Parkin Regulates Eg5 Expression by Hsp70 Ubiquitination-dependent Inactivation of c-Jun NH2-terminal Kinase

Liu, Min; Aneja, Ritu; Sun, Xiaodong; Xie, Songbo; Wang, Hongxia; Wu, Xiaojing; Dong, Jin‐Tang; Li, Minggang; Joshi, Harish C.; Zhou, Jun

doi:10.1074/jbc.m806860200

Cited by 36 publications

(30 citation statements)

References 26 publications

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“…For example, one report describes regulation of Kinesin-5 expression via ubiquitination. The E3 ubiquitin ligase, Parkin, indirectly down-regulated Kinesin-5 gene transcription (Liu et al, 2008a). By blocking the binding of c-Jun NH 2 -terminal kinase to the Kinesin-5 AP1 (activator protein 1) site in its promoter, Parkin could regulate the level of mitotic Kinesin-5 in HEK293 cells (Liu et al, 2008a).…”

Section: Cellular Functions Of Kinesin-5mentioning

confidence: 99%

Kinesin-5: Cross-bridging mechanism to targeted clinical therapy

Wojcik

Buckley

Richard

et al. 2013

Gene

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Kinesin motor proteins comprise an ATPase superfamily that goes hand in hand with microtubules in every eukaryote. The mitotic kinesins, by virtue of their potential therapeutic role in cancerous cells, have been a major focus of research for the past 28 years since the discovery of the canonical Kinesin-1 heavy chain. Perhaps the simplest player in mitotic spindle assembly, Kinesin-5 (also known as Kif11, Eg5, or kinesin spindle protein, KSP) is a plus-end-directed motor localized to interpolar spindle microtubules and to the spindle poles. Comprised of a homotetramer complex, its function primarily is to slide anti-parallel microtubules apart from one another. Based on a multi-faceted analysis of this motor from numerous laboratories over the years, we have learned a great deal about the function of this motor at the atomic level for catalysis and as an integrated element of the cytoskeleton. These data have, in turn, informed the function of motile kinesins on the whole, as well as spearheaded integrative models of the mitotic apparatus in particular and regulation of the microtubule cytoskeleton in general. We review what is known about how this nanomotor works, its place inside the cytoskeleton of cells, and its small-molecule inhibitors that provide a toolbox for understanding motor function and for anticancer treatment in the clinic.

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Section: Cellular Functions Of Kinesin-5mentioning

confidence: 99%

Kinesin-5: Cross-bridging mechanism to targeted clinical therapy

Wojcik

Buckley

Richard

et al. 2013

Gene

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“…Parkin was also found to suppress JNK activation in the Drosophila eye during development by transcriptionally repressing basket (bsk), which is a gene encoding for JNK (48). In addition, Parkin was shown to suppress JNK activation in vitro in EPP85 human pancreatic carcinoma cells via monoubiquitination of heat-shock protein 70 (HSP70), but the exact mechanism for how mono-ubiquitinated HSP70 inhibits activation of JNK is unknown (50). Furthermore, Parkin was shown to inhibit JNK activity in COS1 monkey kidney fibroblasts (49).…”

Section: Jnk Activation Was Differentially Regulated In Parkin Ko Andmentioning

confidence: 99%

Chronic Deletion and Acute Knockdown of Parkin Have Differential Responses to Acetaminophen-induced Mitophagy and Liver Injury in Mice

Williams

Haynes

et al. 2015

Journal of Biological Chemistry

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Background: Parkin is required for mitophagy in cultured cells, but its role in liver injury is not known. Results: APAP-induced mitophagy was impaired in acute Parkin knockdown mouse livers but not whole body Parkin knock-out mice. Conclusion: Chronic, but not acute, loss of Parkin protects against APAP-induced liver injury by multiple mechanisms independent of mitophagy. Significance: This study revealed a novel role of Parkin in APAP-induced liver injury.

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“…To this end, several themes regarding DJ-1 have now emerged that link this protein to neurodegeneration, PD, and oxidative stress. These themes include, but are not limited to the following: (i) DJ-1 protects neurons against oxidative stress (4,9,11,(41)(42)(43)(44); (ii) Loss of DJ-1 on its own does not lead to dopamine neuron death, at least in mice, but DJ-1-deficient animals are sensitized to environmental stress and exhibit impaired dopamine signaling (45)(46)(47)(48); and (iii) DJ-1 modulates signaling pathways critical to cell survival such as PTEN and AKT, at least in select nonneuronal contexts (31).…”

Section: Dj-1 Modulates Akt Translocation To Membranous Fractionsmentioning

confidence: 99%

DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway

Aleyasin

Rousseaux

Marcogliese

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

151

118

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Loss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H 2 O 2 in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover, we show that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.neurodegeneration | Parkinson disease | reactive oxygen species

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Parkin Regulates Eg5 Expression by Hsp70 Ubiquitination-dependent Inactivation of c-Jun NH2-terminal Kinase

Cited by 36 publications

References 26 publications

Kinesin-5: Cross-bridging mechanism to targeted clinical therapy

Kinesin-5: Cross-bridging mechanism to targeted clinical therapy

Chronic Deletion and Acute Knockdown of Parkin Have Differential Responses to Acetaminophen-induced Mitophagy and Liver Injury in Mice

DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway

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