Mohammad Alinoor Rahman
Assistant Professor
University of Arkansas for Medical Sciences
faculty
Biochemistry & Molecular Biology, College of Medicine
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Biography and Research Information
OverviewAI-generated summary
Mohammad Alinoor Rahman investigates the molecular mechanisms underlying cellular processes, with a particular focus on RNA splicing and its role in disease development. His research explores how disruptions in splicing, such as those related to nonsense-mediated mRNA decay, can contribute to tumorigenesis. Rahman has published studies examining the regulation of specific gene isoforms, including those involved in glucose metabolism and neuromuscular junction function, and the impact of splicing factors like SRSF1 and SRSF6 on cancer progression, specifically in pancreatic cancer.
His work also delves into the post-translational modification of proteins, such as the SUMOylation of Leukocyte-Specific Protein 1, and its effects on protein stability and cellular localization. Rahman is the Principal Investigator on a grant from the NIH/National Institute of General Medical Sciences, totaling $376,670, to decode the mechanisms of nonsense-mediated mRNA decay through alternative splicing. His collaborations include researchers at the University of Arkansas for Medical Sciences, such as Preeti Nagar and Md. Rafikul Islam.
With an h-index of 17 and over 1,100 citations across 46 publications, Rahman's scholarship metrics reflect an active research presence in molecular biology and its implications for health and disease.
Research Overview
Alternative splicing (AS) is a highly specialized RNA processing mechanism in higher eukaryotes and a key control point in gene expression regulation. AS enables cells to produce multiple mRNAs and multiple proteins from a single gene, which can facilitate to perform specialized functions. Errors in splicing contribute to many aspects of human diseases, including cancer. AS is regulated by cis-elements in the RNA and trans-acting splicing factors comprised of RNA-binding proteins. Cancer cells often display alterations in splicing, many of which contribute to disease. Some of these alterations are caused by mutations in splicing-regulatory cis-elements, whereas others result from defects in splicing factors, such as abnormal expression, mutation, or post-translational modification. AS often gives rise to transcripts comprising a premature termination codon (PTC). Nonsense-mediated mRNA decay (NMD) is a surveillance mechanism, which selectively degrades mRNAs with PTC. Tumor cells often exploit AS or/and NMD for survival benefit by altering the expression or function of tumor-suppressors, oncogenes, tumor-specific neo-antigens, important proteins in signaling pathways, or RNA-binding proteins. I am interested to study the mechanisms of AS and NMD misregulation in cancer, and the means by which faulty AS or/and NMD can be corrected for therapy. My lab utilizes biochemistry, molecular biology, genome editing, transcriptomics, proteomics, computational biology, and antisense pharmacology to study RNA metabolism in normal and cancer cells to contribute in developing effective cancer therapies.
Metrics
- h-index: 17
- Publications: 46
- Citations: 1,117
Selected Publications
- SUMOylation Protects Endothelial Cell-Expressed Leukocyte-Specific Protein 1 from Ubiquitination-Mediated Proteasomal Degradation and Facilitates Its Nuclear Export (2026) DOI
- Targeting <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction (2026) DOI
- SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform (2025) DOI
- Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing (2024) DOI
- RNA Splicing in Cancer and Targeted Therapies (2023) DOI
- Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis (2023) DOI
Federal Grants 1 $376,670 total
Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing
Grants & Funding
- Loss of FAM60A promotes HBB induced mammary gland tumorigenesis UAMS Cancer Institute (Team of Science Pilot Award) Principal Investigator
- Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Understanding and Targeting Aberrant Splicing and NMD in MDS Edward P. Evans Foundation Principal Investigator
- Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing NIH Principal Investigator
- Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Understanding and Targeting Aberrant Splicing and NMD in MDS Edward P. Evans Foundation Principal Investigator
- Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing NIH/Nat. Inst. of General Medical Sciences Principal Investigator
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