the scaffold protein RACK1 is a new ATG5-interacting protein and an important and novel comp

202 rget of rapamycin blockage) stimulated RACK1-ATG5 interaction.

203 tor activated C-kinase 1, GNB2L1) as a novel ATG5 interactor and an autophagy protein.

204 Interestingly, the autophagy product ATG5 involved in autophagosome elongation positively reg

205 Induction was dependent on Atg5, involved processing of LC3 to LC3II, and led to a

206 Accumulating data indicate that ATG5 is a convergence point for autophagy regulation.

207 ATG5 is a key component of an E3-like ATG12-ATG5-ATG16 p

208 t cancer cell model where the autophagy gene ATG5 is dispensable in A549 cells in vitro, yet promotes

209 Furthermore, while Atg5 is dispensable in alveolar macrophages during M. tu

210 The autophagy protein ATG5 is essential for the formation of autophagosomes by

211 mice, in which the essential autophagy gene Atg5 is specifically deleted in pancreatic acinar cells,

212 Flies in which Atg5 is substituted with the mutant human ATG5 exhibit s

213 Importantly, ATG5 is the only autophagy factor that has been studied

214 allo-immunity, we generated T-cell-specific Atg5 knock-out mice.

215 syncytium formation was markedly reduced by ATG5 knockdown (P < 0.0001).

216 xperiments using chemical inhibitors, stable ATG5 knockdown cell lines, and ATG16L1 knockout cells (g

217 ULK1/2 or VPS34 attenuated secretion, while Atg5 knockdown potentiated FABP4 release.

218 an processing of VZV gE were decreased after ATG5 knockdown, while expression of the nonglycosylated

219 phagy from a lentiviral autophagy-related 5 (Atg5) knockdown were resistant to toxicity from TNF, but

220 athogenesis, we generated adipocyte-specific Atg5 knockout (KO), adipocyte-specific mTOR KO, adipocyt

221 h a tamoxifen-inducible, hepatocyte-specific Atg5 knockout were similarly sensitized to cathepsin-dep

222 In contrast, nonactivated ATG5-knockout BMMs actually restricted C. neoformans gro

223 ATG5-knockout bone marrow-derived macrophages (BMMs) als

224 in mice by bafilomycin A1 or in Becn1+/- and Atg5 KO mice eliminates AGGF1-mediated angiogenesis and

225 Adipocyte-specific Atg5 KO mice had increased circulating levels of fibrobl

226 The expression levels of HuD, ATG5, LC3, and beta-actin were determined by Western blo

227 n of autophagosome formation by depletion of Atg5 led to higher levels of C99 and to its massive accu

228 phagy in PDAC should consider the effects of ATG5 levels to avoid the expansion of resistant and high

229 A5(+/-);Kras mice, with reduced Atg5 levels, developed more tumors and metastases, than

230 Importantly, Atg5 LOF as well as targeting an Atg5-binding peptide de

231 ur data indicate that neutrophilic asthma in Atg5(-/-) mice is glucocorticoid resistant and IL-17A de

232 ped CD11c-specific autophagy-related gene 5 (Atg5)(-/-) mice and used several murine models to invest

233 ependent of canonical autophagy: both WT and Atg5(-/-) mouse embryonic fibroblasts responded similarl

234 bitor bafilomycin and in autophagy-deficient Atg5(-/-) mouse embryonic fibroblasts.

235 cantly higher levels of Cathepsin K mRNA and Atg5 mRNA and protein.

236 We identified ATG5 mRNA as a post-transcriptional target of the mammal

237 Modulating HuD abundance did not alter ATG5 mRNA levels, but HuD silencing decreased ATG5 mRNA

238 TG5 mRNA levels, but HuD silencing decreased ATG5 mRNA translation, and, conversely, HuD overexpressi

239 and, conversely, HuD overexpression enhanced ATG5 mRNA translation.

240 The association of HuD with ATG5 mRNA was analyzed by ribonucleoprotein complex immu

241 HuD associated with the 3'-UTR of the ATG5 mRNA.

242 Autophagy protein 5 (Atg5) mRNA and protein levels were analysed by PCR and W

243 expressing ATG5, but not autophagy-deficient ATG5 mutant K130R, bypasses RAS-induced senescence, wher

244 in for caspase-8 activation, associates with Atg5 on Atg16L- and LC3-positive autophagosomal membrane

245 We find that RILP also interacts with ATG5 on isolation membranes, precluding premature dynein

246 erfering RNAs (siRNAs) targeting beclin 1 or Atg5 on the cytotoxicity of cisplatin.

247 0R, bypasses RAS-induced senescence, whereas ATG5 or ATG3 deficiency predisposes to it.

248 In autophagy-deficient Atg5 or Atg3 null mouse embryonic fibroblasts, OFD1 accu

249 n of autophagosome formation by depletion of Atg5 or Atg3 results in a marked suppression of caspase-

250 e also lacking the essential autophagy genes Atg5 or Atg7 accumulate low-grade, pre-malignant pancrea

251 tissues using small interfering RNAs against Atg5 or Atg7 and chemical antagonists.

252 e expression, the absence of macroautophagy (ATG5 or ATG7 expression), an increase in mitochondrial m

253 ng either of the autophagy-related molecules Atg5 or Atg7 had little to no effect on the proliferatio

254 by depletion of the major autophagy factors Atg5 or Atg7 had no effect on WNV infectious particle pr

255 Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS

256 r knockdown of the essential autophagy genes Atg5 or Atg7 inhibits the in vitro secretion of VWF.

257 ice with a T lymphocyte-specific deletion of Atg5 or Atg7, two members of the macroautophagic pathway

258 Depletion of ATG5 or beclin-1, major mediators of autophagy, prevents

259 ne) or small interfering RNA (siRNA) against ATG5 or beclin-1.

260 Deleting Atg7 or Atg5 or blocking LC3 lipidation or ATG5-ATG12 conjugatio

261 Endothelial-specific deletion of Atg5 or pharmacological inhibition of autophagic flux re

262 ically by shRNA targeting Ulk1, beclin-1, or Atg5 or pharmacologically by 3-methyladenine [3-MA] or s

263 down-regulation of host autophagy protein 5 (ATG5) or autophagy protein 9A (ATG9A) decreased parasite

264 restored in mice deficient in NADPH oxidase, Atg5, or Atg7, demonstrating that CpsA makes a significa

265 RSV infection was promoted in ATG5- or ATG7-silenced plants and was inhibited in GAPC-

266 N1, targeting other autophagy genes, such as ATG5, p62/SQSTM1, or inhibiting autophagy pharmacologica

267 Instead, ATG5 plays a unique role in protection against M. tuberc

268 oss of STX13 also caused the accumulation of Atg5-positive puncta and the formation of multilamellar

269 RNA against the autophagic machinery Atg7 or Atg5 prolonged the survival of neurons co-treated with B

270 by knocking down the core autophagy protein Atg5 promotes cystogenesis, while activation of autophag

271 f varying levels of the autophagy related 5 (Atg5) protein on pancreatic tumor formation and progress

272 ed mice with pancreas-specific disruption of Atg5 (Ptf1aCreex1;Atg5F/F mice) and compared them to con

273 The Atg5-related reactivation defect was partially reversed

274 ATG5 represses transcriptional activation by the TGFbeta

275 intracellular fungal growth, as silencing of Atg5 resulted in impaired phagosome maturation and killi

276 critical autophagy gene autophagy-related 5 (Atg5) resulted in decreased cytokine secretion and incre

277 cin A1, or depletion of autophagy-related 5 (ATG5), results in accumulation of intracellular VEGFA, i

278 etic approaches (siRNA-mediated knockdown of Atg5) sensitized cardiomyocytes to glucose deprivation-i

279 ly, inhibition of autophagosome formation by ATG5 shRNA dramatically increases localization of active

280 ab1A) or down-regulated (3-methyladenine and ATG5 shRNA) by enhancers or inhibitors of autophagy or b

281 vity of Dp44mT was suppressed by Beclin1 and ATG5 silencing, indicating the role of persistent autoph

282 ycin A1) and autophagic (3-methyladenine and Atg5 siRNA) antagonists.

283 y was blocked by 3-methyladenine (3MA) or by Atg5 siRNA, IAP failed to block LPS-mediated effects.

284 lockade of autophagy by autophagy-related 5 (ATG5) siRNA markedly decreased TH-mediated fatty acid be

285 utophagy inhibition using bafilomycin A1 and Atg5 siRNAs only rescues basal insulin secretion, not ki

286 Studies with Atg5 small interfering RNA (siRNA) and the autophagy inh

287 , direct inhibition of autophagy pathways by ATG5 small interfering RNA knockdown inhibited prolifera

288 h 3-MA inhibition, we transfected cells with ATG5 small interfering RNA to block autophagosome format

289 an autophagy inhibitor, 3-methyladenine, or Atg5 small interfering RNA, reduces the expression of EB

290 (-13)), which localize in or near to JARID2, ATG5, SMARCD3, CCAT1, CDKN2A, WAC, RFWD3 and PREX1.

291 We identify the AIM-binding sites in the Atg5 subunit and mutation of these sites impairs selecti

292 e, FMDV yields were reduced in cells lacking Atg5, suggesting that autophagy may facilitate FMDV infe

293 methyladenosine, chloroquine or beclin 1 and Atg5-targeted siRNA also enhanced the sensitivity of SKO

294 Strikingly, TECPR1 localizes to and recruits Atg5 to autolysosome membrane.

295 We overexpressed an inactive mutant of Atg5 to create an autophagy-deficient cell model, and to

296 Treg cell-specific deletion of Atg7 or Atg5, two essential genes in autophagy, leads to loss of

297 own of RACK1 or prevention of its binding to ATG5 using mutagenesis blocked autophagy activation.

298 Atg5 was knocked down in pancreatic cancer cell lines us

299 including single nucleotide polymorphisms in Atg5 which correlate with reduced lung function.

300 Depletion of ATG5, which is essential for autophagic vesicle formatio