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 agy inhibitors and short interfering RNA for ATG5.

4 eins GBP1 or GBP2 and the autophagic protein ATG5.

5 roglial cells is abrogated in the absence of ATG5.

6 oxygen production by the NADPH oxidase, and ATG5.

7 phagy was impaired because of the absence of Atg5.

8 n target, another autophagy regulator called ATG5.

9 NA)-mediated knockdown of the autophagy gene atg5.

10 phagy involving an increase in expression of ATG5.

11 ptides on MHC I was intact 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 mediated silencing of the autophagy mediator ATG5.

15 h promotes lipidation upon its attachment to ATG5.

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

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 dendritic cell (DC)-conditional deletion in Atg5, a key autophagy gene, showed impaired CD4(+) T cel

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

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

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

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

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

25 iated TFEB relocalization required Atg9A and Atg5 activity.

26 we conclude that the formation of the ATG12-ATG5 adduct is essential for ATG8-mediated autophagy in

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

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

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

30 3-kinase (PI3-kinase) prevented induction of ATG5 and activation of LC3-II and blocked autophagosome

31 -5-16L1-positive puncta, and interacted with Atg5 and also with Atg12-5 conjugate.

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

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

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

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

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

37 disruption of the essential autophagy genes Atg5 and Atg7 leads to the accumulation of all detectabl

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

39 Synthesis of the ATG12-ATG5 and ATG8-phosphatidylethanolamine adducts, which ar

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

41 LC3 and two other essential autophagic genes ATG5 and Beclin-1 in an IKK-dependent manner.

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

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

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

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

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

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

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

49 3-methyladenine (3-MA) or siRNA knockdown of Atg5 and the effect on apoptosis was measured using a ca

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

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

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

53 ression of sqstm1, autophagy-related gene 5 (atg5) and light chain 3 gene (lc3) in osteoclast precurs

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

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

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

57 ssical autophagy pathway, including Beclin1, ATG5, and ATG7.

58 Caspase-3, Atg5, and Beclin1 levels were down-regulated by exposing

59 al signaling pathway that involves Beclin-1, atg5, and hVps34.

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

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

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

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

64 ) binding protein, Alfy, interacts with p62, Atg5, and PI3P to coordinate target recognition with sit

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

66 Both in Atg5- and IRGM-deficient cells, the IRG protein Irga6 re

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

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 IFNgamma, via Atg5-Atg12/Atg16L1, inhibited formation of the membranou

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

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

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

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

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

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

88 12 is a component of the ATG12 approximately ATG5-ATG16L1 E3 complex that promotes lipid conjugation

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

90 proteins essential for autophagy, including Atg5, Atg7, Atg4B, and LC3, are important for generating

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

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

93 f other essential autophagy proteins such as ATG5, ATG7, or FIP200 (FAK family-interacting protein of

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

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

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

97 ATG5 but not ULK1 cooperated with ELMO1 in LC3 accumulat

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

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

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

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

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

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

104 L2 but not MoPn grew more efficiently in the ATG5(-/-) cells than in wild-type cells.

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

106 ly, inhibiting ceramide formation suppressed Atg5 cleavage and apoptosis.

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

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

109 or depletion of calpain not only suppressed Atg5 cleavage, it also markedly decreased the robust apo

110 Doxorubicin stimulated calpain activity and Atg5 cleavage, which were significantly enhanced in SPP1

111 leted cells to apoptosis by calpain-mediated Atg5 cleavage.

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

113 g12a and atg12b mutants on forming the ATG12-ATG5 conjugate reveal that the ATG12b locus is more impo

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

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

116 show that ATG8 lipidation requires 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 The most pronounced defect of Atg5(-/-) DCs was the processing and presentation of pha

122 Atg5 deficiency did not alter reactivation from B cells,

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

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 ophagy in WT and Ulk1/2(-/-) MEFs but not in Atg5-deficient MEFs.

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

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

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

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

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

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

133 ed a phenotype similar to those of Atg7- and Atg5-deficient T cells.

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

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

136 A(2) and lipid mediator-induced autophagy is ATG5 dependent.

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

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

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

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

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 ction, localizes to the ruffled border in an Atg5-dependent manner.

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

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

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

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

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

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

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

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

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

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

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

155 tation was reduced by 3MA or by reduction in Atg5 expression.

156 receptor, on LC3-I to LC3-II conversion and Atg5 expression.

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

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

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

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

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

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

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

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

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

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

167 inhibited growth in the autophagy-deficient ATG5(-/-) fibroblasts.

168 Macrophages from uninfected Atg5(fl/fl) LysM-Cre(+) mice displayed a cell-autonomous

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

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

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

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

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

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

175 nic mice with liver-specific knockout of the Atg5 gene, a gene critical for the initiation of autopha

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 -mediated cleavage of the autophagic protein ATG5 in a manner that could facilitate switch to apoptos

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

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

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

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

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

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

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

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

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

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

195 0, beclin 1, Atg14, Atg16l1, Atg7, Atg3, and Atg5, in the myeloid compartment, inhibited MHV68 reacti

196 Down-regulation of Atg5 induced extensive central necrosis in TSC2-null xen

197 -1beta via an export pathway that depends on Atg5, inflammasome, at least one of the two mammalian Go

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

213 the inhibition of autophagy in the livers of Atg5 knockout mice.

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

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

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

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

218 ll culture, which shows that inactivation of Atg5 leads to the selective accumulation of aggregation-

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

220 dent activation of autophagy, with increased Atg5 levels and intraphotoreceptor conversion of LC3-I t

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

222 tophagy inhibitors tested and was reduced in Atg5(-/-) MEFs.

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

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

225 serum or serum-free conditions and in WT or Atg5(-/-) mouse embryonic fibroblasts (MEFs).

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

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

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

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

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

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

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

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

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

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

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

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

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

239 ortantly, downmodulation of autophagy genes (ATG5 or ATG10) rescues the infected cells from being lys

240 0R, bypasses RAS-induced senescence, whereas ATG5 or ATG3 deficiency predisposes to it.

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

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

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

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

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

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

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

248 mphocytes lacking the autophagy-related gene Atg5 or Atg7 have defective survival and contain expande

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

250 autophagy-independent signaling capacity of Atg5 or Atg7 in T lymphocytes remains unknown.

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

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

253 RNAi-mediated knockdown of either Atg5 or Beclin 1, two essential autophagy effectors, was

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

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

256 h effect, requires autophagy-specific genes, atg5 or beclin1, and is associated with the inactivation

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

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

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

260 Moreover, silencing Atg5 or the three sensors of the unfolded protein respon

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

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

263 ysis, and by reduced expression of Beclin 1, Atg5, or microtubule-associated protein 1 light chain 3b

264 By combining mutants eliminating ATG12a/b, ATG5, or the ATG10 E2 required for their condensation wi

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

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

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

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

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

270 lipid phosphatidylethanolamine (PE) and the ATG5 protein, respectively, during formation of the engu

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

272 The Atg5-related reactivation defect was partially reversed

273 ATG5 represses transcriptional activation by the TGFbeta

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

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

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

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

278 ed with caspase activation and is blocked by atg5 silencing and by pharmacological inhibitors.

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

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

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

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

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

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

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

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

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

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

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

290 nal levels of the autophagy proteins LC3 and Atg5, the time course of LC3-I to LC3-II conversion, and

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

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

293 The early autophagosomal marker, Atg5, transiently localizes to punctae on mitochondria,

294 ll-interfering RNA knockdown of Beclin-1 and ATG5 (two key autophagic genes) sensitized the tubular c

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

296 siAMPK or compound C decreases expression of ATG5, ultimately attenuating AEG-1-induced autophagy.

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

298 in the degradation of Abeta and APP-CTF, and Atg5 was necessary for the effect of SMER28.

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

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