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Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury | Molecular Biology Reports
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The ubiquitin-proteasome system (UPS) plays a pivotal role in regulating protein homeostasis and cellular processes, including protein degradation, trafficking, DNA repair, and cell signaling. During cerebral ischemia, ischemic conditions profoundly disrupt UPS activity, leading to proteasomal dysfunction and the accumulation of abnormal proteins. This imbalance contributes to neuronal injury and cell death observed in ischemic stroke. The UPS is intricately linked to various signaling pathways crucial for neuronal survival, inflammation, and cellular stress response, such as NF-κB, TRIM, TRIP, JAK-STAT, PI3K/Akt, and ERK1/2. Alterations in the ubiquitination process can significantly impact the activation and regulation of these pathways, exacerbating ischemic brain injury. Therapeutic approaches targeting the UPS in cerebral ischemia aim to rebalance protein levels, reduce proteotoxic stress, and mitigate neuronal injury. Strategies include proteasome inhibition, targeting specific ubiquitin ligases and deubiquitinating enzymes, and modulating ubiquitination-mediated regulation of key signaling pathways implicated in ischemia-induced pathophysiology. Therefore, the present review discusses the molecular mechanisms underlying UPS dysfunction in ischemic stroke is crucial for developing effective therapeutic interventions. Modulating ubiquitination-mediated pathways through therapeutic interventions targeting specific UPS components holds significant promise for mitigating ischemic brain injury and promoting neuroprotection and functional recovery in patients with cerebral ischemia.
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Keywords {🔍}
pubmed, article, google, scholar, cas, central, cell, cerebral, ischemic, httpsdoiorgs, mol, ischemia, stroke, injury, zhang, therapeutic, sci, chen, ubiquitin, wang, autophagy, signaling, liu, protein, pathway, biol, singh, regulation, mechanisms, role, death, brain, pathways, system, proteasome, disease, med, activation, target, mitochondrial, neuronal, res, neuroinflammation, inflammasome, molecular, int, apoptosis, ubiquitination, httpsdoiorg, mitophagy,
Topics {✒️}
peroxisome proliferator-activated receptor-gamma month download article/chapter wnt/beta-catenin signaling pathway p300/nf-κb/nlrp3 pathway mapk-activated protein kinases cerebral ischemia/reperfusion injury il-1β/il-18 processing inflammasome brain ischaemia/reperfusion injury hpv16 e6-expressing keratinocytes raav8-733-mediated gene transfer wnt/β-catenin signaling targeting nf-κb pathway reelin-dependent gsk3β inhibition wnt/β-catenin signalling creb-mediated dna hypermethylation astrocyte-mediated cerebral edema hypoxia-inducible factor-1β ubiquitin-proteasome proteolytic pathway k63-linked polyubiquitin regulates hypoxia-inducible factor-1α nf-κb signaling pathways e3 ligase chip modulating ubiquitination-mediated pathways full article pdf aggravating microglia-mediated neuroinflammation potential multi-drug target β-catenin destruction complex ubiquitination-mediated protein degradation ischemia-reperfusion injury parkin-mediated mitochondrial dysfunction hif-1α-dependent manner holds exclusive rights related subjects calcium-dependent neuronal death arumugam tv wnt-mediated biology mechanistic exploration modulating ubiquitination-mediated regulation blood-brain barrier function tgfβ-activated kinase 1 nuclear factor-kappa ischemia/reperfusion injuries cerebral ischemia injury ischemia-induced pathophysiology cerebral ischemic injury nf-κb pathway privacy choices/manage cookies post-translational modification article khanra jak-stat
Questions {❓}
- Caldeira MV, Salazar IL, Curcio M et al (2014) Role of the ubiquitin-proteasome system in brain ischemia: friend or foe?
- Caldeira MV, Salazar IL, Curcio M, Canzoniero LM, Duarte CB (2014) Role of the ubiquitin-proteasome system in brain ischemia: friend or foe?
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headline:Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury
description:The ubiquitin-proteasome system (UPS) plays a pivotal role in regulating protein homeostasis and cellular processes, including protein degradation, trafficking, DNA repair, and cell signaling. During cerebral ischemia, ischemic conditions profoundly disrupt UPS activity, leading to proteasomal dysfunction and the accumulation of abnormal proteins. This imbalance contributes to neuronal injury and cell death observed in ischemic stroke. The UPS is intricately linked to various signaling pathways crucial for neuronal survival, inflammation, and cellular stress response, such as NF-κB, TRIM, TRIP, JAK-STAT, PI3K/Akt, and ERK1/2. Alterations in the ubiquitination process can significantly impact the activation and regulation of these pathways, exacerbating ischemic brain injury. Therapeutic approaches targeting the UPS in cerebral ischemia aim to rebalance protein levels, reduce proteotoxic stress, and mitigate neuronal injury. Strategies include proteasome inhibition, targeting specific ubiquitin ligases and deubiquitinating enzymes, and modulating ubiquitination-mediated regulation of key signaling pathways implicated in ischemia-induced pathophysiology. Therefore, the present review discusses the molecular mechanisms underlying UPS dysfunction in ischemic stroke is crucial for developing effective therapeutic interventions. Modulating ubiquitination-mediated pathways through therapeutic interventions targeting specific UPS components holds significant promise for mitigating ischemic brain injury and promoting neuroprotection and functional recovery in patients with cerebral ischemia.
datePublished:2024-11-28T00:00:00Z
dateModified:2024-11-28T00:00:00Z
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Cerebral ischemia
Ubiquitin-proteasome system (UPS)
Proteasomal dysfunction
Signaling pathway modulation (NF-κB
TRIM
TRIP
JAK-STAT
PI3K/Akt
ERK1/2)
Neuroprotection
Animal Biochemistry
Animal Anatomy / Morphology / Histology
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headline:Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury
description:The ubiquitin-proteasome system (UPS) plays a pivotal role in regulating protein homeostasis and cellular processes, including protein degradation, trafficking, DNA repair, and cell signaling. During cerebral ischemia, ischemic conditions profoundly disrupt UPS activity, leading to proteasomal dysfunction and the accumulation of abnormal proteins. This imbalance contributes to neuronal injury and cell death observed in ischemic stroke. The UPS is intricately linked to various signaling pathways crucial for neuronal survival, inflammation, and cellular stress response, such as NF-κB, TRIM, TRIP, JAK-STAT, PI3K/Akt, and ERK1/2. Alterations in the ubiquitination process can significantly impact the activation and regulation of these pathways, exacerbating ischemic brain injury. Therapeutic approaches targeting the UPS in cerebral ischemia aim to rebalance protein levels, reduce proteotoxic stress, and mitigate neuronal injury. Strategies include proteasome inhibition, targeting specific ubiquitin ligases and deubiquitinating enzymes, and modulating ubiquitination-mediated regulation of key signaling pathways implicated in ischemia-induced pathophysiology. Therefore, the present review discusses the molecular mechanisms underlying UPS dysfunction in ischemic stroke is crucial for developing effective therapeutic interventions. Modulating ubiquitination-mediated pathways through therapeutic interventions targeting specific UPS components holds significant promise for mitigating ischemic brain injury and promoting neuroprotection and functional recovery in patients with cerebral ischemia.
datePublished:2024-11-28T00:00:00Z
dateModified:2024-11-28T00:00:00Z
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Cerebral ischemia
Ubiquitin-proteasome system (UPS)
Proteasomal dysfunction
Signaling pathway modulation (NF-κB
TRIM
TRIP
JAK-STAT
PI3K/Akt
ERK1/2)
Neuroprotection
Animal Biochemistry
Animal Anatomy / Morphology / Histology
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