Vivek Sharma

ORCID: 0000-0001-7345-4597
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About
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Research Areas
  • Cancer-related molecular mechanisms research
  • MicroRNA in disease regulation
  • Advanced biosensing and bioanalysis techniques
  • RNA Interference and Gene Delivery
  • Circular RNAs in diseases
  • Crystallization and Solubility Studies
  • Synthesis and biological activity
  • X-ray Diffraction in Crystallography
  • DNA and Nucleic Acid Chemistry
  • interferon and immune responses
  • Synthesis and Reactions of Organic Compounds
  • RNA modifications and cancer
  • CRISPR and Genetic Engineering
  • Biochemical and Molecular Research
  • Histone Deacetylase Inhibitors Research
  • Cancer, Hypoxia, and Metabolism
  • Cancer therapeutics and mechanisms
  • Pluripotent Stem Cells Research
  • Synthesis and Characterization of Heterocyclic Compounds
  • Mosquito-borne diseases and control
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Epigenetics and DNA Methylation
  • Cell death mechanisms and regulation
  • Cytokine Signaling Pathways and Interactions
  • Click Chemistry and Applications

Birla Institute of Technology and Science - Hyderabad Campus
2020-2025

Birla Institute of Technology and Science, Pilani
2020-2025

Norfolk and Norwich University Hospitals NHS Foundation Trust
2024

Banaras Hindu University
2024

University of Massachusetts Chan Medical School
2018-2021

National Botanical Research Institute
2018-2021

National Cancer Institute
2013-2015

University of Southampton
2015

University of Delhi
1981-2015

National Institutes of Health
2013-2014

Abstract While a number of studies have documented the importance microglia in central nervous system (CNS) response to injury, infection and disease, little is known regarding its role viral encephalitis. We therefore, exploited an experimental model Japanese Encephalitis, better understand played by Encephalitis Virus (JEV) infection. Lectin staining performed assess microglial activation indicated robust increase reactive following A difference topographic distribution activated, resting,...

10.1002/glia.20474 article EN Glia 2007-01-03

Abstract Despite recent advances in understanding molecular mechanisms involved glioblastoma progression, the prognosis of most malignant brain tumor continues to be dismal. Because flavonoid kaempferol is known suppress growth a number human malignancies, we investigated effect on cells. Kaempferol induced apoptosis glioma cells by elevating intracellular oxidative stress. Heightened stress was characterized an increased generation reactive oxygen species (ROS) accompanied decrease...

10.1158/1535-7163.mct-06-0788 article EN Molecular Cancer Therapeutics 2007-09-01

Mutations in human induced pluripotent stem cells (iPSCs) pose a risk for their clinical use due to preferential reprogramming of mutated founder cell and selection mutations during maintenance iPSCs culture. It is unknown, however, if are stress associated with oncogene expression reprogramming. We performed whole exome sequencing foreskin fibroblasts derived at two different passages. found that vitro passaging contributed 7% the iPSC coding point mutation load, ultradeep amplicon revealed...

10.1002/stem.1011 article EN Stem Cells 2011-12-12

Glioblastoma multiforme (GBM) are resistant to TNFα-induced apoptosis and blockade of NF-κB activation sensitizes glioma cells apoptosis. As Casein kinase-2 (CK2) induces aberrant as we observed elevated CK2 levels in GBM tumors, investigated the potential inhibitors (CK2-Is) - DRB Apigenin sensitizing CK2-Is small interfering RNA (siRNA) reduced cell viability, inhibited TNFα-mediated activation, sensitized Importantly, activated p53 function wild-type but not mutant cells. Activation...

10.1038/cddis.2012.10 article EN cc-by Cell Death and Disease 2012-02-09

Highlights•During reprogramming, oxidative stress is elevated•Antioxidants reduce genome instability during reprogramming•iPSCs made in the presence of antioxidants have fewer de novo genomic aberrationsSummarySomatic cells can be reprogrammed to induced pluripotent stem (iPSCs) using oncogenic transcription factors. However, this method leads genetic aberrations iPSCs via unknown mechanisms, which may limit their clinical use. Here, we demonstrate that supplementation growth media with...

10.1016/j.stemcr.2013.11.004 article EN cc-by-nc-nd Stem Cell Reports 2014-01-01

Transforming growth factor beta (TGF-β)-regulated long-non-coding RNAs (lncRNAs) modulate several aspects of tumor development such as proliferation, invasion, metastasis, epithelial to mesenchymal transition (EMT), and drug resistance in various cancers, including Glioblastoma multiforme (GBM). We identified novel differentially expressed lncRNAs upon TGF-β treatment glioma cells using genome-wide microarray screening. show that induces lncRNA-MUF cells, its expression is significantly...

10.3389/fonc.2021.788755 article EN cc-by Frontiers in Oncology 2022-02-08

Abstract Immunotherapy often relies on biologics with systemic administration, which can lead to adverse side effects. An innovative approach utilizes a wearable device deliver alternating magnetic fields (AMFs) induce localized immune responses in tumors. Here, we present results from preclinical evaluation of Asha™ Therapy, proprietary, low-intensity (1–3 mT), 50 kHz AMF application, developed locally cancer immunity. To explore the potential for Asha therapy as treatment solid tumors, an...

10.1158/2326-6074.io2025-b085 article EN Cancer Immunology Research 2025-02-23

GalNAc conjugation is emerging as a dominant strategy for delivery of therapeutic oligonucleotides to hepatocytes. The structure and valency the ligand contributes potency conjugates. Here we present panel multivalent variants using two different synthetic strategies. Specifically, novel conjugate based on support-bound trivalent cluster, four others phosphoramidite monomer that was readily assembled into tri- or tetravalent designs during solid phase oligonucleotide synthesis. We compared...

10.1021/acs.bioconjchem.8b00365 article EN Bioconjugate Chemistry 2018-06-13

Resistance to tumor necrosis factor (TNFalpha)-induced apoptosis in various cancer cells has been attributed the activation of transcription NF-kappaB. Ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]one)-a selenoorganic compound is known prevent TNFalpha-mediated NF-kappaB activity. As glioblastoma are resistant cytotoxic effect TNFalpha, we investigated potential sensitizing glioma TNFalpha-induced apoptosis. Although treatment with reduced viability cells, cotreatment TNFalpha enhanced...

10.1002/ijc.23771 article EN International Journal of Cancer 2008-08-15

Abstract The present study identified a novel mechanism of induction apoptosis in glioblastoma cells by scriptaid – histone deacetylase (HDAC) inhibitor. Scriptaid reduced glioma cell viability increasing Jun N‐terminal kinase (JNK) activation. Although induced activation both p38MAPK and JNK, it was the inhibition JNK that attenuated scriptaid‐induced significantly. also increased expression ( i ) p21 p27 involved cell‐cycle regulation ii γH2AX associated with DNA damage response...

10.1111/j.1582-4934.2009.00844.x article EN other-oa Journal of Cellular and Molecular Medicine 2009-07-06

New cycloartane triterpenoids (2–4) have been recently discovered in the bark of Dysoxylum malabaricum .

10.1039/d3nj04057g article EN New Journal of Chemistry 2024-01-01

The anti-neoplastic property of alkyl phospholipids has been tested for the treatment several malignancies. In this study, we evaluated efficacy miltefosine (Hexadecylphosphocholine--an analogue) on glioblastoma multiforme. demonstrate that miltefosine-induced apoptosis is accompanied by elevated Fas, Fas-associated death domain (FADD) expression, caspase-8 activity and increased distribution Fas FADD towards lipid raft microdomain to form inducing signaling complex. Treatment with resulted...

10.1111/j.1471-4159.2008.05625.x article EN Journal of Neurochemistry 2008-08-15
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