ライフサイエンスコーパス: ATG7

1 cal macroautophagy gene autophagy-related 7 (Atg7).

2 bsence of a key gene required for autophagy (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 entional initiation pathway still depends on ATG7.

14 ced activity of the autophagy genes atg5 and atg7.

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

16 require the autophagic activity mediated by ATG7.

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

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

19 Using a conditional KO mouse model where Atg7, a critical gene for macroautophagy, is specificall

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

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

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

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

24 R or the suppression of expression of LC3 or Atg7, a protein that mediates LC3 lipidation, suppressed

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

26 pe CryAB or CryAB(R120G) and coinfected with Atg7 adenovirus or with Atg7 silencing siRNAs to produce

27 Atg7-/- adults are short-lived, hypersensitive to nutrie

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

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

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

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

32 RIPK-2), autophagy-related protein-5 (ATG5), ATG7 and ATG16L1 but not NLR family, pyrin domain contai

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

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

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

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

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

38 A/R markedly decreased Atg7 and Beclin-1 concomitantly with a progressive incre

39 onclusion: Calpain 2-mediated degradation of Atg7 and Beclin-1 impairs mitochondrial autophagy, and t

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

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

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

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

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

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

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

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

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

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

50 tingly, RNAi knockdown of autophagy proteins Atg7 and LC3/Atg8 also decreased mitochondrial fragmenta

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

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

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

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

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

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

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

58 ncoding green fluorescent protein (control), Atg7, and Beclin-1 to augment autophagy.

59 Taken together, our results indicate that atg7, and by inference autophagy, plays an important rol

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

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

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

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

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

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

66 These findings indicate that Atg7- and Beclin1-induced autophagy plays a cytoprotecti

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

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

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

70 ATG12-ATG3 complex formation requires ATG7 as the E1 enzyme and ATG3 autocatalytic activity as

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

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

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

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

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

76 report that the unique N-terminal domain of Atg7 (Atg7(NTD)) recruits a unique "flexible region" fro

77 ockdown of p300 reduces acetylation of Atg5, Atg7, Atg8, and Atg12, although overexpressed p300 incre

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

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

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

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

82 Expression of autophagy-related protein 7 (Atg7), Beclin-1, and Atg12, autophagy regulatory protein

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

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

85 Short hairpin RNA knockdown of Atg7, but not Beclin1, expression significantly inhibite

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

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

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

89 al effects on cell survival, suggesting that Atg7 can activate autophagy with no apparent cytotoxic e

90 sruption of autophagy by mutation of Atg5 or Atg7 can lead to neurodegeneration.

91 TG10 that, similar to plants missing ATG5 or ATG7, cannot form the ATG12-ATG5 conjugate.

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

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

94 Atg7 cKO mice were viable but exhibited structural and f

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

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

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

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

99 Furthermore, p300 and Atg7 colocalize within cells, and the two proteins physi

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

101 34 (VPS34), and autophagy-related protein 7 (ATG7), could rescue the PA-induced death of endothelial

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

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

104 Atg7 deficiency produced an autophagy-deficient phenotyp

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

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

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

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

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

110 Atg7-deficient neutrophil precursors had increased glyco

111 Atg7-deficient RPE displayed abnormal morphology with in

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

113 indicate that the expanded ER compartment in Atg7-deficient T cells contains increased calcium stores

114 Atg7-deficient T cells stimulated through the TCR displa

115 vated Ca(2+) channel opening, is impaired in Atg7-deficient T cells.

116 cium, and ER calcium stores are increased in Atg7-deficient T cells.

117 igargin rescues the calcium influx defect in Atg7-deficient T lymphocytes, suggesting that this impai

118 Atg7-deficient Treg cells show increased apoptosis and r

119 atg7-deficient tumors accumulated dysfunctional mitochon

120 Atg7-deficient tumors display evidence of endoplasmic re

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

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

123 Although Atg7 deletion resulted in increased mitochondrial mutati

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

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

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

127 Atg7(Deltapan) mice also exhibit spontaneous activation

128 Atg7(Deltapan) mice exhibit severe acinar cell degenerat

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

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

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

132 Rheb inhibits autophagy mostly through Atg7 depletion.

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

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

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

136 35(S34F) have a similar increased use of the ATG7 distal CP site, and previous studies have shown tha

137 Analyses of Pik3c3/Atg7 double mutant neurons revealed that this unconventi

138 ana mutants affecting the ATG5 target or the ATG7 E1 required to initiate ligation of both ATG8 and A

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

140 Mammalian homologs of Atg8 are unmodified in Atg7(-/-) erythroid cells, indicating that canonical aut

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

142 ine the gain and loss of function effects of Atg7 expression on CryAB(R120G) protein misfolding and a

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

144 to the core autophagy genes such as atg5 and atg7, expression of ulk1 is not essential for induction

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

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

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

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

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

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

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

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

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

154 lencing siRNAs to produce gain-of or loss-of Atg7 function.

155 at inhibition of autophagy by disrupting the atg7 gene has a unique anti-obesity and insulin sensitiz

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

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

158 An adipocyte-specific mouse knockout of Atg7 generated lean mice with decreased white adipose ma

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

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

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

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

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

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

165 toprotective role during starvation but that Atg7 has a unique pro-apoptotic function in response to

166 s lacking the autophagy-related gene Atg5 or Atg7 have defective survival and contain expanded mitoch

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

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

169 Knockdown of Atg7 in 3T3-L1 preadipocytes inhibited lipid accumulatio

170 A mouse model with a targeted deletion of atg7 in adipose tissue was generated.

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

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

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

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

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

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

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

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

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

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

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

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

183 gy-independent signaling capacity of Atg5 or Atg7 in T lymphocytes remains unknown.

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

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

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

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

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

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

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

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

192 he autophagy-specific genes (ATGs) (ATG5 and ATG7) in some human prostate cancer cells and immortaliz

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

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

195 Sustained Atg7-induced autophagy in the CryABR120G hearts decrease

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

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

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

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

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

201 Atg7 is a noncanonical, homodimeric E1 enzyme that inter

202 Atg7 is an autophagy protein and an E1-like enzyme, whic

203 Collectively, these data show that Atg7 is an essential regulator of adult HSC maintenance.

204 d Baf A1-induced cell death, indicating that Atg7 is an upstream mediator of lysosome dysfunction-ind

205 The interaction between p300 and Atg7 is dependent on nutrient availability.

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

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

208 Thus, we conclude that the autophagy protein Atg7 is required for membrane trafficking and turnover i

209 Atg7 is required for the conjugation of Atg12 to Atg5, a

210 re we show that the essential autophagy gene Atg7 is required in a cell-intrinsic manner for the surv

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

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

213 ted by either Atg7 or Beclin1 knockdown, and Atg7 knockdown had no effect on starvation-induced death

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

215 3-methyladenine, an inhibitor of autophagy; Atg7 knockdown using small interfering RNA; or L-carniti

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

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

218 BCN1- or ATG7-knockdown IHHs, when they were infected with HCV, e

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

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

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

222 on of the essential autophagy genes Atg5 and Atg7 leads to the accumulation of all detectable Ub-Ub t

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

224 The increase in Ub conjugates in Atg7(-/-) liver and brain is completely suppressed by si

225 atg7 loss altered tumor fate from adenomas and carcinoma

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

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

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

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

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

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

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

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

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

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

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

237 In the absence of Atg7, mitochondrial clearance from reticulocytes is dimi

238 ce AuCD in autophagy-deficient ATG5(-/-) and ATG7(-/-) mouse embryonic fibroblast cells, suggesting t

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

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

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

242 hough metamorphic cell death is perturbed in Atg7 mutants, the larval-adult midgut transition proceed

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

244 t that the unique N-terminal domain of Atg7 (Atg7(NTD)) recruits a unique "flexible region" from Atg3

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

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

247 al autophagy gene, autophagy-related gene 7 (atg7), on adipogenesis.

248 Upregulation of ATG5 and ATG7 only occurred in cells displaying PI-induced phosph

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

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

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

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

253 uced AV accumulation was inhibited by either Atg7 or Beclin1 knockdown, and Atg7 knockdown had no eff

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

255 Furthermore, knockdown of beclin 1 or Atg7 or treatment with the lysosome inhibitor chloroquin

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

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

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

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

260 Atg7 overexpression effectively induced basal autophagy

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

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

263 1 regulates autophagy by directly binding to ATG7 promoter and transcriptionally up-regulating its ex

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

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

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

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

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

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

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

271 g autophagy alone by conditional deletion of Atg7 results in a completely distinct phenotype in all s

272 ophagy or molecular targeting of beclin 1 or Atg7 results in reversal of the suppressive effects of A

273 ells before elimination, remain polarized in Atg7(-/-) reticulocytes in culture.

274 3-methyladenine, dominant-negative Vps34, or Atg7 shRNA rescued T cells expressing a dominant-negativ

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

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

277 and coinfected with Atg7 adenovirus or with Atg7 silencing siRNAs to produce gain-of or loss-of Atg7

278 ever, although inhibition of autophagy using Atg7 small interfering RNA inhibited cell death during s

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

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

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

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

283 s on the autophagy pathway proteins ATG5 and ATG7; this process is preceded by recruitment of beclin

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

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

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

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

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

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

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

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

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