Publications by authors named "Rupsha Mondal"
Article Synopsis
- The exposure of the protein PHB2 during the process of mitophagy is regulated by the ubiquitin-proteasome system and is linked to mitochondrial depolarization.
- Research found that the interaction between VDAC1 (a voltage-dependent channel) and PHB2 increases during mitochondrial stress, facilitating the exposure of PHB2.
- The study indicates that VDAC1 plays a critical role in optimizing PHB2 exposure at mitochondrial rupture sites, which could have implications for understanding neurodegenerative diseases.
Parkinson's disease (PD) is one of the most prevalent age-related neurodegenerative disorders. Behavioral complexities worsen over time due to progressive dopaminergic (DArgic) neuronal loss at substantia nigra region of brain. Available treatments typically aim to increase dopamine (DA) levels at striatum.
View Article and Find Full Text PDFBackground: Parkinson's disease (PD), a highly prevalent neuro-motor disorder is caused due to progressive loss of dopaminergic (DAergic) neurons at substantia nigra region of brain. This leads to depleted dopamine (DA) content at striatum, thus affecting the fine tuning of basal ganglia. In patients, this imbalance is manifested by akinesia, catalepsy and tremor.
View Article and Find Full Text PDFIn the recent past, many of the deubiquitinases (DUB) were found to modulate mitochondrial clearance or mitophagy and thus they are currently projected as therapeutic targets against neurodegeneration. Among these DUBs, USP14 stands at a distinctive juncture, since it can influence both proteasome complex activity and autophagy process. USP14 interference can enhance mitochondrial clearance and thus can protect Parkinsonian phenotypes in model.
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