ライフサイエンスコーパス: ATG7

1 n and of autophagy-related proteins Ulk1 and Atg7.

2 require the autophagic activity mediated by ATG7.

3 ion of p300-dependent acetylation of p53 and ATG7.

4 ssibility of p300 to its substrates, p53 and ATG7.

5 is not related to the autophagic function of Atg7.

6 ndent on the autophagy proteins Beclin 1 and Atg7.

7 tabases, demonstrating a prognostic value of ATG7.

8 onal up-regulation of autophagy-related gene ATG7.

9 dicted site in the 3' untranslated region of ATG7.

10 ophagy pathway, including Beclin1, ATG5, and ATG7.

11 d progenitors was impaired in the absence of Atg7.

12 pecific delivery of lentiviral shRNA against Atg7.

13 d expression of the autophagy genes Atg5 and Atg7.

14 eversed by knockdown of autophagy-related 7 (ATG7), a component of the autophagy machinery.

15 ble Tg mouse expressing autophagy-related 7 (Atg7), a critical and rate-limiting autophagy protein.

16 in HSCs, which was inhibited by knockdown of ATG7, a critical autophagy mediator.

17 te that deletion of a conditional allele for Atg7, a gene essential for autophagy, from osteocytes ca

18 inishing autophagy directly by knock-down of atg7, a key autophagy gene, reduces branch density, whil

19 while limiting p300-dependent acetylation of ATG7, a mechanism known to inhibit autophagy.

20 Atg7, a mediator of autophagosomal biogenesis, is a puta

21 Depletion of Atg7, a necessary component of the autophagy pathway, in

22 acking the essential autophagy genes Atg5 or Atg7 accumulate low-grade, pre-malignant pancreatic intr

23 vo targeting of the essential autophagy gene ATG7 also disrupted tumor growth when combined with beva

24 Atg7 also suppressed apoptosis induced by p53 activator

25 Loss of ATG7 also up-regulates TGFbeta signaling and key pro-fib

26 gnaling, but instead involved suppression of ATG7, an autophagy-associated gene.

27 In this study, we investigated the role of ATG7, an essential autophagy regulator with no autophagy

28 Moreover, conditional deletion of Atg7, an essential regulator of autophagy, in mouse fore

29 autophagy or knockdown of autophagy proteins ATG7 and ATG13 induced and accelerated the death of ATP7

30 vented brain damage in SE rats by inhibiting Atg7 and Atg16L1 expression and autophagosome formation

31 We found that Atg7 and Atg16L1 were up-regulated in the neurons after

32 onserved autophagy proteins including ATG4B, ATG7 and ATG3.

33 g8 protein that could not be reconjugated by Atg7 and Atg3.

34 RNAi-mediated knockdown of ATG7 and ATG5, essential autophagy proteins, abolished S

35 The protein levels of ATG7 and beclin 1 are also reduced in ccRCC tumors.

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

37 targeting the essential autophagy components ATG7 and Beclin-1, effectively attenuated Chal-24-induce

38 es autophagy by transcriptional induction of ATG7 and BECLIN1 in a p53-dependent manner.

39 key autophagic markers and mediators LC3-II, Atg7 and Beclin1 were reduced in DeltaKlf6 mice livers.

40 hed as a direct transcriptional activator of ATG7 and BECLIN1, but was dependent on the presence of p

41 shows how inhibiting the autophagy proteins ATG7 and BECN1 can regulate IRF1-dependent and -independ

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

43 Coexpression of Atg7 and CryAB(R120G) significantly reduced preamyloid o

44 inhibits autophagy by reducing expression of ATG7 and impairs viability of HCC cells under hypoxic co

45 antiestrogens, whereas combined silencing of ATG7 and IRF1 restored sensitivity to these agents.

46 d on Lyn coimmunoprecipitation with Ulk1 and Atg7 and on the presence of Ulk1 in Lyn-containing high-

47 cytoplasm with DOR, where it is able to bind Atg7 and other autophagy factors and undergo phosphatidy

48 ty of ISC and highlight the key functions of Atg7 and p53.

49 lysis also supported the association between ATG7 and SVO stroke.

50 Mechanistic investigations identified ATG7 and the cell death modulator beclin-1 (BECN1) as ne

51 ssess the expression of autophagy-related 7 (Atg7) and Atg16L1 and the status of autophagosome format

52 inst MNV in macrophages required Atg5-Atg12, Atg7, and Atg16L1, but not induction of autophagy, the d

53 hagy protein expression (i.e., Atg6/Beclin1, Atg7, and Atg8/LC3) and mitophagy protein Bnip3 expressi

54 er cells, which have a biallelic deletion of Atg7, and in H460 Atg7-knockout cells.

55 y is mediated by its direct interaction with Atg7, and it is not related to the autophagic function o

56 NAs targeting autophagic proteins (Beclin 1, ATG7, and LC3) as well as by overexpression of Bcl-2, vi

57 gy-elongation proteins ATG5, ATG16L1, ATG4B, ATG7, and LC3B.

58 These findings strongly suggest that Atg7, and likely microenvironment autophagy in general,

59 derstood despite association of Atg3, the E1 Atg7, and the composite E3 Atg12-Atg5-Atg16 with patholo

60 ss and/or mutation of autophagy-related gene ATG7, and the low expression level of autophagy genes co

61 es displayed a phenotype similar to those of Atg7- and Atg5-deficient T cells.

62 atg7- and p53-deficient tumor-derived cell lines (TDCLs)

63 Thus, the inhibition of Atg7 appears to be a valid strategy to enhance chemosens

64 , atg-16.2/ATG16L, atg-18/WIPI1/2, and atg-7/ATG7 are required for the late larval expansion of germl

65 Using autophagy-related protein 7 (Atg7) as an autophagic marker, this work showed that aut

66 Atg) genes Fip200, beclin 1, Atg14, Atg16l1, Atg7, Atg3, and Atg5, in the myeloid compartment, inhibi

67 (LC3) to phosphatidylethanolamine, including Atg7, Atg3, and the Atg12-Atg5-Atg16L1 complex play cruc

68 ins essential for autophagy, including Atg5, Atg7, Atg4B, and LC3, are important for generating the o

69 amycin (Mtor) (mTOR(f/f):Villin-cre mice) or Atg7 (Atg7(flox/flox); Villin-Cre).

70 ta allow modeling of a full-length, dimeric (Atg7~Atg8-Atg3)(2) complex.

71 bal autophagy-network genes, including Tfeb, Atg7, Atgl, and Fgf21, through demethylation of histone

72 ther studies indicated that the knockdown of ATG7 attenuated the expression of CD44 standard (CD44s),

73 with autophagy inhibition by repressing HSF1/ATG7 axis represents a promising strategy for future can

74 Mice with B cell-specific deletion of Atg7 (B/Atg7(-/-) mice) showed normal primary antibody r

75 We identified Atg5, Atg7, Bax, Bid, Bik, and Noxa as potential therapeutic t

76 autophagy-related proteins, including Atg5, Atg7, Beclin-1 and LC3A/B-II, seen in HFD-fed control mi

77 es, including autophagy-related gene (Atg)5, Atg7, beclin-1, and microtubule-associated proteins 1A/1

78 expression of the autophagy-related proteins ATG7, Beclin1, and LC3bI/II were significantly suppresse

79 vation, skeletal muscle-specific deletion of ATG7 blunts the beneficial effects of beta(2) -adrenocep

80 Microlipophagy does not require ATG7 but does requires ESCRT components and a newly iden

81 cotreatment with chloroquine or knockdown of Atg7, but not Beclin-1 or Ambra1, prevented THC-induced

82 ic deletion of the autophagy regulatory gene Atg7 by generating Atg7(flox/flox);VMD2-rtTA-cre+ mice t

83 studies demonstrated that the deficiency of ATG7 by its shRNA dramatically reduced sphere formation

84 Deletion of autophagy-related 7 (ATG7) by genome editing completely blocked macroautophag

85 also report the structure of the homodimeric Atg7 C-terminal domain, which is homologous to canonical

86 We propose that the Atg7.caspase-9 complex performs a dual function of linki

87 By crossing Atg7 cKO mice to the SOD1(G93A) mouse model, we found th

88 Atg7 cKO mice were viable but exhibited structural and f

89 was specifically disrupted in motor neurons (Atg7 cKO).

90 11+/-0.004 in wild type and 0.152+/-0.019 in atg7 cKO; P<0.05) and induced systolic dysfunction (end

91 4.86+/-2.46 in wild type and 15.93+/-1.76 in atg7 cKO; P<0.05) during HFD feeding.

92 prisingly, however, lifespan was extended in Atg7 cKO; SOD1(G93A) double-mutant mice.

93 uronal autophagy-deficient mice or Tsc2 +/- :Atg7(CKO) double mutants.

94 pruning defects in Tsc2 +/- mice, but not in Atg7(CKO) neuronal autophagy-deficient mice or Tsc2 +/-

95 dependent of its E1-like enzymatic activity, Atg7 could bind to the tumor suppressor p53 to regulate

96 34 (VPS34), and autophagy-related protein 7 (ATG7), could rescue the PA-induced death of endothelial

97 The entire exercised Atg7-crossed CryABR120G cohort survived to 7 months.

98 autophagy-deficient CryABR120G mice and the Atg7-crossed CryABR120G mice to voluntary exercise, whic

99 Atg7 deficiency produced an autophagy-deficient phenotyp

100 atg7 deficiency reduced fatty acid oxidation (FAO) and i

101 Interestingly, ATG7-deficient and -proficient cells were equally sensit

102 Genetic analyses using ATG7-deficient cells indicate that neutrophils secrete I

103 In contrast, Atg7-deficient DA neurons in the midbrain exhibit early

104 Finally, p53 deletion prevents the death of Atg7-deficient Lgr5(+)ISC but promotes genetic instabili

105 gh the overall LSK compartment was expanded, Atg7-deficient LSK cells failed to reconstitute the hema

106 However, Atg7-deficient MCs entered into premature growth arrest

107 Atg7-deficient neutrophil precursors had increased glyco

108 Atg7-deficient RPE displayed abnormal morphology with in

109 d retinal histology were normal in mice with Atg7-deficient RPE in both fasted and fed states.

110 Atg7-deficient Treg cells show increased apoptosis and r

111 atg7-deficient tumors accumulated dysfunctional mitochon

112 Atg7-deficient tumors display evidence of endoplasmic re

113 Surprisingly, lipid accumulation occurred in atg7-deficient tumors only when p53 was deleted.

114 The protection afforded by both Myr-Akt and Atg7 deletion is robust and lasting, because it is still

115 Although Atg7 deletion resulted in increased mitochondrial mutati

116 Nrf2(-/-)Atg7 (Delta/Delta) mice died rapidly due to small intest

117 o test whether increased oxidative stress in Atg7 (Delta/Delta) mice was responsible for p53 activati

118 Compared with Atg7 (Delta/Delta) mice, the life span of Atg7 (Delta/De

119 th Atg7 (Delta/Delta) mice, the life span of Atg7 (Delta/Delta) p53 (Delta/Delta) mice was extended d

120 and not merely a consequence of NEC, because ATG7(DeltaIEC) mice were protected from NEC development.

121 or autophagy function (Atg16l1(DeltaIEC) or Atg7(DeltaIEC)) in intestinal epithelial cells results i

122 gy gene ATG7 from the intestinal epithelium (ATG7(DeltaIEC)), the induction of autophagy was determin

123 Atg7(Deltapan) mice also exhibit spontaneous activation

124 Atg7(Deltapan) mice exhibit severe acinar cell degenerat

125 To address this question, we generated Atg7(Deltapan) mice that lack the essential autophagy-re

126 in mice deficient in NADPH oxidase, Atg5, or Atg7, demonstrating that CpsA makes a significant contri

127 heir progenitors and that this protection is Atg7 dependent.

128 Intriguingly, they activate ULK1-ATG7-dependent autophagy as a survival mechanism to miti

129 mmary, the results of our study suggest that Atg7-dependent autophagy is dispensable for melanogenesi

130 are mobilized to the vacuole in an ATG5- and ATG7-dependent manner.

131 ppaBalpha in the cytosol was not affected in ATG7-depleted cells, suggesting a defect in the transloc

132 ofilin1, an actin-depolymerizing protein, in ATG7-depleted cells.

133 Rheb inhibits autophagy mostly through Atg7 depletion.

134 n that mice with hematopoietic cells lacking Atg7 develop an MDS-like syndrome.

135 genetic deletion of the autophagy initiator ATG7 developed beta cell apoptosis and overt diabetes.

136 and biochemical data provide a rationale for Atg7 dimerization: Atg8 is transferred in trans from the

137 35(S34F) have a similar increased use of the ATG7 distal CP site, and previous studies have shown tha

138 Our results demonstrate that CD44s is a key ATG7 downstream regulator of the sphere formation, invas

139 rs2594973, rs4684776) clustered at 3p25.3 in ATG7 (encoding Autophagy Related 7), with P values betwe

140 patient sample study revealed that a higher ATG7 expression level is associated with poor patient su

141 sion, the absence of macroautophagy (ATG5 or ATG7 expression), an increase in mitochondrial mutationa

142 patic stellate cells from C57BL/6 wild-type, Atg7(F/F), and Atg7(F/F)-GFAP-Cre mice, as well as the m

143 cells from C57BL/6 wild-type, Atg7(F/F), and Atg7(F/F)-GFAP-Cre mice, as well as the mouse stellate c

144 lacking the essential autophagy gene product Atg7 failed to undergo cell cycle arrest.

145 (Mtor) (mTOR(f/f):Villin-cre mice) or Atg7 (Atg7(flox/flox); Villin-Cre).

146 autophagy regulatory gene Atg7 by generating Atg7(flox/flox);VMD2-rtTA-cre+ mice to determine whether

147 umans, deletion of Abca4 was introduced into Atg7(flox/flox);VMD2-rtTA-cre+ mice to investigate the r

148 he eyes of 6-month-old mice with and without Atg7 from both Abca4(-/-) and Abca4(+/+) backgrounds.

149 arboring mtDNA mutations in vivo, we deleted Atg7 from erythroid progenitors of wild-type and mtDNA-m

150 ch we selectively deleted the autophagy gene ATG7 from the intestinal epithelium (ATG7(DeltaIEC)), th

151 g sequence (PQFS) in the first intron of the Atg7 gene folds into a G4.

152 tinas lacking the rod photoreceptor-specific Atg7 gene were coincubated with 20 muM all-trans-retinal

153 ed structures occurred in the absence of the Atg7 gene, a gene essential for autophagy.

154 A with G4 ligands strongly downregulates the Atg7 gene.

155 ified polymorphisms in the Atg5 and possibly Atg7 genes, involved in both canonical autophagy and LAP

156 en tumor suppressor and autophagy-related-7 (Atg7) genes.

157 CRAF, together with the autophagy E1 ligase ATG7, gives the best therapeutic window between KRAS mut

158 2 activity irrespective of cell type: ATG12, ATG7, GOSR1, IFT172, NRXN2, RAB6A, VPS37A, and the well-

159 Interestingly, exercise-trained Atg7(h&mKO) mice were better protected against obesity a

160 disruption of the Autophagy related 7 gene (Atg7(h&mKO)).

161 r of the autophagy-related molecules Atg5 or Atg7 had little to no effect on the proliferation and fu

162 etion of the major autophagy factors Atg5 or Atg7 had no effect on WNV infectious particle production

163 h mice with endothelial-specific deletion of Atg7 have normal vessel architecture and capillary densi

164 Deletion of atg7 impaired mitophagy, increased lipid accumulation, e

165 ues from Atg3 engaging a conserved groove in Atg7, important for Atg8 conjugation.

166 deletion of the essential autophagy mediator Atg7 in adult mice also achieves striking axon protectio

167 Knockdown of Atg7 in AML cells using short hairpin RNA markedly incre

168 further enhanced by concomitant knockdown of Atg7 in both AML and stromal cells.

169 st study demonstrating a prognostic value of ATG7 in breast cancer patients.

170 avior by generating conditional knockouts of Atg7 in either dSPNs or iSPNs.

171 in that loss of the essential autophagy gene ATG7 in endothelial cells (ECs) leads to impaired autoph

172 In addition, chorein associated with Atg7 in healthy but not in chorea-acanthocytosis erythro

173 of nuclear IRF1 and the autophagy regulator ATG7 in human breast cancer cells that directly affects

174 Thus, conditional ablation of Atg5 or Atg7 in intestinal APCs resulted in enhanced ROS and TH1

175 ther, these data uncover a novel function of ATG7 in mediating EC inflammation and permeability, and

176 pecific deletion of essential autophagy gene Atg7 in midbrain DA neurons causes delayed neurodegenera

177 agy genes including Atg14, Fip200, Atg5, and Atg7 in myeloid cells also led to elevated basal lung in

178 autophagy, including Beclin1 systemically or Atg7 in only rod photoreceptors resulted in increased su

179 Mice lacking the autophagy gene Atg7 in T cells failed to establish CD8(+) T cell memory

180 erated mice with the conditional deletion of Atg7 in the dopamine neurons of the substantia nigra par

181 Mice lacking Atg7 in the entire osteoblast lineage had low bone mass

182 onally deleting the essential autophagy gene Atg7 in the hematopoietic system.

183 nal deletion of the essential autophagy gene Atg7 in the T-cell compartment (CD4 Cre-Atg7(-/-)), thym

184 tion was observed between levels of HSF1 and ATG7 in triple-negative breast cancer patient samples, t

185 eport that loss of autophagy-related gene 7 (Atg7) in DCs ameliorated experimental autoimmune encepha

186 lin 1 (BCN1) or autophagy-related protein 7 (ATG7) in immortalized human hepatocytes (IHHs) inhibited

187 k the essential autophagy-related protein 7 (ATG7) in pancreatic epithelial cells.

188 ential autophagy components ATG5, ATG16L1 or ATG7-in mediating quiescence of tissue-resident macropha

189 iver-specific deletion of the autophagy gene Atg7 increases hepatic fat content, mimicking the human

190 We find that ATG7-independent autophagy still requires canonical ATG

191 observed in mice with intestinal deletion of ATG7, indicating that autophagy is required for the redu

192 Sustained Atg7-induced autophagy in the CryABR120G hearts decrease

193 Atg7 induces basal autophagy, rescues the CryAB(R120G) a

194 cells or in Lgr5(+)ISC, we show that loss of Atg7 induces the p53-mediated apoptosis of Lgr5(+)ISC.

195 Up-regulating miR-375 or down-regulating ATG7 inhibited mitochondrial autophagy of HCC cells, red

196 inhibitor chloroquine or siRNA knockdown of Atg7 inhibited ORMDL1 degradation by cholesterol, wherea

197 Moreover, ATG7 inhibition stabilized AUF1 protein and thereby redu

198 own of the essential autophagy genes Atg5 or Atg7 inhibits the in vitro secretion of VWF.

199 e that the autophagy related genes Atg4c and Atg7 (involved in the lipidation of microtubule-associat

200 Atg7 is a critical gene for the initiation of autophagy

201 Atg7 is a noncanonical, homodimeric E1 enzyme that inter

202 As Atg7 is critical for the canonical autophagy pathway, it

203 vely in the cytosol, autophagy is abrogated, ATG7 is hyperacetylated, p53 acetylation is abolished, a

204 ion; that it forms a complex with Atg7; that Atg7 is not a direct substrate for caspase-9 proteolytic

205 tudies report that autophagy-related gene 7 (ATG7) is overexpressed in BCs, the regulatory effects of

206 ve regulator of NRF2, KEAP1 Of these, ATG12, ATG7, KEAP1, and VPS37A are known to be involved in auto

207 In vivo, EC-specific ATG7 knock-out mice exhibit a basal reduction in endothe

208 Finally, in a mouse model of human leukemia, Atg7 knockdown extended overall survival after chemother

209 Mechanistic studies revealed that Atg7 knockdown induced a proapoptotic phenotype in AML c

210 Defective autophagy, as established by ATG7 knockdown, results in prolonged cytosolic retention

211 utic agents, and this was reversed following Atg7 knockdown.

212 Furthermore, ATG7 knockout did not sensitize cells to irradiation or

213 ve a biallelic deletion of Atg7, and in H460 Atg7-knockout cells.

214 for autophagy-dependent cells to circumvent ATG7 KO and maintain protein homeostasis.

215 identifying genes required for NBR1 flux in ATG7(KO) cells.

216 genomes of wild-type or autophagy-deficient (Atg7(-/-)) Kras-driven lung tumors.

217 sease patients, hepatic expression of JMJD3, ATG7, LC3, and ULK1 is substantially decreased.

218 on of two essential autophagy genes ATG5 and ATG7 leads to failure of CHK1 activation by 20A and subs

219 Furthermore, whole-brain-specific loss of Atg7 leads to presynaptic accumulation of alpha-syn and

220 anslated inefficiently, leading to decreased ATG7 levels and an autophagy defect that predisposes cel

221 Thus, Atg7 limits p53 activation and p53-mediated neurodegener

222 atg7 loss altered tumor fate from adenomas and carcinoma

223 Whereas ATG7 loss leads to the expected decrease in autophagic f

224 Atg7(-)/(-) macrophages exhibited higher bacterial uptak

225 Atg7(-)/(-) macrophages had increased expression of two

226 ccumulated sequestosome 1 (SQSTM1 or p62) in Atg7(-)/(-) macrophages.

227 Moreover, depletion of ATG7 markedly reduced the binding of RelA/p65 to DNA in

228 These observations indicate that Atg7-mediated autophagy is dispensable for retinoid recy

229 f caspase-9, whereas the latter enhances the Atg7-mediated formation of light chain 3-II.

230 In addition, BCG-infected Atg7(-)/(-) mice showed increased bacterial loads and ex

231 specific autophagy-related gene 7-deficient (Atg7(-)/(-)) mice.

232 ice with B cell-specific deletion of Atg7 (B/Atg7(-/-) mice) showed normal primary antibody responses

233 hk2 partially rescued postnatal lethality in Atg7(-/-) mice.

234 rmacologic inhibitors, siRNA approaches, and Atg7-/- mice, that autophagy initiated by ULK1 is requir

235 This longer Atg7 mRNA is translated inefficiently, leading to decrea

236 its showed greater impairment in parkin than Atg7 mutants, and RC turnover was also selectively impai

237 than the slowing seen in autophagy-deficient Atg7 mutants, consistent with the model that Parkin acts

238 We found that atg2, atg3, and atg7 mutations suppressed lon2 defects in auxin metaboli

239 e, depletion of the essential autophagy gene Atg7 normalizes the excess autophagy and corrects the vi

240 The structure of an Atg7(NTD)-Atg3(FR) complex reveals hydrophobic residues

241 In mice harboring mutant Atg7, nuclear IRF1 was increased in mammary tumors, sple

242 rexpressed in BCs, the regulatory effects of ATG7 on cancer stem-like phenotypes and invasion have no

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

244 Deleting Atg7 or Atg5 or blocking LC3 lipidation or ATG5-ATG12 co

245 shRNA against the autophagic machinery Atg7 or Atg5 prolonged the survival of neurons co-treate

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

247 Silencing ATG7 or BECN1 caused estrogen receptor-alpha to exit the

248 Genetic knockout of autophagy-related 7 (ATG7) or pharmacologic inhibition of SYK activity with f

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

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

251 ty and/or molecular targeting of p62/SQSTM1, Atg7, or cathepsin B result in partial reversal of the s

252 r essential autophagy proteins such as ATG5, ATG7, or FIP200 (FAK family-interacting protein of 200 k

253 egative form of ATG4B or silencing Beclin-1, Atg7, or p62 indicated that macroautophagy does not prot

254 Targeted depletion of Atg3, Atg7, or p62/sequestosome-1 to inactivate autophagy rest

255 Mechanistic studies revealed that ATG7 overexpression stabilized CD44s proteins accompanie

256 was rescued by reactivation of autophagy by Atg7 overexpression, indicating that the effect of Nox4

257 d the G4-DNA-binding protein PC4 bind to the Atg7 PQFS.

258 formed cells the autophagy-related factor 7 (Atg7) pre-mRNA is abnormally processed, which unexpected

259 1 regulates autophagy by directly binding to ATG7 promoter and transcriptionally up-regulating its ex

260 sed Beclin1 and autophagy-related protein 7 (Atg7), proteins involved in phagophore-autophagosome for

261 in trans from the catalytic cysteine of one Atg7 protomer to Atg3 bound to the N-terminal domain of

262 und to the N-terminal domain of the opposite Atg7 protomer within the homodimer.

263 Restoration of autophagy, through Atg7 reexpression and inhibition of mTORC1, increased ce

264 Thus, when nutrients are limited, Atg7 regulates p53-dependent cell cycle and cell death p

265 and that, depending on the cellular context, Atg7 represses the apoptotic capability of caspase-9, wh

266 y delete Stk11 and autophagy essential gene, Atg7, respectively or simultaneously, throughout the adu

267 h prolonged metabolic stress, the absence of Atg7 resulted in augmented DNA damage with increased p53

268 sion of the essential autophagy gene product ATG7 resulted in cell death, indicating that survival of

269 vity in the inhibition of EC inflammation in ATG7-silenced cells.

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

271 ATG7 silencing also reduced thrombin-mediated EC permeab

272 aling hypotheses, we developed evidence that ATG7 silencing could resensitize IRF1-attenuated cells t

273 Conversely, Atg7 silencing in the CryAB(R120G) background significan

274 nucleus, and indeed our results showed that ATG7 silencing inhibited this response via inactivation

275 bited by 3MA or autophagy-related protein 7 (Atg7) small interfering RNA (siRNA).

276 ional mice models lacking the autophagy gene Atg7 specifically in all intestinal epithelial cells or

277 we inactivated the essential autophagy gene Atg7 specifically in MCs using the Cre-loxP system.

278 agy response in cells lacking autophagy gene Atg7, suggesting that Beclin 1 may regulate DSB repair i

279 some formation; that it forms a complex with Atg7; that Atg7 is not a direct substrate for caspase-9

280 reafter) and/or the essential autophagy gene Atg7 throughout adult mice.

281 gene Atg7 in the T-cell compartment (CD4 Cre-Atg7(-/-)), thymic iNKT cell development--unlike convent

282 with the model that Parkin acts upstream of Atg7 to promote mitophagy.

283 itional deletion of essential autophagy gene Atg7 to test whether autophagy compensates for LKB1 loss

284 a T lymphocyte-specific deletion of Atg5 or Atg7, two members of the macroautophagic pathway, we obs

285 at the silencing of the expression of LC3 or Atg7, two protein factors critical for the formation of

286 CREB upregulated autophagy genes, including Atg7, Ulk1 and Tfeb, by recruiting the coactivator CRTC2

287 se melanocytes lacking the autophagy protein Atg7 undergo premature senescence in vitro and accumulat

288 role of autophagy in osteoblasts by deleting Atg7 using an Osterix1-Cre transgene, which causes recom

289 Knockdown of ATG7 using si-RNA significantly attenuated thrombin-indu

290 we downregulated autophagy genes BCLN-1 and ATG7 using small interfering RNA (siRNA) and monitored v

291 ta) mice was responsible for p53 activation, Atg7 was deleted in the presence or absence of the maste

292 ed mice in which the critical autophagy gene Atg7 was specifically disrupted in motor neurons (Atg7 c

293 ssential autophagy gene autophagy-related-7 (atg7) was deleted concurrently with K-ras(G12D) activati

294 of the essential autophagy-related protein, Atg7, was associated with shorter remission in newly dia

295 ree autophagy-related genes, Atg3, Atg5, and Atg7 were identified to be inhibited by MPA treatment.

296 and coupling of stress-acetylated FOXO1 with ATG7 (which remains uncoupled without lacritin) and be s

297 CaMKIalpha activates AMPK, thereby inducing ATG7, which also localizes to this CaMKIalpha/AMPK compl

298 ersely, overexpressing constitutively active Atg7, which forces autophagy and raises ER cholesterol e

299 ATG7, which has been implicated in autophagy, could prov

300 toprotective autophagy through regulation of ATG7, which is distinct from the HSF1 function in the he