ライフサイエンスコーパス: beclin 1

1 negatively controlling K63 ubiquitination of Beclin 1.

2 nown to stimulate the autophagic function of Beclin 1.

3 tivity resulting from haploinsufficiency for Beclin 1.

4 hich BCL2 inhibits the autophagy function of Beclin 1.

5 sential for the tumor suppressor function of Beclin 1.

6 and in vivo by BCL2, a negative regulator of Beclin 1.

7 was required for maintaining basal levels of Beclin 1.

8 xidative stress through the up-regulation of beclin 1.

9 to modulate the ubiquitination of RIPK1 and beclin 1.

10 nti-T. gondii activity dependent on ULK1 and beclin 1.

11 and activate autophagy through induction of beclin 1.

12 ith the autophagy complex proteins Vps34 and Beclin-1.

13 -xL and dissociation of Bcl-2 or Bcl-xL from Beclin-1.

14 -II and the autophagy-associated BH3 protein Beclin-1.

15 ng an autophagy-dependent phosphorylation of beclin-1.

16 he cell surface interaction between Her2 and Beclin-1.

17 athway through transcriptional regulation of BECLIN-1.

18 protein to the cellular proautophagy protein beclin-1.

19 ant, Delta68H, which is incapable of binding beclin-1.

20 nd with the subsequent increase in cytosolic Beclin-1.

21 autophagy and apoptosis through ATG16L1 and Beclin-1.

22 duced by Bax reduced autophagy by decreasing Beclin-1.

23 itination at lysine residues K32 and K263 on Beclin-1.

24 agy by promoting inactive dimer formation of Beclin-1.

25 We have shown that inhibition of Beclin 1, a key activator in the initiation phase of aut

26 ormation of the autophagophore by binding to Beclin 1, a key factor involved in the elongation of the

27 enables wild-type ataxin 3 to interact with beclin 1, a key initiator of autophagy.

28 and ROS generation result in upregulation of beclin-1, a protein associated with transcriptional supp

29 Conversely, overexpression of beclin-1 activates mTOR to inhibit TFEB, resulting in de

30 Beclin-1 (also known as Atg6 in yeast) is a core protein

31 n of pro-autophagic proteins (ATG5, ATG7 and Beclin-1) also restores Delta133p53alpha expression.

32 tophagy by upregulating the transcription of Beclin 1, an essential autophagy gene.

33 at negatively regulate autophagy by blocking Beclin 1, an essential component of the autophagy initia

34 of Bcl-2 and dissociation between Bcl-2 and Beclin 1, an event known to stimulate the autophagic fun

35 irradiation resistance-associated gene, and Beclin 1 and a block of autophagy.

36 er90 to promote K63-linked ubiquitination of Beclin 1 and activation of autophagy.

37 Mechanistically, SNX5 interacts with beclin 1 and ATG14-containing class III phosphatidylinos

38 aracterized by increased calpain activation, beclin 1 and ATG5 cleavage, and intestinal epithelial ce

39 proautophagic and proapoptotic functions of beclin 1 and ATG5 during inflammation.

40 optosis by protecting the autophagy proteins beclin 1 and ATG5 from calpain-mediated cleavage during

41 es of enteroids verified that HMGB1 protects beclin 1 and ATG5 from calpain-mediated cleavage events

42 dii were dependent on the autophagy proteins Beclin 1 and Atg7.

43 lineate a function of the autophagy proteins Beclin 1 and FIP200-but not of other essential autophagy

44 Beclin 1 and its interacting proteins, including the cla

45 Peg3 coimmunoprecipitated with Beclin 1 and LC3 and was required for maintaining basal

46 creased expression of the autophagy proteins Beclin 1 and LC3 II, enhanced autophagy flux, and led to

47 essor gene Peg3 and its co-localization with Beclin 1 and LC3 in autophagosomes, suggesting a major r

48 n-mediated activation and co-localization of Beclin 1 and LC3, thereby reducing autophagic progressio

49 in an increased level of autophagic proteins Beclin 1 and LC3-II.

50 eg3 relocated into autophagosomes labeled by Beclin 1 and microtubule-associated light chain 3.

51 , and VEGFR2 was required for decorin-evoked Beclin 1 and microtubule-associated protein 1 light chai

52 Decorin, via Peg3, induced transcription of Beclin 1 and microtubule-associated protein 1 light chai

53 IRGM interacts with ULK1 and Beclin 1 and promotes their co-assembly thus governing t

54 sease (AD) brains show significantly reduced beclin 1 and retromer protein levels.

55 osphorylation and functional inactivation of Beclin 1 and the consequent suppression of autophagy.

56 endothelial cells but was also dependent on beclin 1 and the expression of inducible Hsp70 in dendri

57 the direct binding of p65 to the promoter of Beclin 1 and to its transcriptional activation.

58 out the effects of cell-mediated immunity on Beclin 1 and ULK1, key regulators of autophagy.

59 3-kinase complex (PI3KC3-C2)-which contains beclin 1 and UVRAG-in skeletal muscle during exercise, a

60 These results help clarify the mechanism of beclin-1 and Atg14 during autophagy.

61 3B-positive neurons, and expression of LC3B, Beclin-1 and Bcl-2 in peri-infarct cortex were evaluated

62 Physical interactions between Beclin-1 and Bcl-2 were increased in the VDR-deficient e

63 ced autophagy by reducing the interaction of Beclin-1 and Bcl-2.

64 Human beclin-1 and its yeast homologue, Atg6/Vps30, are scaffo

65 alleled with induction of autophagy markers, beclin-1 and LC3-II.

66 induced, as indicated by increased levels of beclin-1 and LC3-II.

67 hagy-related proteins, including Atg5, Atg7, Beclin-1 and LC3A/B-II, seen in HFD-fed control mice, bu

68 ith reduced levels of the autophagic markers Beclin-1 and LC3B.

69 The expression levels of Beclin-1 and lysozyme were decreased in VDR(DeltaIEC) or

70 c vesicle formation and markers of autophagy BECLIN-1 and microtubule-associated protein 1 light chai

71 ased levels of autophagy-associated proteins Beclin-1 and P62, and increased LC3b-II/LC3b-I ratio, we

72 eport a newly identified interaction between Beclin-1 and the protein tyrosine kinase receptor Her2.

73 nated TRIM21, autophagy regulators (ULK1 and beclin 1) and effectors (LC3 and p62), and lysosome-asso

74 autophagy-related proteins (LC3, Atg-5, and Beclin-1) and augmented recruitment of phagosomal (EEA1

75 (vacuolar protein sorting) 34, VPS15, BECN1 (Beclin 1), and ATG (autophagy-related) 14.

76 nsisting of Vps34, Vps15 (p150), Vps30/Atg6 (Beclin 1), and Vps38 (UVRAG).

77 TLR9 binds beclin 1, and this interaction is increased by energy st

78 n regulates ATG14 interaction with VPS34 and Beclin 1, and thus plays a key role in ATG14 complex ass

79 itioning inhibited these changes in p-Bcl-2, Beclin-1, and Bcl-2/Beclin-1 complex expression.

80 In situ monitoring of GFAP, Ki67, caspase-3, Beclin-1, and LC-3 in the tumor samples together with TU

81 ssion of lysosomal cathepsin B, cathepsin D, Beclin-1, and microtubule-associated protein light chain

82 cluding autophagy-related gene (Atg)5, Atg7, beclin-1, and microtubule-associated proteins 1A/1B ligh

83 otubule-associated protein 1 light chain 3), Beclin-1, and p62.

84 rdiac damage was substantially attenuated in beclin 1- and Atg16-deficient mice as shown by improved

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

86 Autophagy-related proteins such as Beclin-1 are involved in an array of complex processes,

87 sion levels of ATG4 family members, ATG5 and BECLIN-1 are significantly increased in CD34(+) cells fr

88 These findings position beclin 1 as a link between autophagy, retromer trafficki

89 utophagosome initiating molecules FIP200 and Beclin 1, as well as molecules involved in the autophago

90 th Bnip3-mediated displacement of Bcl-2 from Beclin-1, as determined by immunoblotting and immunoprec

91 nhanced binding to inhibitors, and decreased Beclin 1-associated VPS34 kinase activity.

92 Here we report that ATG14 (also known as beclin-1-associated autophagy-related key regulator (Bar

93 show that CaMKII can directly phosphorylate Beclin 1 at Ser90 to promote K63-linked ubiquitination o

94 report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-

95 Interaction of Rubicon and Beclin-1 at 1 h postinfection affirmed the prevalence of

96 removing the K11-linked ubiquitin chains of Beclin-1 at lysine 437.

97 by phosphorylating an essential ATG protein, Beclin 1, at serine 90, and that this phosphorylation si

98 ith upregulation of most autophagic markers (Beclin-1, ATG10, p62/SQSTM1, LC3) and of the HSPB8-media

99 We found that depletion of Beclin-1, Atg12, Atg14, Atg16, or LC3 with specific smal

100 ion of autophagy-related (Atg) genes Fip200, beclin 1, Atg14, Atg16l1, Atg7, Atg3, and Atg5, in the m

101 nd autophagy by blocking the activity of the Beclin-1/Atg14/PI3KIII complex in regard to synthesis of

102 utophagy by secreting Ats-1 that hijacks the Beclin 1-Atg14L autophagy initiation pathway likely to a

103 ical for understanding how modulation of the Beclin 1-ATG14L interaction affects autophagy.

104 We hypothesize that disruption of the Beclin 1-ATG14L protein-protein interaction, which is re

105 agy by directly binding to the BH3 domain of Beclin 1/Atg6.

106 ine or shRNAs targeting autophagic proteins (Beclin 1, ATG7, and LC3) as well as by overexpression of

107 dominant negative form of ATG4B or silencing Beclin-1, Atg7, or p62 indicated that macroautophagy doe

108 phagy-related (Atg) proteins including Ulk1, Beclin-1, Atg9A, Atg4B, and Bnip3, suggesting that FoxO3

109 f Bcl-2 and prevented the formation of Bcl-2/Beclin 1 autophagy suppressor complexes.

110 the direct interaction between cGAS and the Beclin-1 autophagy protein not only suppresses cGAMP syn

111 these results indicate that the ROS-ATM-CHK2-Beclin 1-autophagy axis serves as a physiological adapta

112 ings reveal novel dual functions of theUSP19-Beclin-1 axis by balancing autophagy and the production

113 s Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1-Bcl-2 autophagy-regulatory complex formation in

114 olished isoflurane-induced disruption of the Beclin 1/Bcl-2 association.

115 nduced autophagy, possibly by disrupting the Beclin 1/Bcl-2 interaction.

116 Beclin 1 (Becn1) functions as a tumor suppressor, and Be

117 Conditional deletion of beclin 1 (Becn1) in mouse lung epithelial cells (Becn1Ep

118 Beclin 1 (BECN1) is a key regulator of autophagy, a crit

119 identified ATG7 and the cell death modulator beclin-1 (BECN1) as negative regulators of IRF1.

120 of the major pro-autophagy proteins ULK1 and Beclin-1 (BECN1), increased LC3-II levels, and accumulat

121 that SS-12 commonly interacts with Bcl-2 and Beclin 1 BH3 domain proteins and enhances autophagic flu

122 othermal titration calorimetry to identify a Beclin 1 BH3 domain-derived peptide that selectively bin

123 xplored the effect of deleting the gamma34.5 Beclin 1 binding domain (BBD).

124 Pi promoted beclin 1 binding to its negative regulator BCL2, which i

125 tion(3,5) that blocks the disruption of BCL2-beclin 1 binding.

126 effect when 3-methyladenine or knockdown of beclin 1 blocked early stages of autophagy.

127 lizes the autophagy core-machinery component Beclin-1 by promoting K27-linked ubiquitination at lysin

128 interferon (IFN) signaling.USP19 stabilizes Beclin-1 by removing the K11-linked ubiquitin chains of

129 ver, with time, B. abortus infection induced Beclin-1 cleavage with concomitant cleavage of caspase-3

130 We here addressed the mechanism of beclin-1 complex activation and reveal two critical step

131 was accompanied by dissociation of the Bcl-2/Beclin-1 complex and increased Beclin-1 expression.

132 Changes in Bcl-2/Beclin-1 complex association and Bcl-2 phosphorylation (

133 hese changes in p-Bcl-2, Beclin-1, and Bcl-2/Beclin-1 complex expression.

134 on, a negative autophagy regulator, from the Beclin-1 complex, activating phosphatidylinositol 3-kina

135 JCI, Tan et al. describe the effects of the beclin-1 conditional myeloid cell-specific deletion in m

136 First, we identified a unique domain in beclin-1, conserved in the yeast homologue Atg6, which i

137 d ULK1, but dependent upon the activation of Beclin 1-containing class III PI3-kinase.

138 iated membrane protein-2 and upregulation of BECLIN-1, contributing to increased cardiomyocyte death.

139 Beclin 1 controls the trafficking fate of growth regulat

140 Indeed, we found that Beclin 1 could directly interact with DNA topoisomerase

141 Finally, adoptive transfer of RSV-infected Beclin-1(+/-) DCs into the airways of wild-type mice pro

142 Further examination indicated that Beclin-1(+/-) DCs stimulated less IFN-gamma and IL-17 pr

143 Tat-beclin 1 decreases the accumulation of polyglutamine exp

144 Rhes robustly binds the autophagy regulator Beclin-1, decreasing its inhibitory interaction with Bcl

145 BECLIN-1 deficiency in ECs abolished the XBP1-induced au

146 cancers may be, at least in part, due to the Beclin 1-dependent autophagy activation by IAPs describe

147 plasmic reticulum to functionally antagonize Beclin 1-dependent autophagy.

148 SR-BI was a key driver of beclin-1-dependent autophagy during acute bacterial infe

149 thway, by blockingRIG-I-MAVSinteraction in a Beclin-1-dependent manner.

150 -penetrating autophagy-inducing peptide, Tat-Beclin 1, derived from the autophagy protein Beclin 1, t

151 Here we show that a peptide, Tat-beclin 1-derived from a region of the autophagy protein,

152 Inhibition of Beclin 1 did not change the levels of several key inflam

153 Here we delineate Beclin 1 differential specificity determinants for bindi

154 phosphorylation-Bcl-2 phosphorylation-Bcl-2-Beclin 1 dissociation and AMPK phosphorylation-ULK1 phos

155 ux through up-regulating autophagy initiator beclin 1 during redox stress and is an important cell su

156 the essential autophagy components ATG7 and Beclin-1, effectively attenuated Chal-24-induced cell de

157 Conditional deletion of the beclin 1-encoding gene (Becn1) specifically within lung

158 Akt-mediated phosphorylation of Beclin 1 enhanced its interactions with 14-3-3 and vimen

159 SiRNA knockdown of autophagy initiator beclin-1 enhanced Mtb survival, whereas rapamycin-induce

160 Therefore, we examined the effects of the Beclin-1 evolutionarily conserved domain in TB1 on viral

161 The Beclin-1 evolutionarily conserved domain is required bot

162 utosis during the late phase of I/R with Tat-Beclin 1 exacerbated injury.

163 In human breast tumors, beclin 1 expression is inversely correlated with AKT and

164 ling and reveal a mechanism by which loss of beclin 1 expression would enhance breast cancer progress

165 In tumors with low Beclin 1 expression, endosomal HRS recruitment was dimin

166 by upregulation of the LC3II/LC3I ratio and Beclin-1 expression as well as inhibition of p62 express

167 atient lymphoid malignancies and showed that beclin-1 expression in neutrophils positively correlated

168 of the Bcl-2/Beclin-1 complex and increased Beclin-1 expression.

169 provide an explanation for how low levels of Beclin 1 facilitate tumor proliferation and contribute t

170 /IL-24 regulated autophagy through a miR-221/beclin-1 feedback loop.

171 ubiquitinase activity of ataxin 3 to protect beclin 1 from proteasome-mediated degradation and thereb

172 hibitor Rubicon, which in turn disassociates Beclin 1 from Rubicon to initiate autophagy.

173 inducer of autophagy that acts by displacing beclin-1 from BCL2.

174 correlatively associated with the release of Beclin-1 from its complex with Her2 and with the subsequ

175 at-containing protein (LRPPRC), and releases Beclin-1 from LRPPRC-mediated sequestration, thereby ena

176 d autophagic flux by physically dissociating Beclin-1 from the Vps34-Vps15 complex independent of its

177 However, Beclin 2, but not Beclin 1, functions in an additional lysosomal degradati

178 lian-specific protein, Beclin 2, which, like Beclin 1, functions in autophagy and interacts with clas

179 rboring significant autophagy defects due to Beclin-1 haploinsufficiency (Beclin-1(+/-)) were used.

180 Beclin 1 has nonautophagic functions that include its ab

181 Overexpressing Beclin 1 improved the repair of IR-induced DSB, but did

182 cribe an alternative mechanism of action for beclin 1 in breast cancer involving its control of growt

183 The function of beclin 1 in cancer has been attributed primarily to its

184 ly, our results demonstrate a novel role for Beclin 1 in impeding tumor growth by coordinating the re

185 Atg6 (beclin 1 in mammals) is a core component of the Vps34 co

186 muli, this is not observed in mice that lack Beclin 1 in myeloid cells, establishing the dominance of

187 Likewise, overexpressing Beclin 1 in PAI-2-deficient cells rescued the suppressio

188 Our data identify a novel role for beclin 1 in regulating growth factor signaling and revea

189 These findings reveal a novel function of Beclin 1 in regulation of DNA damage repair independent

190 core autophagy regulators ATG16L1, ULK1, and Beclin 1 in response to damaged endomembranes.

191 ors and act as platforms assembling ULK1 and Beclin 1 in their activated states.

192 However, the roles of Atg14 and beclin-1 in the activation of this complex remain unclea

193 ceptor 9 (TLR9)(4), and its interaction with beclin 1, in exercise-induced activation of AMPK in skel

194 th the autophagy enhancers rapamycin and Tat-Beclin-1 increased ureagenesis and protected against hyp

195 Here we show that Tat-Beclin 1 induces dose-dependent death that is blocked by

196 Depletion of eitherUSP19 or Beclin-1 inhibits autophagic flux and promotes type IIFN

197 clear receptor binding factor 2 (Nrbf2) as a Beclin 1-interacting protein from Becn1(-/-);Becn1-EGFP/

198 ults suggest that targeting the Bcl-2/Bcl-xL-Beclin 1 interaction may hold promise for ameliorating h

199 We also found that Nrbf2-Beclin 1 interaction required the N terminus of Nrbf2.

200 Thus, the cGAS-Beclin-1 interaction shapes innate immune responses by r

201 However, beclin 1 is a core component of the vacuolar protein sor

202 Beclin 1 is a haploinsufficient tumor suppressor that is

203 Here, we show that Beclin 1 is a prenatal primary cytoplasmic protein but r

204 Beclin 1 is a well-established core mammalian autophagy

205 Here we show that the autophagy protein beclin 1 is required for efficient phagocytosis in vitro

206 Beclin-1 is a key regulator of autophagy that functions

207 The activity of Beclin-1 is tightly regulated by multiple post-translati

208 ring exercise, and a core autophagy protein, beclin 1, is required for AMPK activation in skeletal mu

209 Beclin 1 knockdown abolished preconditioning-induced aut

210 Partial beclin-1 knockdown transcriptionally stimulates lysosome

211 ly, of the cytoprotective effects of partial beclin-1 knockdown, indicating a critical role for both

212 ted in marked upregulation of phosphorylated Beclin 1, known to play an important role in both autoph

213 interacts with a dominant negative binder of Beclin-1, known as leucine-rich pentatricopeptide repeat

214 utophagy as indicated by an up-regulation of Beclin-1/LC-3 and downregulation of p62, and aggravated

215 helial cells by modulating the expression of Beclin 1, LC3, and p62, three established autophagic mar

216 Bim bridges the Beclin 1-LC8 interaction and thereby inhibits autophagy

217 Active EGFR binds the autophagy protein Beclin 1, leading to its multisite tyrosine phosphorylat

218 ights the novelty of the mda-7/IL-24-miR-221-beclin-1 loop in mediating cancer cell-specific death.

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

220 Conversely, animals overexpressing Beclin 1 manifested an amplified cardiotoxic response.

221 lacking autophagy gene Atg7, suggesting that Beclin 1 may regulate DSB repair independent of autophag

222 s by inhibiting K63-linked ubiquitination of beclin 1 mediated by TRAF2, cIAP1 and cIAP2, thereby red

223 tant selectively prevents down-regulation of Beclin 1-mediated autophagy by Bcl-XL, but not by M11.

224 inities, resulting in the down-regulation of Beclin 1-mediated autophagy.

225 Furthermore, we show that beclin 1-mediated impairments in phagocytosis are associ

226 uncover a transcriptional feedback loop for beclin-1-mediated regulation of TFEB activation and impl

227 Beclin 1(+/-) mice exposed to doxorubicin were protected

228 though isolated airway epithelial cells from Beclin-1(+/-) mice demonstrated little change compared w

229 Upon RSV infection in vivo, lungs of Beclin-1(+/-) mice showed increased Th2 cytokine product

230 the expression of a tyrosine phosphomimetic Beclin 1 mutant leads to reduced autophagy, enhanced tum

231 11 or Bcl-XL, and we show that a G120E/D121A Beclin 1 mutant selectively prevents down-regulation of

232 tophagy levels in cells expressing different Beclin 1 mutants and either M11 or Bcl-XL, and we show t

233 Consequently, ubiquitination of Beclin-1 negatively regulates autophagy by promoting ina

234 perturbation of quiescence in mice that lack Beclin 1 or FIP200 in myeloid cells results in spontaneo

235 etal muscle during exercise, and knockout of beclin 1 or UVRAG inhibits the cellular AMPK activation

236 th chloroquine or knockdown of Atg7, but not Beclin-1 or Ambra1, prevented THC-induced autophagy and

237 autophagic genes such as Ulk1/2, Fip200, or Beclin-1 or chemical inhibition of ULK1/2 or VPS34 atten

238 LC in the subventricular region co-expressed beclin-1 or LC3, markers for autophagosome or autophagol

239 (e.g., genetically by shRNA targeting Ulk1, beclin-1, or Atg5 or pharmacologically by 3-methyladenin

240 gy in diabetic hearts was further reduced in beclin 1- or Atg16-deficient mice but was restored parti

241 c damage was dose-dependently exacerbated by beclin 1 overexpression.

242 ay aggravated infarct phenotypes and reduced Beclin 1 p-Ser90/Ser93 in a cerebral stroke model, sugge

243 vation of autophagy using a specific inducer Beclin-1 peptide ameliorates cysts in the pkd1a model.

244 mycin (mTOR)/Unc-51-like kinase 1 (ULK1) and Beclin-1/phosphatidylinositol 3-kinase (PI3K) pathways w

245 Moreover, MK2/MK3-dependent Beclin 1 phosphorylation (and starvation-induced autopha

246 on the downstream autophagy-related proteins Beclin 1, PI3K, and ATG5, but not on the upstream autoph

247 36, which blocks Bcl-2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy

248 Beclin 1 promoted endosomal recruitment of hepatocyte gr

249 nd that de novo expression of Peg3 increased Beclin 1 promoter activity and protein expression.

250 e spliced XBP1 isoform bound directly to the BECLIN-1 promoter at the region from nt -537 to -755.

251 ce transcriptional activation of a truncated BECLIN-1 promoter.

252 little change compared with wild-type mice, Beclin-1(+/-) pulmonary and bone marrow-derived DCs show

253 stage of autophagosomes by interacting with Beclin 1/Rab7 and dysregulating TFEB localization and ce

254 A deficiency in Beclin-1 reduces viral infection in mice and abolishes A

255 Beclin 1 regulates PI3P production in response to growth

256 and identify the blockade of MK2/3-dependent Beclin 1 S90 phosphorylation as a mechanism by which BCL

257 nsive kinases that promote autophagy through Beclin 1 S90 phosphorylation, and identify the blockade

258 xpressing breast carcinoma cell lines and in Beclin-1 signaling in these cells.

259 autophagosome machinery proteins Atg16L1 and Beclin 1 significantly ameliorated cell death in these c

260 Interestingly, both ITPR1 and Beclin-1 silencing in 786-0 cells inhibited NK-induced a

261 on of autophagy by 3-methyladenine (3-MA) or Beclin-1 small interfering RNA (siRNA) partially suppres

262 Here, we provide in vivo evidence that Beclin 1 suppresses tumor proliferation by regulating th

263 The Tat-Beclin-1 (TB1) peptide has been reported as an autophagy

264 through the characterization of a domain of beclin 1 that interacts with HIV-1 Nef, we have develope

265 rly endosome maturation that is regulated by beclin 1, the transition of APPL1-containing phosphatidy

266 partially or completely by overexpression of beclin 1 to different levels.

267 ndritic cell (DC) maturation, and binding to Beclin 1 to interfere with autophagy.

268 bsequently stabilized the autophagic protein Beclin 1 to promote autophagy, resulting in decreases in

269 eam molecules by which CD40 acts on ULK1 and Beclin 1 to stimulate autophagy and killing of T. gondii

270 thereby inhibits autophagy by mislocalizing Beclin 1 to the dynein motor complex.

271 serves as a novel anchorage site, recruiting Beclin-1 to mitochondria, promoting its polyubiquitinati

272 Beclin 1, derived from the autophagy protein Beclin 1, to investigate whether high levels of autophag

273 ed to translocate to the nucleus and promote Beclin 1 transcription.

274 ycoprotein Thrombospondin 1 independently of Beclin 1 transcriptional induction.

275 sine kinase inhibitor (TKI) therapy disrupts Beclin 1 tyrosine phosphorylation and binding to its inh

276 Upon its interaction with Her2, Beclin-1 up-regulates the phosphorylation levels of Her2

277 Inhibition of autophagy by targeting Beclin 1 using siRNA significantly suppresses cell growt

278 -induced AMPK activation, glucose uptake and beclin 1-UVRAG complex assembly.

279 n addition, the molecule did not disrupt the Beclin 1-UVRAG interaction, critical for VPS34 Complex I

280 AG), reducing the activity of the associated Beclin 1-Vps34 complex and thereby inhibiting phosphoino

281 The Beclin 1-Vps34 complex, the core component of the class

282 rbf2 is a component of the Atg14L-containing Beclin 1-Vps34 complex.

283 rbf2 may interact with the Atg14L-containing Beclin 1-Vps34 protein complex to modulate protein-prote

284 el aspect of the intricate mechanism for the Beclin 1-Vps34 protein-protein interaction network to ac

285 on of mTORC1 signaling or stimulation of the Beclin 1-Vps34-UVRAG complex rescued the autophagy flux,

286 NRBF2 in the assembly of the specific Atg14L-Beclin 1-Vps34-Vps15 complex for autophagy induction.

287 Rubicon is a protein known to engage the Beclin-1/Vps34-PI3K/UVRAG complex and inhibit endosome a

288 This Slamf1/Beclin-1/Vps34/UVRAG protein complex is formed in intrac

289 in 3 and its polyQ-mediated interaction with beclin 1 was competed for by other soluble proteins with

290 f cells with 3-methyladenine or knockdown of beclin 1 was protective, whereas chloroquine treatment h

291 Until recently, beclin-1 was a protein known mainly for its role as a cr

292 Beclin-1 was identified as a new transcriptional target

293 reover, although post-ischemic expression of Beclin-1 was not altered in the ethanol groups, post-isc

294 ion-induced autophagy, which is regulated by beclin 1, was particularly inhibited in ataxin-3-deplete

295 as autophagy related 16 like 1 (ATG16L1) and Beclin-1 were decreased in the intestines of VDR(DeltaIE

296 defects due to Beclin-1 haploinsufficiency (Beclin-1(+/-)) were used.

297 ived from a region of the autophagy protein, beclin 1, which binds human immunodeficiency virus (HIV)

298 BH3 domain within the key autophagy effector Beclin 1 with comparable affinities, resulting in the do

299 Moreover, HO-1 promoted the association of Beclin-1 with Bcl-xL and Rubicon, a novel negative regul

300 main is required both for the interaction of Beclin-1 with Her2 and for the increased Her2 and Akt ph