Microtubule-associated protein light chain 3 regulates Cdc42-dependent actin ring formation in osteoclast

Chung, Yeon‐Ho; Yoon, Seung-Yong; Choi, Bok Kyoung; Sohn, Dong Hyun; Yoon, Kwang-Ho; Kim, Wan-Jong; Kim, Dong-Hou; Chang, Eun‐Ju

doi:10.1016/j.biocel.2012.03.007

Cited by 64 publications

(55 citation statements)

References 25 publications

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“…Autophagy proteins, such as LC3 and Atg5, have been shown to be important factors for generating the osteoclast ruffled border [46]. However, previous findings have indicated that autophagy proteins such as LC3 and beclin-1 may be involved in osteoclast formation and function via non-autophagic pathways [47,48]. In our study, autophagosome/ autolysosome formation and autophagic marker LC3 were observed.…”

Section: Discussioncontrasting

confidence: 57%

Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Shi

Wang

Zhang

et al. 2015

Bone

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Section: Discussioncontrasting

confidence: 57%

Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Shi

Wang

Zhang

et al. 2015

Bone

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“…In contrast to other RNA viruses such as coronaviruses and equine arteritis virus that require non-lipidated LC3 to anchor replication complexes to ER membranes [29], [38], RV, which does not need ER-derived membranes for genome replication, requires Atg7 indicating a role for the lipidated form of LC3 in virus morphogenesis. Interestingly, an autophagy-independent role for lipidated LC3 has been recently described in microtubule dynamics [39]. It is therefore possible that the microtubule network might be involved in an LC3-dependent localization of viral proteins participating in the final stages of virus morphogenesis (such as NSP4 and VP7), also considering that such network has been already shown to participate in the dynamics of RV viroplasms [40].…”

Section: Discussionmentioning

confidence: 93%

Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation

et al. 2014

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Replication of many RNA viruses benefits from subversion of the autophagic pathway through many different mechanisms. Rotavirus, the main etiologic agent of pediatric gastroenteritis worldwide, has been recently described to induce accumulation of autophagosomes as a mean for targeting viral proteins to the sites of viral replication. Here we show that the viral-induced increase of the lipidated form of LC3 does not correlate with an augmented formation of autophagosomes, as detected by immunofluorescence and electron microscopy. The LC3-II accumulation was found to be dependent on active rotavirus replication through the use of antigenically intact inactivated viral particles and of siRNAs targeting viral genes that are essential for viral replication. Silencing expression of LC3 or of Atg7, a protein involved in LC3 lipidation, resulted in a significant impairment of viral titers, indicating that these elements of the autophagic pathway are required at late stages of the viral cycle.

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“…A similar increase in RhoA has been reported in SHSY-5Y cells by Petratos et al (2008), supporting our assumption that the simultaneous abundance of Aβ, AICD and Grb2 in and around these cells could be a true reflection of an AD-like condition. Elevation of Cdc42 activity is justified as it is known to be agonistically regulated with autophagy by phosphatidylethanolamine-conjugated LC3 proteins (LC3II) (Chung et al, 2012), and our group has previously demonstrated autophagy induction in a similar context (Roy et al, 2014). Considering that Rac1 activity decreases significantly in our model, the expression of PAK1, the downstream effector of both Cdc42 and Rac1, relies on the fine balance of the activities of both.…”

Section: Discussionmentioning

confidence: 99%

Cellular levels of growth factor receptor bound protein 2 (Grb2) and cytoskeleton stability are correlated in a neurodegenerative scenario

Majumder

Roy

Singh

et al. 2017

Disease Models &Amp; Mechanisms

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Alzheimer's disease (AD) manifests as neuronal loss. On the premise of Grb2 overexpression in AD mouse brain and brain tissues of AD patients, our study primarily focuses on the stability of cytoskeletal proteins in the context of degenerative AD-like conditions. Two predominant molecular features of AD, extracellular accumulation of β-amyloid oligomers and intracellular elevation of amyloid precursor protein intracellular domain levels, have been used to closely inspect the series of signalling events. In their presence, multiple signalling pathways involving ROCK and PAK1 proteins lead to disassembly of the cytoskeleton, and Grb2 partially counterbalances the cytoskeletal loss. Increased Grb2-NOX4 interactions play a preventive role against cytoskeletal disassembly, in turn blocking the activity of nitrogen oxides and decreasing the expression of slingshot homolog 1 (SSH-1) protein, a potent inducer of cytoskeleton disassembly. This study unravels a unique role of Grb2 in protecting the cytoskeletal architecture in AD-like conditions and presents a potential new strategy for controlling neurodegeneration.

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Microtubule-associated protein light chain 3 regulates Cdc42-dependent actin ring formation in osteoclast

Cited by 64 publications

References 25 publications

Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Rotavirus Increases Levels of Lipidated LC3 Supporting Accumulation of Infectious Progeny Virus without Inducing Autophagosome Formation

Cellular levels of growth factor receptor bound protein 2 (Grb2) and cytoskeleton stability are correlated in a neurodegenerative scenario

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