ライフサイエンスコーパス: beclin 1

1 sential for the tumor suppressor function of Beclin 1.

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

3 was required for maintaining basal levels of Beclin 1.

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

5 and activate autophagy through induction of beclin 1.

6 g to Bim, leading to dissociation of Bim and Beclin 1.

7 negatively controlling K63 ubiquitination of Beclin 1.

8 nown to stimulate the autophagic function of Beclin 1.

9 tivity resulting from haploinsufficiency for Beclin 1.

10 hich BCL2 inhibits the autophagy function of Beclin 1.

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

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

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

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

15 athway through transcriptional regulation of BECLIN-1.

16 protein to the cellular proautophagy protein beclin-1.

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

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

19 mall interfering RNA (siRNA) against ATG5 or beclin-1.

20 SC2/AMPK-mediated mTOR inhibition but not on beclin-1.

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

22 and the formation of an autophagy-inhibitory Beclin 1/14-3-3/vimentin intermediate filament complex.

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

24 (Ats-1), a type IV secretion effector, binds Beclin 1, a subunit of the class III PI3K and Atg14L, an

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

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

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

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

29 Bim inhibits autophagy by interacting with Beclin 1, an autophagy regulator, and this interaction i

30 Here, we show that Beclin 1, an essential autophagy and tumor suppressor pr

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

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

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

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

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

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

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

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

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

40 tment with 3-methyladenosine, chloroquine or beclin 1 and Atg5-targeted siRNA also enhanced the sensi

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

42 Beclin 1 and its interacting proteins, including the cla

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

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

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

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

47 nally, glutamate activated autophagy markers Beclin 1 and LC3-II, while selenium prevented the activa

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

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

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

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

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

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

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

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

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

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

58 knockout cells showed an interaction between Beclin-1 and Atg3, a protein required for autophagosome

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

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

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

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

63 reased the expression of autophagic proteins Beclin-1 and LC3B-II; while knockdown of HO-1 down-regul

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

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

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

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

68 h the class III PI3K Vps34 in a complex with Beclin-1 and UVRAG.

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

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

71 ired the autophagy-initiation proteins ULK1, Beclin 1, and ATG14L and PI3-kinase activity.

72 ssociated with significantly decreased ULK1, beclin 1, and LC3 expression in the cartilage superficia

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

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

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

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

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

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

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

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

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

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

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

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

85 y-related 14 (Atg14), also called Barkor for Beclin 1-associated autophagy-related key regulator.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

103 High Beclin 1, Bcl-xL and Bad levels in CH and CIRR tissues s

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

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

106 that knockdown of autophagy-related protein beclin 1 (BCN1) or autophagy-related protein 7 (ATG7) in

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

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

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

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

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

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

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

114 Hsp90 specifically interacted with Beclin 1 but not with other adapter proteins in the TLR

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

116 ecute, autophagy is unleashed due to lack of Beclin 1 cleavage by caspases and can contribute to canc

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

118 ted gene) and FEZ1 and may regulate ULK1 and Beclin 1 complex activities.

119 53 is thus a negative regulator of the HMGB1/Beclin 1 complex, and HMGB1 promotes autophagy in the se

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

121 vent stimulus-induced disruption of the BCL2-beclin-1 complex and autophagy activation.

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

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

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

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

126 4 resulted in reduced stability of Vps15 and Beclin-1, components of the class III PI3K complex, and

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

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

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

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

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

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

133 Tat-beclin 1 decreases the accumulation of polyglutamine exp

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

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

136 umbers, the peripheral T cell compartment of Beclin 1-deficient Rag1(-/-) chimeras is largely normal.

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

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

139 that normal lymphocyte development involves Beclin 1-dependent, early-stage and distinct, Beclin 1-i

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

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

142 s host cytoplasmic delivery of anti-Ats-1 or Beclin 1 depletion by siRNA suppressed the infection; be

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

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

145 Here we delineate Beclin 1 differential specificity determinants for bindi

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

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

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

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

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

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

152 The Beclin-1 evolutionarily conserved domain is required bot

153 ys from mice deficient in autophagic protein Beclin 1 exhibited profibrotic phenotype, with increased

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

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

156 Reduced Beclin 1 expression, through genetic disruption of becli

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

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

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

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

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

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

163 Bnip3 that displaces the autophagic effector Beclin-1 from inactive Bcl-XL complexes.

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

165 Drug-induced dissociation of Beclin-1 from Rubicon and the induction of autophagy wer

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

167 Thus, Akt-mediated phosphorylation of Beclin 1 functions in autophagy inhibition, oncogenesis,

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

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

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

171 depletion by siRNA suppressed the infection; beclin 1 heterozygous-deficient mice were resistant to A

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

173 ectively promoted proteasomal degradation of Beclin 1 in a concentration-dependent (EC(50) 100 nM) an

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

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

176 This further suggested a role of the Hsp90/Beclin 1 in controlling autophagy in response to microbi

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

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

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

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

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

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

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

184 Heterozygous deletion of beclin 1 increased accumulation of aggregated Col-I unde

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

186 eclin 1-dependent, early-stage and distinct, Beclin 1-independent, late-stage processes.

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

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

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

190 The RUN domain Beclin-1-interacting cysteine-rich-containing Rubicon pr

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

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

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

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

195 Beclin 1 is a haploinsufficient tumor suppressor that is

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

197 Beclin 1 is a well-established core mammalian autophagy

198 In contrast, Beclin 1 is largely dispensable for the initial generati

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

200 Collectively, our results suggest that Beclin 1 is required for maintenance of undifferentiated

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

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

203 Beclin 1 knockdown abolished preconditioning-induced aut

204 ipid levels after inhibition of autophagy by Beclin 1 knockdown or lysosome inhibitors.

205 ane protein-2 levels synergizes with partial BECLIN-1 knockdown to restore autophagosome processing a

206 Partial beclin-1 knockdown transcriptionally stimulates lysosome

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

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

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

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

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

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

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

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

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

216 Therefore, Beclin 1 may be a useful target for inhibiting autophagy

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

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

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

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

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

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

223 ity was reduced in macrophages isolated from Beclin-1(+/-) mice compared with wild-type mice.

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

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

226 Beclin 1 mRNA levels were lower in HCC than in CH (P = 0

227 Beclin 1 mutant knockin resulted in markedly increased a

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

229 Expression of a Beclin 1 mutant resistant to Akt-mediated phosphorylatio

230 11 or Bcl-XL, and we show that a G120E/D121A Beclin 1 mutant selectively prevents down-regulation of

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

232 In this study we evaluated the expression of Beclin 1 (one of the main autophagocytic agents, which b

233 cell differentiation to address the role of Beclin 1, one of the key autophagic proteins, in lymphoc

234 nd small interfering RNAs (siRNAs) targeting beclin 1 or Atg5 on the cytotoxicity of cisplatin.

235 1 expression, through genetic disruption of beclin 1 or knockdown by specific siRNA in primary mouse

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

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

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

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

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

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

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

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

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

245 36, which blocks Bcl-2 and Bcl-xL binding to Beclin 1, prevented hypercapnic inhibition of autophagy

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

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

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

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

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

251 Beclin 1 regulates PI3P production in response to growth

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

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

254 eIF2alpha, while inhibition of autophagy, by Beclin 1 short hairpin RNA (shRNA) knockdown or pharmaco

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

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

257 dly, allelic loss of the autophagy regulator Beclin-1 significantly delayed tumor development in ATM-

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

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

260 Simultaneous knockdown of GRP78 and beclin-1 synergistically restored antiestrogen sensitivi

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

262 gy was confirmed using ectopic expression of Beclin 1 that conferred cytoprotection.

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

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

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

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

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

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

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

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

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

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

273 ycoprotein Thrombospondin 1 independently of Beclin 1 transcriptional induction.

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

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

276 ompanied by reactive oxygen species-mediated BECLIN-1 upregulation and a reduction in lysosome-associ

277 hereas reperfusion stimulates autophagy with BECLIN-1 upregulation and is implicated in causing cell

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

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

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

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

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

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

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

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

286 ine-rich protein that functions as part of a Beclin-1-Vps34-containing autophagy complex.

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 Beclin-1 was identified as a new transcriptional target

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

293 which can also form a complex with Vps34 and Beclin-1, we conclude that Slamf1 recruits a subset of V

294 Both the BD and CCD domains of Beclin-1 were required for efficient binding to Slamf1.

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

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

297 prosurvival BCL-2 family member, MCL-1, from beclin 1, which was essential for the initiation of auto

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