Pravir Kumar

Department of Biotechnology, Delhi Technological University India


Dr. Pravir Kumar is working as a Professor in the Department of Biotechnology at DTU. Before joining DTU, Dr. Kumar has served as an Associate Professor (Biosciences) and Assistant Director (Center) at VIT University, Vellore. He has obtained MS degree from BHU, Varanasi with Molecular and clinical genetics specialization, and PhD degree from J. W. Goethe University, Germany in the field of coronary artery diseases and cardiovascular physiology. Before returning to India, he has spent several years in the Neurology Department at Tufts University School of Medicine, Boston, USA as a postdoctoral fellow and later at faculty position. Until April 2016, he was holding an adjunct Faculty status in the Neurology Department at Tufts University School of Medicine (TUSM). His areas of research interest and expertise include molecular chaperone and ubiquitin E3 ligase in neurodegenerative disorders along with the aberrant cell cycle re-entry into aged neurons and muscles. He is an editorial board member in the prestigious journals such as, Scientific Reports, Journal of Alzheimer’s disease, and adhoc reviewers of 30 leading Elsevier, Springer, BMC, Bentham, Oxford and other reputed journals. He has published more than 65 papers in peer- reviewed journals and more than 100 abstracts in international symposium, proceedings and as an invited speaker. Until now, he has guided 08 PhD students, 30 M.Tech and more than 30 students at MS and BS levels. Currently, he is guiding 06 PhD and 4 M.Tech. students. He has also severed as a member of many national-level selection committees, including prestigious USIEF Nehru Fulbright program, Life Science Research Board- DRDO committee, National Research Development Foundation (NRDC). He has successfully completed LSRB-DRDO funded research defense project on hypoxia induced neurodegeneration for soldiers in India. He is a life and regular member of various professional societies across the globe. Dr.Kumar has served as Dean of alumni affair, from January 2018-March 2020. Prof. Kumar has raised approx. 7 crores (given or pledged) for DTU infrastructure development, endowment, fellowship, interaction, centre establishment, and MoU between DTU and overseas universities. He was also organized homecoming meet of golden and diamond jubilee along with the team which was a grand celebration in Feb 2019 and in Jan 2020.

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Discovery of novel compounds targeting DJ-1 as neuroprotectants for Parkinson’s disease by virtual screening and in silico method

Aim: To screen zinc database for structurally similar molecules to compound 23 that targets DJ1 for use as a neuroprotective agent for Parkinson’s disease. Background: Parkinson’s disease (PD), the second most common chronic neurodegenerative disorder characterized by progressive loss of dopaminergic neurons of the substantia nigra. To date, several proteins account for the recessive familial PD-forms, namely, Parkin, PINK-1, DJ-1, SNCA, PARK2, and LRRK2 Genes. DJ1 is one of the important central points that may be targeted for PD therapy. Recently, Compound 23 has been observed to exert the neuroprotective effect against neurodegeneration in PD model, but due to its toxic substructure, the hunt for better nontoxic compound continues. Objective: The overall objective of our work is to apply in silico approaches to screen structure similar compounds that interacts potentially with DJ1 and may serve as a good therapeutic molecule for PD. Method: Initial data mining was done from zinc database and then screened compounds were additionally screened with toxicity checker, carcinopred, ADMET analysis and docking analysis. Results: The basic screening of database for structurally similar chemicals to compound 23 resulted in 50 compounds, which were further screened to twenty-three and finally seven compounds have been screened based on the toxicity and carcinopred test. Later, the seven compounds were docked and analysed for its docking efficiency with DJ1. Our result of molecular docking and molecular simulation analysis highlights Molecule 42(SS2), to exhibit best binding affinity against DJ-1 protein target and can be proposed to be used as a therapeutic agent to modulate neurodegenerative proteins. Conclusion: Therefore, we conclude discovery of novel, non-toxic, non-carcinogenic; ADMET investigated capable of crossing BB barrier but structurally similar compounds of Compound-23, specifically molecule 42(SS2) and potentially molecule 34(SS1) to be used as a neuroprotective agent for Parkinson’s disease.

Cancer Fighting SiRNA-RRM2 loaded nanorobots

Background: Silencing of several genes are critical for cancer therapy. These genes may be apoptotic gene, cell proliferation gene, DNA synthesis gene etc. Ribonucleotide Reductase (RR) two subunit RRM1 and RRM2 are critical for DNA synthesis. Hence targeting the blockage of DNA synthesis at tumour site can be a smart mode of cancer therapy. Specific targeting of blockage of RRM2 has been done effectively by SiRNA. The drawback of siRNA delivery in the body is pool uptake by all kinds of cell, questionable stability under physiological condition, non-target effect and ability to trigger immune response. These obstacles may be overcome by target delivery of siRNA at tumour site. This review presents a holistic overview about role of RRM2 in controlling cancer progression. The nanoparticles are more effective due to its specific characters like cell membrane penetration capacity, less toxicity etc. RRM2 have been found to be elevated in different type of cancer and has been identified as the prognostic and predictive marker of the disease. Reductase. RRM1 and RRM2 regulate the protein and gene expression of E2F which is critical for protein expression and progression of cell cycle and cancer. Knockdown of RRM2 leads to apoptosis via Bcl2 in cancer. Both Bcl2 and E2F is critical in progression of cancer, hence a gene that can affect both in regulating DNA replication is essential for cancer therapy. Aim: The aim of the review is to identify critical and related gene whose silencing may inhibit cancer progression. Conclusion: In this review, we illuminate the critical link between RRM-E2F, RRM-Bcl2, RRM-HDAC for the therapy of cancer. Altogether, this review presents an overview on all type of SiRNA targeted for cancer therapy with especial emphasis on RRM2 for controlling tumour progression.

Comparative evaluation of 99mTc-MBIP-X/11[C] MBMP for visualization of 18 kDa translocator protein

An elevated translocator protein (18 kDa, TSPO) density is observed during inflammation in the brain and peripheral organs making it a viable target for imaging.

Aβ, Tau, and α-Synuclein aggregation and integrated role of PARK2 in the regulation and clearance of toxic peptides

Publication date: Available online 13 September 2019

Source: Neuropeptides

Author(s): Dhiraj Kumar, Pravir Kumar


Alzheimer's and Parkinson's diseases are one of the world's leading causes of death. >50 million people throughout the world are suffering with these diseases. They are two distinct progressive neurodegenerative disorders affecting different regions of the brain with diverse symptoms, including memory and motor loss respectively, but with the advancement of diseases, both affect the whole brain and exhibit some common biological symptoms. For instance, >50% PD patients develop dementia in their later stages, though it is a hallmark of Alzheimer's disease. In fact, latest research has suggested the involvement of some common pathophysiological and genetic links between these diseases, including the deposition of pathological Aβ, Tau, and α-synuclein in both the cases. Therefore, it is pertinent to diagnose the shared biomarkers, their aggregation mechanism, their intricate relationships in the pathophysiology of disease and therapeutic markers to target them. This would enable us to identify novel markers for the early detection of disease and targets for the future therapies. Herein, we investigated molecular aspects of Aβ, Tau, and α-Synuclein aggregation, and characterized their functional partners involved in the pathology of AD and PD. Moreover, we identified the molecular-crosstalk between AD and PD associated with their pathogenic proteins- Aβ, Tau, and α-Synuclein. Furthermore, we characterized their ubiquitinational enzymes and associated interaction network regulating the proteasomal clearance of these pathological proteins.

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