Ph.D in Biotechnology from Babasaheb Bhimrao Ambedkar University, Lucknow on the Thesis title " Investigation(s) on the HCMV miRNAs role on cellular Apoptosis" under the supervision of Dr Sunil Babu Gosipatala, Associate Professor, Department of Biotechnology, School of Life Sciences, Babasaheb Bhimrao Ambedkar University Lucknow. I have completed my Masters in Biotechnology from Department of Biotechnology, School of Life Sciences, Babasaheb Bhimrao Ambedkar University Lucknow.
RESEARCH, TEACHING, or OTHER INTERESTS
Biochemistry, Genetics and Molecular Biology, Biotechnology, Applied Microbiology and Biotechnology, Neuroscience
18
Scopus Publications
Scopus Publications
Predictive performance of HOMA-IR and TyG index across FTO rs9939609 genotypes in type 2 diabetes mellitus Dinesh Kumar, Jyoti Batra, Abhishek Pandeya, Sumesh Prasad Sah, Sudeep Kumar, Juhi Aggarwal Clinical Epidemiology and Global Health, 2026 Background:The fat mass and obesity-associated (FTO) gene variant rs9939609 has been linked to obesity, Insulin Resistance (IR), and Type 2 Diabetes Mellitus (T2DM).Conventional IR indicators such as Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) require insulin measurement, whereas the triglyceride-glucose (TyG) index offers a cost-effective alternative that reflects metabolic disturbances involving glucose and lipid metabolism.This study assessed whether the predictive performance of IR indices differs across FTO rs9939609 genotypes in North India. Methods:A case-control study was conducted among 120 T2DM patients and 120 age-and sex-matched healthy controls.Fasting glucose, triglycerides, lipid profile, and insulin levels were measured.HOMA-IR and TyG indices were calculated.FTO rs9939609 (T>A) genotyping was performed using Polymerase Chain Reaction -Restriction Fragment Length Polymorphism (PCR-RFLP) followed by ScaI digestion.Associations between IR indices and genotype models were examined using logistic regression under additive, recessive, and dominant models.Receiver operating characteristic (ROC) analysis evaluated the discriminatory performance of the indices for T2DM. Results:The A allele was significantly more frequent in T2DM cases than controls (43.9% vs. 27.9%,p<0.001.Both TyG and HOMA-IR values increased progressively from TT < AT < AA genotypes.In the additive model, TyG (OR=2.84;95% CI: 1.80-4.47)and HOMA-IR (OR=2.39;95% CI: 1.53-3.73)were associated with T2DM.ROC analysis demonstrated superior discriminatory performance of TyG, particularly under the dominant model (AUC=0.742vs. 0.666 for HOMA-IR). Conclusions:FTO rs9939609 strongly influences IR and T2DM susceptibility.The TyG index outperforms J o u r n a l P r e -p r o o f HOMA-IR across genotype models, making it a practical and genetically informed screening marker.
Targeting TDP-43 Proteinopathy in hiPSC-Derived Mutated hNPCs with Mitoxantrone Drugs and miRNAs Uzair A. Ansari, Ankita Srivastava, Ankur K. Srivastava, Abhishek Pandeya, Pankhi Vatsa, Renu Negi, Akash Singh, Aditya B. Pant Pharmaceutics, 2025 Background/Objectives: TDP-43 mutation-driven Amyotrophic Lateral Sclerosis (ALS) motor neuron disease is one of the most prominent forms (approximately 97%) in cases of sporadic ALS. Dysfunctional autophagy and lysosomal function are the prime mechanisms behind ALS. Mitoxantrone (Mito), a synthetic doxorubicin analog, is an inhibitor of DNA and RNA synthesis/repair via intercalating with nitrogenous bases and inhibiting topoisomerase II. The therapeutic potential of miRNAs associated with disease conditions has also been reported. This study explores the therapeutic potential of Mito along with miRNAs against mutated TDP-43 protein-induced proteinopathy in human-induced pluripotent stem cell (hiPSC)-derived human neural progenitor cells (hNPCs). Methods: HiPSCs mutated for TDP-43 were differentiated into hNPCs and used to explore the therapeutic potential of Mito at a concentration of 1 μM for 24 h (the identified non-cytotoxic dose). The therapeutic effects of Mito on miRNA expression and various cellular parameters such as mitochondrial dynamics, autophagy, and stress granules were assessed using the high-throughput Open Array technique, immunocytochemistry, flow cytometry, immunoblotting, and mitochondrial bioenergetic assay. Results: Mutated TDP-43 protein accumulation causes stress granule formation (G3BP1), mitochondrial bioenergetic dysfunction, SOD1 accumulation, hyperactivated autophagy, and ER stress in hNPCs. The mutated hNPCs also show dysregulation in six miRNAs (miR-543, miR-34a, miR-200c, miR-22, miR-29b, and miR-29c) in mutated hNPCs. A significant restoration of TDP-43 mutation-induced alterations could be witnessed upon the exposure of mutated hNPCs to Mito. Conclusions: Our study indicates that miR-543, miR-29b, miR-22, miR-200c, and miR-34a have antisense therapeutic potential alone and in combination with Mitoxantrone.
HCMV miR-UL70-3p downregulates the rapamycin-induced autophagy by targeting the autophagy-related protein 9A (ATG9A) Raj Kumar Khalko, Abhishek Pandeya, Sangeeta Saxena, Sunil Babu Gosipatala International Reviews of Immunology, 2024 Human cytomegalovirus (HCMV) is a representative β-herpesvirus that establishes persistent infections in humans, and exhibits high seropositivity rates in adults. It has co-evolved with its human host and employs various strategies to evade antiviral mechanisms by utilizing a significant portion of its genome. HCMV-encoded proteins and miRNAs have been implicated in regulating these mechanisms, enabling viral survival within the human body. During viral infections, autophagy, a conserved catabolic process essential for cellular homeostasis, acts as an antiviral defense mechanism. Multiple studies have reported that HCMV can modulate autophagy through its proteins and miRNAs, thereby influencing its survival within the host. In this study, we showed the potential involvement of HCMV miRNAs in cellular autophagy. We employed various bioinformatic tools to predict putative HCMV miRNAs that target autophagy-related genes and their corresponding cellular autophagy genes. Our results show that the 3'UTR of autophagy-related genes, including ATG9A, ATG9B, ATG16L2, SQSTM1, and EIF2AK2, harbors potential binding sites for hcmv-miR-UL70-3p. Experimental manipulation involving ectopic expression of hcmv-miR-UL70-3p demonstrated a significant reduction in rapamycin-induced autophagy, with ATG9A as its functional target. These findings establish that hcmv-miR-UL70-3p acts as an autophagy inhibitor by suppressing the expression of ATG9A.
Proteome architecture of human‑induced pluripotent stem cell‑derived three‑dimensional organoids as a tool for early diagnosis of neuronal disorders R. Negi, A. Srivastava, A. Srivastava, Abhishek Pandeya, P. Vatsa, U. A. Ansari, A. Pant Indian Journal of Pharmacology, 2023 BACKGROUND AND OBJECTIVES: Induced pluripotent stem cells (iPSCs) derived three-dimensional (3D) model for rare neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS) is emerging as a novel alternative to human diseased tissue to explore the disease etiology and potential drug discovery. In the interest of the same, we have generated a TDP-43-mutated human iPSCs (hiPSCs) derived 3D organoid model of ALS disease. The high-resolution mass spectrometry (MS)-based proteomic approach is used to explore the differential mechanism under disease conditions and the suitability of a 3D model to study the disease. MATERIALS AND METHODS: The hiPSCs cell line was procured from a commercial source, grown, and characterized following standard protocols. The mutation in hiPSCs was accomplished using CRISPR/Cas-9 technology and predesigned gRNA. The two groups of organoids were produced by normal and mutated hiPSCs and subjected to the whole proteomic profiling by high-resolution MS in two biological replicates with three technical replicas of each. RESULTS: The proteomic analysis of normal and mutated organoids revealed the proteins associated with pathways of neurodegenerative disorders, proteasomes, autophagy, and hypoxia-inducible factor-1 signaling. Differential proteomic analysis revealed that the mutation in TDP-43 gene caused proteomic deregulation, which impaired protein quality mechanisms. Furthermore, this impairment may contribute to the generation of stress conditions that may ultimately lead to the development of ALS pathology. CONCLUSION: The developed 3D model represents the majority of candidate proteins and associated biological mechanisms altered in ALS disease. The study also offers novel protein targets that may uncloud the precise disease pathological mechanism and be considered for future diagnostic and therapeutic purposes for various neurodegenerative disorders.
Corona Viruses: Emergence, Evolution, and Recurrence R. C. Sobti, Bharti Kotarya, Abhishek Pandeya, Raj Kumar Khalko, Neelam Yadav, Sudipta Saha, Y. Vasudeva Rao, Sunil Babu Gosipatala Delineating Health and Health System Mechanistic Insights into Covid 19 Complications, 2021
Prospects of sars-cov-2 vaccines and their landscape Bharti Kotarya, , Abhishek Pandeya, Raj Kumar Khalko, Anup Mishra, Arti Priyadarshini, N. Vijaya, Manoj Kumar Singh, Sudipta Saha, Sunil Babu Gosipatala, , , , , , , , and Journal of Experimental Biology and Agricultural Sciences, 2020
