ライフサイエンスコーパス: parkin

1 es as a pro-fission signal, independently of Parkin.

2 y PTEN-induced putative kinase 1 (PINK1) and Parkin.

3 elease of exosomes in the presence of mutant Parkin.

4 se a loss of function of the encoded protein Parkin.

5 the E2~Ub conjugate, thus leading to active parkin.

6 IF-1alpha as a major ubiquitination site for Parkin.

7 e mitochondrial outer membrane and activates Parkin.

8 o suppressed VDAC1-induced redistribution of Parkin.

9 re marked for disposal via ubiquitylation by Parkin.

10 g in poorer autoinhibition in phosphorylated parkin.

11 ucture of the phosphorylated UBL domain from parkin.

12 Parkin, a E3 ubiquitin ligase associated with familial P

13 TRAF2 also colocalizes and interacts with PARKIN, a previously described E3 ubiquitin ligase and m

14 Mutations in Parkin, a ubiquitinating enzyme, lead to the selective l

15 Physiological regulation of PARKIN abundance, however, and the impact on pUb accumul

16 , our work demonstrates the critical role of PARKIN abundance, identifies regulating genes, and revea

17 gned to discover physiological regulators of PARKIN abundance, we performed a pooled genome-wide CRIS

18 entified and negatively regulates endogenous PARKIN abundance.

19 Parkin accumulation on mitochondria and subsequent Parki

20 on of K572 for modification, suggesting that Parkin activation and acquisition of substrate specifici

21 d relative importance of these events during PARKIN activation and mitochondria quality control remai

22 er, the results underscore the importance of parkin activation by the PINK1 phosphorylation signal an

23 the brains of Mutator mice, indicating PINK1-Parkin activation.

24 ns up new avenues to identify small-molecule PARKIN activators.

25 sorafenib as a mitocan and suggest that high Parkin activity levels could make tumor cells more sensi

26 domains from elimination by unchecked PINK1-Parkin activity.

27 The lack of Parkin affected mitochondrial morphology in dopaminergic

28 Our results suggest that Parkin affects mtDNA levels in a mitophagy-independent m

29 related proteins-alpha-synuclein, LRRK2, and Parkin-alpha-synuclein might be a major link.

30 Accumulating evidence indicates that Parkin also has an important role in excitatory glutamat

31 PARKIN, an E3 ligase mutated in familial Parkinson's dis

32 It encodes parkin, an E3 ubiquitin ligase of the RBR family.

33 Mutations in the gene encoding Parkin, an E3 ubiquitin ligase, lead to juvenile-onset P

34 ggest a functional epistatic relationship to Parkin and a protective role of SLP-2 in neurons.

35 with dilated cardiomyopathy showed excessive Parkin and CHOP induction.

36 KI links mitochondrial stress with the PINK1/Parkin and DJ-1 mechanisms of mitophagy.

37 The regulatory PINK1/Parkin and DJ-1 pathways are strongly induced by mitocho

38 dependent protein kinase regulates the PINK1/Parkin and DJ-1 pathways of mitophagy during sepsis.

39 KI that precedes the colocalization of PINK1/Parkin and DJ-1.

40 s a master mitophagy regulator by activating Parkin and DRP1 in response to damage.

41 structural insights into the RBR E3 ligases Parkin and HHARI in their overall auto-inhibited forms a

42 OIP RBR E3 ligase cycle, and comparison with Parkin and HHARI suggests a general mechanism for RBR E3

43 The RBR family includes Parkin and HOIP, the central catalytic factor of the LUB

44 The E3 ubiquitin ligases PARKIN and MUL1 play redundant roles in elimination of p

45 f small-molecule activators or inhibitors of PARKIN and other RBR E3 ligases.

46 qk transcription but does not extend to the Parkin and Parkin coregulated genes, which are affected

47 biquitin-conjugating enzyme UbcH7 binding to Parkin and Parkin E3 ligase activity suggest that Parkin

48 se results highlight the combined effects of Parkin and PGC-1alpha in the maintenance of mitochondria

49 Mutations in Parkin and PINK1 cause an inherited early-onset form of

50 Together, parkin and PINK1 regulate the mitophagy pathway, which r

51 ophagy linked to dysfunction in the proteins Parkin and PTEN-induced putative kinase 1 (PINK1) is imp

52 Mice lacking both parkin and RET exhibited accelerated dopaminergic cell a

53 The physical and genetic interaction between Parkin and SLP-2 and the compensatory potential of SLP-2

54 hila studies showed a genetic interaction of Parkin and SLP-2, and further, tissue-specific or global

55 es both Ser65 (S65) in the UB-like domain of PARKIN and the conserved Ser in UB itself, but the tempo

56 These genes encode the E3 ubiquitin ligase parkin and the protein kinase PTEN-induced kinase 1 (PIN

57 rate that there is genetic crosstalk between parkin and the receptor tyrosine kinase RET in two diffe

58 serine 65 (Ser(65)) of the ubiquitin ligase Parkin and ubiquitin to stimulate Parkin E3 ligase activ

59 PINK1 phosphorylates both Parkin and ubiquitin to stimulate ubiquitination of doze

60 NK1 activates Parkin by phosphorylating both Parkin and ubiquitin.

61 ulates the phosphorylation of the substrates Parkin and Ubiquitin.

62 al homeostasis and functions in concert with Parkin and VCP for Marf degradation to promote damaged m

63 disease-associated proteins alpha-Synuclein, Parkin, and Huntingtin (Htt).

64 issue homeostasis upon reduction of Pink1 or Parkin appears to result from reduction of age- and stre

65 ecruited Parkin to the mitochondria, and via Parkin arrested axonal transport of mitochondria.

66 and SAXS, we show that pUb binds to RING1 of Parkin at a site formed by His302 and Arg305.

67 Loss of Parkin at least partially mediates the prodeath actions

68 kedly delayed compared to phosphorylation of Parkin at Ser(65).

69 e here that vps35 genetically interacts with parkin but interestingly not with pink1.

70 PINK1 activates Parkin by phosphorylating both Parkin and ubiquitin.

71 Activation of Parkin by phosphorylation or by binding of pUb is requir

72 omain and ubiquitin are required to activate parkin by releasing the UBL domain, forming an extended

73 uor can quantify activation or inhibition of PARKIN by structural mutations.

74 The kinase PINK1 and ubiquitin ligase Parkin can regulate the selective elimination of damaged

75 Loss-of-function mutations of Parkin cause some monogenic forms of Parkinson's disease

76 cts naturally occurring activation states of PARKIN caused by Ser(65) phosphorylation (pPARKIN) and p

77 ed that meiosis-expressed gene 1 (MEIG1) and Parkin co-regulated gene (PACRG) interact, and that sper

78 Parkin colocalizes on polarized mitochondria harboring m

79 ctopic expression of the ubiquitin E3 ligase Parkin, combined with short-term mitochondrial uncoupler

80 The phosphoUb binding site on PARKIN comprises a conserved phosphate pocket and harbou

81 ate the nonmotile ciliary signaling roles of parkin coregulated gene (PACRG), a protein linked to cil

82 iption but does not extend to the Parkin and Parkin coregulated genes, which are affected in the qk a

83 utophagy-forced reactivation that clears the Parkin-decorated mitochondria is as effective in inhibit

84 Here, we show that Parkin deficiency leads to decreased AMPA receptor-media

85 Contrary to our expectations, we found that Parkin-deficient animals do not accumulate senescent mit

86 aminergic cell and axonal loss compared with parkin-deficient animals, which showed none, and RET-def

87 Both endogenous Rab7 in Parkin-deficient cells and overexpressed K38 R-Rab7 muta

88 increased secretion of exosomes observed in Parkin-deficient cells, suggesting that Rab7 deregulatio

89 hese alterations in the endocytic pathway in Parkin-deficient cells, we found that Parkin regulates t

90 esting the impairment of retromer pathway in Parkin-deficient cells.

91 ible for the endocytic phenotype observed in Parkin-deficient cells.

92 sence of Drp1, while it induces mitophagy in Parkin-deficient cells.

93 We find that Parkin-deficient neurons exhibit significantly reduced A

94 Cardiac Parkin deletion or expression of Mfn2 AA from birth, but

95 A crystal structure of Parkin Delta86-130 at 2.54 A resolution allowed the desi

96 SOD1 induced reductions in Miro1 levels were Parkin dependent.

97 also reduces cytosolic pH and induces PINK1/PARKIN-dependent and -independent mitophagy.

98 Furthermore, while cultured neurons display Parkin-dependent axonal mitophagy, we find this is vanis

99 response, sorafenib treatment triggers PINK1/Parkin-dependent cellular apoptosis, which is attenuated

100 (PTEN)-induced Putative Kinase 1 (PINK1) and Parkin-dependent degradation of Miro1 and consequently s

101 n mitochondrial turnover in vivo, or whether Parkin-dependent events of the mitochondrial life cycle

102 red for the delivery of stress-induced PINK1/parkin-dependent MDVs to the late endosome/lysosome.

103 AMPA receptor internalization and suggest a Parkin-dependent mechanism for hippocampal dysfunction t

104 transport of mitochondria by inducing PINK1/Parkin-dependent Miro1 degradation.

105 orylation influences the decision to undergo Parkin-dependent mitochondrial arrest, which, in the con

106 Miro ubiquitination, Parkin recruitment, and Parkin-dependent mitochondrial arrest.

107 tion via modulation of redox homeostasis and Parkin-dependent mitochondrial clearance.

108 ission, whereas Ubc13 inactivation abrogates parkin-dependent mitochondrial fusion.

109 indicate that the cell body is the focus of Parkin-dependent mitochondrial quality control in neuron

110 d glucose intolerance due to activation of a Parkin-dependent mitophagic pathway, leading to the form

111 accumulation on mitochondria and subsequent Parkin-dependent mitophagy is abrogated in glucose-free

112 c or selective autophagic stimuli, including parkin-dependent mitophagy, and cells lacking all ATG8 p

113 creased respiration rates, exacerbated PINK1/Parkin-dependent mitophagy, and transcriptional upregula

114 hysiological conditions effectively triggers Parkin-dependent mitophagy, thus establishing a foundati

115 vitro, mature motor neurons rarely displayed Parkin-dependent mitophagy.

116 imination, in which these organelles undergo Parkin-dependent sequestration into Rab5-positive early

117 Damaged mitochondria undergo Parkin-dependent ubiquitin conjugation and are specifica

118 However, recent work uncovered a PINK1/parkin-dependent vesicle transport pathway wherein oxidi

119 RNA interference-mediated Parkin depletion attenuates CD44H cell generation.

120 Parkin depletion in cardiac HL-1 cells increased CHOP le

121 We found that the loss of Parkin did not exacerbate the parkinsonian pathology alr

122 However, the loss of Parkin did produce abnormal tubular and reticular mitoch

123 Using Drosophila motor neurons, we show that parkin disruption generates an abnormal mitochondrial ne

124 First, we confirmed that PARKIN does not require an E2 enzyme for substrate ubiqu

125 d as a Parkin substrate and its turnover was Parkin-dose and proteasome-dependent.

126 Parkin downregulation in breast cancer cells promotes me

127 f mitochondria-derived cargos independent of Parkin, Drp1, and autophagy.

128 njugating enzyme UbcH7 binding to Parkin and Parkin E3 ligase activity suggest that Parkin phosphoryl

129 hPINK1 activates Parkin E3 ligase activity, involving phosphorylation of

130 tin ligase Parkin and ubiquitin to stimulate Parkin E3 ligase activity.

131 The E3 ubiquitin ligase PARKIN (encoded by PARK2) and the protein kinase PINK1 (

132 RNAseq analysis revealed the PARKIN-encoding locus as a prime THAP11 target, and THAP

133 l content and mitochondrial translocation of Parkin, essential in mitophagy.

134 In this protocol, we explain how to generate Parkin-expressing, mitochondria-depleted cells from scra

135 Importantly, Parkin expression is inversely correlated with HIF-1alph

136 aces further emphasis on the significance of Parkin for the maintenance of mitochondrial function in

137 mitochondrial alterations caused by reduced Parkin function in these cells.

138 We showed that loss of Parkin function led to decreased endosomal tubulation an

139 However, it is not clear how Parkin functions in mitochondrial turnover in vivo, or w

140 This study identifies that Parkin functions to blunt excessive CHOP to prevent mala

141 Mutations in the Parkin gene (PARK2) have been linked to a recessive form

142 own-regulating expression of either Pink1 or Parkin genes ameliorated FUS-induced neurodegeneration p

143 own link between FUS proteinopathy and PINK1/Parkin genes, providing new insights into the pathogenes

144 To study whether Parkin has a role in vivo in the context of mitochondria

145 Parkin has also been implicated in mitosis through mecha

146 Parkin has been proposed to police mitochondrial fidelit

147 Parkin has been shown to participate in mitochondrial tu

148 In vivo, Parkin has significant protective effects on the surviva

149 Mutations in E3 ubiquitin ligase Parkin have been linked to familial Parkinson's disease.

150 ctions between some PD genes, like PINK1 and parkin, have been identified, but whether other ones int

151 text of mitochondrial damage, we knocked out Parkin in a mouse model in which the mitochondrial DNA i

152 ely assess the activity of the RBR E3 ligase PARKIN in a simple experimental setup and in real time u

153 n ligase Parkin, we investigated the role of Parkin in cardiac ER stress.

154 t the crystal structure of Pediculus humanus PARKIN in complex with Ser65-phosphorylated ubiquitin (p

155 s demonstrate a novel and essential role for Parkin in glutamatergic neurotransmission, as a stabiliz

156 The role of Parkin in hearts is unclear.

157 escribe the 1.8 A crystal structure of human parkin in its fully inhibited state and identify the key

158 s system, we investigated the involvement of Parkin in mitochondrial dynamics, distribution, morpholo

159 These findings establish a role for Parkin in regulating the endo-lysosomal pathway and retr

160 These findings demonstrate a novel role for Parkin in synaptic AMPA receptor internalization and sug

161 rial quality control in vivo by knocking out Parkin in the PD-mito-PstI mouse (males), where the mito

162 While several studies implicated Parkin in the regulation of mitophagy and proteasomal de

163 and uncover a collaboration between MUL1 and PARKIN in this process.

164 ur results reveal an important mechanism for Parkin in tumor suppression and HIF-1alpha regulation.

165 Combining p-S65-UB and p-S65-PARKIN in vitro showed accelerated transfer of nonphosph

166 se results shed new light on the function of Parkin in vivo.

167 rtical neurons, co-expressing PGC-1alpha and Parkin increases the number of mitochondria, enhances ma

168 s and is also implicated in PINK1-driven and Parkin-independent mitophagy.

169 PHB2 is required for Parkin-induced mitophagy in mammalian cells and for the

170 and identify the key interfaces to maintain parkin inhibition.

171 teasomal ubiquitin receptor Rpn13/ADRM1 as a parkin-interacting protein.

172 Parkin interacts with HIF-1alpha and promotes HIF-1alpha

173 on endogenous proteins, we demonstrate that Parkin interacts with mitochondrial Stomatin-like protei

174 Accumulating evidence suggests that Parkin is a tumor suppressor, but the underlying mechani

175 Here we show that Parkin is an E3 ubiquitin ligase for hypoxia-inducible f

176 Parkin is associated with autosomal recessive early-onse

177 Additionally, Parkin is identified as a novel post-translational regul

178 Native parkin is inactive and exists in an autoinhibited state

179 Moreover, endogenous PINK1 or parkin is indispensable for the proper autophagic remova

180 ation group C (FANCC) protein interacts with Parkin, is required in vitro and in vivo for clearance o

181 elerated transfer of nonphosphorylated UB to PARKIN itself, its substrate mitochondrial Rho GTPase (M

182 I is required and serves as both a PINK1 and Parkin kinase.

183 e, we found that mitophagy still occurred in Parkin knock-out (KO) mice after APAP treatment based on

184 induced cell death when CHOP was depleted in Parkin knockdown cardiomyocytes.

185 diates the prodeath actions of Trib3 in that Parkin knockdown in cellular PD models abolishes the pro

186 artially restore mitophagy in the setting of PARKIN knockdown, suggesting redundancy in their ubiquit

187 However, Parkin knockout (KO) mice do not display signs of neurod

188 Parkin knockout mice exposed to aortic constriction-indu

189 Underlying the Parkin knockout rescue was suppression of Drp1-induced h

190 Mechanistically, we found that Parkin KO mice had decreased activated c-Jun N-terminal

191 nalysis for some mitochondrial proteins, and Parkin KO mice were protected against APAP-induced liver

192 tivation upregulated PINK1 and downregulated Parkin levels.

193 ontribute to the development of pathology in Parkin-linked Parkinson's disease.

194 Parkin loss caused mitochondrial dysfunction and affecte

195 Parkin loss of function has also been shown to alter hip

196 Accordingly, Parkin loss of function leads to the reduced density of

197 mechanism leading to neurodegeneration upon Parkin loss of function remains incompletely understood.

198 ions, providing one possible explanation why Parkin may be a tumor suppressor gene.

199 vealed that these proteins partly facilitate Parkin-mediated mitochondrial clearance.

200 PINK1/Parkin-mediated mitochondrial quality control (MQC) requ

201 mpairs the protective functions of the PINK1/parkin-mediated mitochondrial quality control.

202 cardiomyocyte mitochondria undergo perinatal Parkin-mediated mitophagy and replacement by mature adul

203 Here, we found that PINK1-Mfn2-Parkin-mediated mitophagy directs this metabolic transfo

204 Parkin-mediated mitophagy is reportedly either irrelevan

205 hondrial unfolded protein response and PINK1-Parkin-mediated mitophagy to mitigate proteotoxicity.

206 impair parkin recruitment to mitochondria or parkin-mediated mitophagy upon carbonyl cyanide m-chloro

207 for mitochondria-associated degradation and Parkin-mediated mitophagy.

208 in, are the primary receptors for PINK1- and parkin-mediated mitophagy.

209 ial stress and motility before activation of Parkin-mediated mitophagy.

210 Although the mechanism by which Parkin mediates mitophagy in a PINK1-dependent manner is

211 This review focuses on non-Parkin members such as HOIP/HOIL-1L (the only E3s known

212 irement of ATP for elevated PINK1 levels and Parkin mitochondrial recruitment, local or individual mi

213 ily members as primary contributors to PINK1/Parkin mitophagy and starvation autophagy.

214 cusing on the PTEN-induced putative kinase 1-Parkin mitophagy pathway.

215 In this study, we found that Parkin modulates the endocytic pathway through the regul

216 ophagy pathway is required for the rescue of parkin mutant defects by mask loss of function.

217 Isogenic Parkin mutant iPSC-derived cardiomyocytes showed exagger

218 l overexpression of SLP-2 transgenes rescued parkin mutant phenotypes, in particular loss of dopamine

219 of Drosophila Clu complements PINK1, but not parkin, mutant muscles.

220 oteasome system, whereas clinically relevant parkin mutants fail to do so.

221 d pluripotent stem cell-derived neurons from Parkin mutation carriers, showed decreased complex I act

222 ta suggest that, in the case of at least one parkin mutation, Q311X, detrimental effects are due to i

223 ical and cellular defects caused by pink1 or parkin mutations in a cell-autonomous manner.

224 lpha mutation and specific cancer-associated Parkin mutations largely abolish the functions of Parkin

225 autosomal recessive parkinsonism, PINK1 and Parkin, normally work together in the same pathway to go

226 Mfn2 protein, a key ubiquitylation target of Parkin on mitochondria.

227 We studied the role of Parkin on mitochondrial quality control in vivo by knock

228 h ubiquitin and the ubiquitin-like domain of Parkin on structurally protected Ser65 residues, trigger

229 We show that PINK1 recruits Parkin onto mitochondrial subdomains after actinonin-ind

230 els are elevated on acute down-regulation of parkin or in PARK2 KO rat striatum.

231 SH-SY5Y cells with a stable knockdown of Parkin or SLP-2, as well as induced pluripotent stem cel

232 ins, accompanied with depletion of cytosolic Parkin over disease progression.

233 ly, alpha-synuclein inactivation phenocopies parkin overexpression and suppresses stress-induced mito

234 is also promoted by two other PD-lined genes parkin (PARK2) and PINK1 (PARK6).

235 ant brains had elevated auxilin (PARK19) and parkin (PARK2) levels.

236 Mutations in PARKIN (PARK2), an ubiquitin ligase, cause early onset P

237 r the genes encoding the E3 ubiquitin ligase Parkin (PARK2, also known as PRKN) and its upstream prot

238 Finally, down-regulating PINK1 or Parkin partially rescued the locomotive defects and enha

239 The PTEN-induced putative kinase 1 (PINK1)/Parkin pathway can tag damaged mitochondria and trigger

240 However, the role of the PINK1/Parkin pathway in mitochondrial turnover is unclear in t

241 lation of autophagy, activation of the PINK1/parkin pathway or decreased levels of mitofusin result i

242 ver, it is unknown whether and how the PINK1/Parkin pathway regulates the mitochondrial life cycle in

243 n and Parkin E3 ligase activity suggest that Parkin phosphorylation regulates E3 ligase activity down

244 agement of the Ubl from RING1 and subsequent Parkin phosphorylation.

245 The convergence of parkin, PINK1, and alpha-synuclein on mitochondrial dyna

246 OS may act as a trigger for the induction of Parkin/PINK1-dependent mitophagy.

247 Our data indicate that PINK1 and Parkin play an important role in FUS-induced neurodegene

248 that the C-terminal GTPase (cGTPase) of the Parkin primary substrate human Miro is necessary and suf

249 The lack of Parkin promoted earlier onset of dopaminergic neurodegen

250 Mutations in PARK2 (parkin), which encodes Parkin protein, an E3 ubiquitin ligase, are associated w

251 drial proteotoxicity and that PINK1 recruits Parkin proximal to focal misfolded aggregates of the mit

252 Taken in total, our data suggest that the parkin Q311X mutation impacts on mitochondrial quality c

253 NAT1 R64W and Parkin R42P are naturally occurring misfolded variants o

254 Parkin R42P full length protein is trafficked poorly to

255 We also find that artificially directing Parkin R42P to ER by fusion with the Sec61beta ER-direct

256 However, the mechanisms by which Parkin recognizes specific proteins for modification rem

257 Parkin reconstitution rescued this phenotype and the con

258 hosphoUb), revealing the molecular basis for PARKIN recruitment and activation.

259 s expansion of Tie2(+) HSCs through enhanced Parkin recruitment in mitochondria.

260 Although Miro S156E promoted Parkin recruitment it was insufficient to trigger mitoph

261 damage via photoirradiation does not affect Parkin recruitment to damaged mitochondria as long as a

262 In contrast, silencing Rpn13 did not impair parkin recruitment to mitochondria or parkin-mediated mi

263 These phosphorylation events lead to PARKIN recruitment to mitochondria, and activation by an

264 inhibited PINK1-induced Miro ubiquitination, Parkin recruitment, and Parkin-dependent mitochondrial a

265 way in Parkin-deficient cells, we found that Parkin regulates the levels and activity of Rab7 by prom

266 substantia nigra of PD patients, and loss of Parkin results in the reduction of complex I activity sh

267 Here, we investigate Parkin's role at glutamatergic synapses of rat hippocamp

268 However, very little is known about Parkin's specific sites or mechanisms of action at gluta

269 de a structural picture of the unraveling of parkin's ubiquitin ligase potential.

270 PINK1 phosphorylation of serine 65 in parkin's UBL and serine 65 of ubiquitin fully activate u

271 CHOP was identified as a Parkin substrate and its turnover was Parkin-dose and pr

272 We also provide evidence that Parkin substrate recognition is functionally separate fr

273 down of the mitophagy-related genes Pink1 or Parkin suppresses the age-related loss of tissue homeost

274 Specifically, PARKIN-synthesized ubiquitin chains represent targets fo

275 as the autophagy signal on mitochondria, and parkin then acts to amplify this signal.

276 vates recruitment of the ubiquitin E3 ligase Parkin to damaged mitochondria.

277 s exhibit increased recruitment of cytosolic Parkin to depolarized mitochondria.

278 ad, loss of Drp1 enhances the recruitment of Parkin to fused mitochondrial networks and the rate of m

279 ulates on damaged mitochondria and activates Parkin to induce mitophagy.

280 of Parkinson's disease (PD)-linked PINK1 and Parkin to Miro by showing that a third PD-related protei

281 tein quantity of PINK1 in the recruitment of Parkin to mitochondria.

282 found to interact genetically with PINK1 and parkin to regulate mitochondrial clustering in germ cell

283 r, these findings implicate Rpn13 in linking parkin to the 26 S proteasome and regulating the clearan

284 ro ubiquitination and degradation, recruited Parkin to the mitochondria, and via Parkin arrested axon

285 n mutations largely abolish the functions of Parkin to ubiquitinate HIF-1alpha and inhibit cancer met

286 nhibited the ROS upsurge and PINK1-dependent Parkin translocation to mitochondria in response to carb

287 ge-dependent anion channel 1 (VDAC1) induced Parkin translocation to mitochondria, presumably by stim

288 protein level of PINK1 was not necessary for Parkin translocation to mitochondria.

289 volving phosphorylation of ubiquitin and the Parkin ubiquitin-like (Ubl) domain via as yet poorly und

290 phosphorylates polyubiquitin as well as the PARKIN ubiquitin-like (Ubl) domain.

291 Then, Parkin ubiquitinates outer mitochondrial membrane protei

292 In cellular models, parkin ubiquitinates STEP61 and thereby regulates its le

293 Loss of clu leads to the recruitment of Parkin, VCP/p97, p62/Ref(2)P and Atg8a to depolarized sw

294 wnstream target of the E3 ligase activity of Parkin, was also increased in cells overexpressing FUS p

295 attempt to further elucidate the function of parkin, we have identified the proteasomal ubiquitin rec

296 ignaling upregulates the E3-ubiquitin ligase Parkin, we investigated the role of Parkin in cardiac ER

297 The protein levels of PINK1 and Parkin were elevated in cells overexpressing FUS.

298 Mutations in PARK2 (parkin), which encodes Parkin protein, an E3 ubiquitin l

299 s ubiquitin to activate the ubiquitin ligase parkin, which builds ubiquitin chains on mitochondrial o

300 tein kinase PINK1 or the E3 ubiquitin ligase Parkin, which function together to eliminate damaged mit

301 of Miro on S156 promoted the interaction of Parkin with Miro, stimulated Miro ubiquitination and deg