Ashish Kumar

ORCID: 0000-0002-8018-0237
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About
Contact & Profiles
Research Areas
  • Endoplasmic Reticulum Stress and Disease
  • Ubiquitin and proteasome pathways
  • Prostate Cancer Diagnosis and Treatment
  • Mitochondrial Function and Pathology
  • Cancer Cells and Metastasis
  • Urologic and reproductive health conditions
  • Autophagy in Disease and Therapy
  • Cancer, Hypoxia, and Metabolism
  • Cancer Risks and Factors
  • Congenital heart defects research
  • Tissue Engineering and Regenerative Medicine
  • Therapeutic Uses of Natural Elements
  • Machine Learning in Bioinformatics
  • Genetics, Aging, and Longevity in Model Organisms
  • Congenital Diaphragmatic Hernia Studies
  • Proteoglycans and glycosaminoglycans research
  • PI3K/AKT/mTOR signaling in cancer
  • Medicinal Plants and Bioactive Compounds
  • Urological Disorders and Treatments
  • Microtubule and mitosis dynamics
  • Coenzyme Q10 studies and effects
  • Pancreatic function and diabetes
  • Hormonal and reproductive studies
  • ATP Synthase and ATPases Research
  • Kidney Stones and Urolithiasis Treatments

University of Helsinki
2020-2025

York Teaching Hospital NHS Foundation Trust
2024

Vellore Institute of Technology University
2023

National Institute of Immunology
2018

Wansbeck General Hospital
2011

Mitophagy, the selective degradation of mitochondria by autophagy, is crucial for maintenance healthy mitochondrial pool in cells. The critical event mitophagy translocation cytosolic Parkin, a ubiquitin ligase, to surface defective mitochondria. This study elucidates novel role SESN2/Sestrin2, stress inducible protein, PARK2/Parkin during mitophagy. data demonstrates that SESN2 downregulation inhibits BECN1/Beclin1 and Parkin interaction, thereby preventing optimum accumulation Parkin....

10.1038/s41598-017-19102-2 article EN cc-by Scientific Reports 2018-01-08

Differential utilization of metabolites and metabolic plasticity can confer adaptation to cancer cells under stress. Glutamine is one the vital versatile nutrients that consume avidly for their proliferation, therefore mechanisms related glutamine metabolism have been identified as targets. Recently, sestrin2 ( SESN2 ), a stress‐inducible protein, has reported regulate survival in glutamine‐depleted cells; based on this, we explored if could during glucose starvation. This report highlights...

10.1111/febs.14406 article EN FEBS Journal 2018-02-13

ABSTRACT Epithelial tissues undergo fetal-like cellular reprogramming to regenerate after damage 1,2 . Although the mesenchyme and extracellular matrix (ECM) play critical roles in tissue homeostasis regeneration 2–5 , their role repurposing developmental programs epithelium is unknown. To model epithelial regeneration, we culture intestinal on decellularized small scaffold (iECM), identify Asporin (Aspn), an ECM bound proteoglycan, as a mediator of reprogramming. Aspn produced by...

10.1101/2021.06.24.449590 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2021-06-25

Abstract Background: Obesity-related factors such as adipokines, insulin, insulin-like growth factors, and sex steroid hormones have been reported to be involved in breast carcinogenesis. Studies across the world suggest an important, but still controversial, role of obesity cancer risk. This study aims evaluate association obesity-related insulin resistance, with risk Indian population. Materials Methods: Anthropometric biochemical measurements were taken 60 newly diagnosed histologically...

10.4103/ijc.ijc_727_20 article EN cc-by-nc-sa Indian Journal of Cancer 2024-01-09

Paneth cell niche promotes the function of intestinal stem cells (ISCs) during reduced food intake, but how ISC activity can be boosted when availability resources is simultaneously remains unknown. Here, we show that increase in upon dietary restriction (DR) dependent on mitochondrial alanine transaminase Gpt2 cells. Metabolic tracing Alanine directly showed DR, catabolizes increased amounts to produce lactate, which transported ISCs fuel their TCA cycle. Correspondingly, inhibition lactate...

10.2139/ssrn.3959329 article EN SSRN Electronic Journal 2021-01-01
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