Vidur Sabharwal

ORCID: 0000-0001-5070-985X
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Genetics, Aging, and Longevity in Model Organisms
  • Mitochondrial Function and Pathology
  • Microtubule and mitosis dynamics
  • Photosynthetic Processes and Mechanisms
  • Cellular Mechanics and Interactions
  • Cellular transport and secretion
  • ATP Synthase and ATPases Research
  • Endoplasmic Reticulum Stress and Disease
  • Neurogenesis and neuroplasticity mechanisms
  • Planarian Biology and Electrostimulation
  • Nuclear and radioactivity studies
  • COVID-19 epidemiological studies
  • Hippo pathway signaling and YAP/TAZ
  • Bone health and treatments
  • Machine Learning in Bioinformatics
  • Bone Metabolism and Diseases

Tata Institute of Fundamental Research
2017-2024

Karolinska Institutet
2024

University of Toronto
2001

Significance In many organisms axonal fragments can rejoin by self-fusion after neuronal injury. It is hypothesized that cell fusion would be an efficient way to repair functional loss this study, we tested hypothesis using the Caenorhabditis elegans sensory neurons are responsible for gentle touch sensation. We found between proximal and distal of injured posterior neuron (the lateral microtubule) promotes recovery in age-dependent manner. also discovered let-7 miRNA inhibits restoration...

10.1073/pnas.1704372114 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2017-11-06

Abstract We investigate the role of axonal transport in regulating neuronal mitochondrial density. show that density mitochondria touch receptor neuron (TRN) adult Caenorhabditis elegans is constant. Mitochondrial and are controlled both by Kinesin heavy chain Dynein-Dynactin complex. However, unlike other models, presence C . TRNs depends on a light as well. Mutants three miro genes do not alter TRNs. Kinesin-1 associated proteins, UNC-16/JIP3 UNC-76/FEZ1, increased also have elevated...

10.1038/s41598-018-27211-9 article EN cc-by Scientific Reports 2018-06-06

Axonal transport in neurons is essential for cargo movement between the cell body and synapses. Caenorhabditis elegans UNC-104 its homolog KIF1A are kinesin-3 motors that anterogradely precursors of synaptic vesicles (pre-SVs) degraded at However, C. elegans, touch neuron-specific knockdown E1 ubiquitin-activating enzyme, uba-1, leads to accumulation neuronal ends Here, we performed an RNAi screen identified depletion fbxb-65, which encodes F-box protein, distal ends, alters net anterograde...

10.1242/jcs.261553 article EN publisher-specific-oa Journal of Cell Science 2024-03-13

Abstract Neuronal regeneration after injury depends on the intrinsic growth potential of neurons. Our study shows that UNC-16, a Caenorhabditis elegans JIP3 homolog, inhibits axonal by regulating initiation and rate regrowth. This occurs through inhibition regeneration-promoting activity long isoform DLK-1 independently inhibitory short DLK-1. We show UNC-16 promotes punctate localization in concentration-dependent manner limiting availability at cut site, minutes injury. negatively...

10.1093/genetics/iyab139 article EN Genetics 2021-08-28

ABSTRACT First Person is a series of interviews with the first authors selection papers published in Journal Cell Science, helping researchers promote themselves alongside their papers. Vidur Sabharwal author on ‘ F-box protein FBXB-65 regulates anterograde transport kinesin-3 motor UNC-104 through PTM near its cargo-binding PH domain’, JCS. conducted research described this article while PhD student Sandhya P. Koushika's lab at Tata Institute Fundamental Research, Mumbai, India. He now...

10.1242/jcs.262138 article EN other-oa Journal of Cell Science 2024-04-01

Cargo distribution within eukaryotic cells relies on the active transport mechanisms driven by molecular motors. Despite their critical role, intricate relationship between motor properties and cargo binding - its impact remains inadequately understood. Additionally, improper regulation of ubiquitination, a pivotal post-translational modification that affects protein degradation, activation, localization, is associated with several neurodegenerative diseases. Recent data showed...

10.48550/arxiv.2409.02655 preprint EN arXiv (Cornell University) 2024-09-04

Abstract Axonal transport is essential for cargo movement between the neuronal cell body and synapses. UNC-104/KIF1A, a Kinesin-3 motor in C. elegans that anterogradely transports precursors of synaptic vesicles (pre-SVs), known to be degraded at synapses through ubiquitin pathway. Knockdown E1 ubiquitin-activating enzyme, uba-1 , leads increased accumulation UNC-104 ends touch receptor neurons (TRNs). Loss F-box protein FBXB-65, putative E3 ligase, distal neurons, alters net anterograde...

10.1101/2023.08.13.553108 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-08-15

Abstract Neuronal regeneration after injury depends on the intrinsic growth potential of neurons. UNC-16, a C. elegans JIP3 homologue, inhibits axonal by regulating regrowth initiation and rate regrowth. UNC-16/JIP3 promoting activity DLK-1 long but acts additively to independently inhibitory short isoform. promotes punctate localization in concentration dependent manner limiting availability at cut site minutes injury. UNC-16 negatively regulates actin dynamics microtubule independent...

10.1101/484683 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-12-02

Abstract We investigate the role of axonal transport in regulating neuronal mitochondrial density. show that density mitochondria touch receptor neuron (TRN) adult Caenorhabditis elegans is constant. Mitochondrial and are controlled both by Kinesin heavy chain Dynein-Dynactin complex. However, unlike other models, presence C. TRNs depends on light as well. Mutants three miro genes do not alter TRNs. Kinesin-1 associated proteins, UNC-16/JIP3 UNC-76/FEZ1, increased also have elevated levels...

10.1101/279372 preprint EN cc-by-nd bioRxiv (Cold Spring Harbor Laboratory) 2018-03-26

10.17504/protocols.io.zn4f5gw preprint EN 2019-04-01
Coming Soon ...