The Centrosomal E3 Ubiquitin Ligase FBXO31-SCF Regulates Neuronal Morphogenesis and Migration

Vadhvani, Mayur; Schwedhelm-Domeyer, Nicola; Mukherjee, C. D.; Stegmüller, Judith

doi:10.1371/journal.pone.0057530

Cited by 45 publications

(52 citation statements)

References 51 publications

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“…The proteasome, itself, may be a target of oxidative stress [109, 110], and once sufficiently damaged its function is impaired [110]. Generally, this is detrimental to neuronal function as the proteasome is responsible for several aspects of synaptic function, such as spinogenesis [111], presynaptic neurotransmission [112], long-term potentiation [113], synaptic scaling [114], apical dendrite outgrowth/polarization [115, 116], dendritic arborization [117], and synapse formation/elimination [118]. Animals that live with chronic oxidative stress are likely to have evolved mechanisms to protect and maintain proteasome function.…”

Section: Lessons From Hypoxia-tolerant Animalsmentioning

confidence: 99%

Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates

Garbarino¹,

Orr

Rodriguez³

et al. 2015

Archives of Biochemistry and Biophysics

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The Oxidative Stress Theory of Aging has had tremendous impact in research involving aging and age-associated diseases including those that affect the nervous system. With over half a century of accrued data showing both strong support for and against this theory, there is a need to critically evaluate the data acquired from common biomedical research models, and to also diversify the species used in studies involving this proximate theory. One approach is to follow Orgel’s second axiom that “evolution is smarter than we are” and judiciously choose species that may have evolved to live with chronic or seasonal oxidative stressors. Vertebrates that have naturally evolved to live under extreme conditions (e.g., anoxia or hypoxia), as well as those that undergo daily or seasonal torpor encounter both decreased oxygen availability and subsequent reoxygenation, with concomitant increased oxidative stress. Due to its high metabolic activity, the brain may be particularly vulnerable to oxidative stress. Here, we focus on oxidative stress responses in the brains of certain mouse models as well as extremophilic vertebrates. Exploring the naturally evolved biological tools utilized to cope with seasonal or environmentally variable oxygen availability may yield key information pertinent for how to deal with oxidative stress and thereby mitigate its propagation of age-associated diseases.

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Section: Lessons From Hypoxia-tolerant Animalsmentioning

confidence: 99%

Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates

Garbarino¹,

Orr

Rodriguez³

et al. 2015

Archives of Biochemistry and Biophysics

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“…In the nervous system, the UPS regulates several aspects of synaptic function, such as spinogenesis (Hamilton et al, 2012), presynaptic neurotransmission (Willeumier et al, 2006;Jiang et al, 2010), long-term potentiation (Dong et al, 2008;Cajigas et al, 2010;Pavlopoulos et al, 2011), synaptic scaling , apical dendrite outgrowth/ polarization (Hamilton and Zito, 2013;Miao et al, 2013;Vadhvani et al, 2013), dendritic arborization (Puram et al, 2013), axon growth (Yang et al, 2013), and synapse formation and elimination (Yi and Ehlers, 2007).…”

Section: Role Of Ups In Nervous Systemmentioning

confidence: 99%

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

Caldeira

Salazar

Curcio

et al. 2014

Progress in Neurobiology

110

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A B S T R A C TThe ubiquitin-proteasome system (UPS) is a catalytic machinery that targets numerous cellular proteins for degradation, thus being essential to control a wide range of basic cellular processes and cell survival. Degradation of intracellular proteins via the UPS is a tightly regulated process initiated by tagging a target protein with a specific ubiquitin chain. Neurons are particularly vulnerable to any change in protein composition, and therefore the UPS is a key regulator of neuronal physiology. Alterations in UPS activity may induce pathological responses, ultimately leading to neuronal cell death. Brain ischemia triggers a complex series of biochemical and molecular mechanisms, such as an inflammatory response, an exacerbated production of misfolded and oxidized proteins, due to oxidative stress, and the breakdown of cellular integrity mainly mediated by excitotoxic glutamatergic signaling. Brain ischemia also damages protein degradation pathways which, together with the overproduction of damaged proteins and consequent upregulation of ubiquitin-conjugated proteins, contribute to the accumulation of ubiquitincontaining proteinaceous deposits. Despite recent advances, the factors leading to deposition of such aggregates after cerebral ischemic injury remain poorly understood. This review discusses the current knowledge on the role of the UPS in brain function and the molecular mechanisms contributing to UPS dysfunction in brain ischemia with consequent accumulation of ubiquitin-containing proteins. Chemical inhibitors of the proteasome and small molecule inhibitors of deubiquitinating enzymes, which promote the degradation of proteins by the proteasome, were both shown to provide neuroprotection in brain ischemia, and this apparent contradiction is also discussed in this review. ß

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“…FBXO31 located in chromosome 16q24.3 and played a crucial role in multiple pathways such as neuronal development [12],DNA damage response [13,14]and tumorigenesis [13,15,16, 17]. FBXO31 was initially considered as a candidate tumor suppressor since decreased FBXO31 expression was found in breast cancer.…”

Section: Introductionmentioning

confidence: 99%

F-box protein FBXO31 is down-regulated in gastric cancer and negatively regulated by miR-17 and miR-20a

Zhang

Kong

et al. 2014

Oncotarget

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FBXO31, a subunit of the SCF ubiquitin ligase, played a crucial role in neuronal development, DNA damage response and tumorigenesis. Here, we investigated the expression and prognosis value of FBXO31 in human primary gastric cancer (GC) samples. Meanwhile, the biological role and the regulation mechanism of FBXO31 were evaluated. We found that FBXO31 mRNA and protein was decreased dramatically in the GC tissue compared with the adjacent non-cancerous tissues. FBXO31 expression was significantly associated with tumor size, tumor infiltration, clinical grade and patients' prognosis. FBXO31 overexpression significantly decreased colony formation and induced a G1-phase arrest and inhibited the expression of CyclinD1 protein in GC cells. Further evidence was obtained from knockdown of FBXO31. Ectopic expression of FBXO31 dramatically inhibited xenograft tumor growth in nude mice. miR-20a and miR-17 mimics inhibited, whereas the inhibitor of miR-20a and miR-17 increased, the expression of FBXO31, respectively. miR-20a and miR-17 directly bind to the 3'-UTR of FBXO31. The level of miR-20a and miR-17 in GC tissue was significantly higher than that in surrounding normal mucosa. Moreover, a highly significant negative correlation between miR-20a (miR-17) and FBXO31 was observed in these GC samples. Therefore, effective therapy targeting the miR-20a (miR-17)-FBXO31-CyclinD1 pathway may help control GC progression.

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The Centrosomal E3 Ubiquitin Ligase FBXO31-SCF Regulates Neuronal Morphogenesis and Migration

Cited by 45 publications

References 51 publications

Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates

Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates

Role of the ubiquitin–proteasome system in brain ischemia: Friend or foe?

F-box protein FBXO31 is down-regulated in gastric cancer and negatively regulated by miR-17 and miR-20a

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