Sahir Sultan Alvi

About

Currently, I am working as a post-doctoral fellow at the Department of Immunology and Microbiology, University of Texas Rio Grande Valley, Texas, USA, aiming to understand the biology of the Ribosome biogenesis (RiBi) and to develop therapeutic regimens against pancreatic and hepatocellular carcinoma via targeting the RiBi, particularly the RNA pol-I activity and ribosomal proteins (RPs) i.e., RPA135, RPS20, and RPL6. Before moving to USA, I worked as a Young Scientist Fellow and Principal Investigator (PI) as I was awarded with the prestigious Young Scientist Fellowship in 2019 by the Department of Health Research (DHR), Ministry of Health & Family Welfare (MoHFW), Govt. of India. During this tenure, I particularly focused on cardiovascular pharmacology via targeting the proprotein convertase subtilisin Kexin/type-9 (PCSK-9) and 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMG-R) as it is quite imperative to develop novel therapeutic agents in order to regulate cholesterol homeostasis.

Employment

• South Dakota State University Post Doctoral Research Associate-I
  2025 - Present
• The University of Texas Rio Grande Valley - Edinburg Campus Post-Doctoral Fellow
  2022 - 2025
• Integral University Young Scientist Fellow (Principal Investigator)
  2019 - 2022
• Integral University Research Scholar
  2013 - 2018

Education

• Integral University Ph.D.
  2013 - 2018
• Integral University M.Sc.
  2011 - 2013
• C.S.J.M. University B.Sc.
  2008 - 2011

Projects & Funding

Projects & funding information is unavailable.

Publications (55)

• Data from Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  2026 DOI: 10.1158/1535-7163.c.8547693
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• N‐Acetyl Cysteine Mitigates d‐Ribose‐Induced Protein Glycation and Aggregation Through Multiple Protective Mechanisms
  IUBMB Life 2026 DOI: 10.1002/iub.70126
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• Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  Molecular Cancer Therapeutics 2026 DOI: 10.1158/1535-7163.MCT-25-0097
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• Repurposing of FDA-approved Drugs Identifies Glipizide as a Potent HMG-CoA Reductase Inhibitor: a High-Throughput Virtual Screening and Molecular Dynamics Approach for Targeting Hypercholesterolemia
  Journal of Pharmaceutical Innovation 2026 DOI: 10.1007/s12247-025-10349-1
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• Prognostic significance and interplay of circulatory PCSK-9–ApoCIII–chemokine axis in type 2 diabetes and its complications: a pilot study in North Indian patients
  The Egyptian Journal of Internal Medicine 2026 DOI: 10.1186/s43162-026-00624-z
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• Diallyl trisulfide attenuates metabolic syndrome via integrated modulation of PCSK-9/LDL-R axis, redox homeostasis, and inflammatory cytokine networks in high-carbohydrate high-fat (HCHF) diet-fed rats
  Frontiers in Pharmacology 2026 DOI: 10.3389/fphar.2026.1781950
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• Supplementary Tables from Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  2026 DOI: 10.1158/1535-7163.32743290
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• Supplementary Figure 9 from Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  2026 DOI: 10.1158/1535-7163.32743293
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• Supplementary Figure 8 from Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  2026 DOI: 10.1158/1535-7163.32743296
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• Supplementary Figure 6 from Ubiquitination of Oncogenic Mutant p53 via Attenuation of Ribosome Biogenesis Machinery Effectively Inhibits Pancreatic Tumor Growth
  2026 DOI: 10.1158/1535-7163.32743302
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