Mohammad Alinoor Rahman

Federal Grant PI

Assistant Professor

UAMS

Last publication 2026 Last refreshed 2026-05-22

faculty

Biochemistry & Molecular Biology, College of Medicine

marahman@uams.edu

17 h-index 47 pubs 1,153 cited

Research Areas

Links

ORCID Lab Website UAMS TRI Profile

OverviewAI-generated summary

Mohammad Alinoor Rahman, Assistant Professor of Biochemistry & Molecular Biology at the University of Arkansas for Medical Sciences, investigates the complex interplay between alternative splicing (AS) and nonsense-mediated mRNA decay (NMD) in gene expression regulation and disease. His research focuses on how errors in these fundamental RNA processing mechanisms contribute to human diseases, particularly cancer. AS allows a single gene to produce multiple protein variants, a process crucial for cellular specialization. However, dysregulation of AS can lead to the production of aberrant transcripts, often containing premature termination codons (PTCs).

Rahman's work examines how cellular surveillance pathways, such as NMD, normally eliminate these aberrant transcripts. However, cancer cells can exploit or evade NMD to promote tumor growth by altering the expression of key proteins, including tumor suppressors and oncogenes. His federally funded research, supported by a $376,670 grant from the NIH/National Institute of General Medical Sciences, aims to decode the mechanisms by which NMD is influenced by alternative splicing. Collaborating with researchers at the University of Arkansas for Medical Sciences, including Preeti Nagar and Md. Rafikul Islam, Rahman has published extensively on topics such as the role of splicing factor SRSF1 in pancreatitis and pancreatic cancer, and the broader implications of NMD in tumorigenesis. His scholarly output includes 47 publications with 1,134 citations and an h-index of 17.

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: 47
Citations: 1,153

Selected Publications

Loss of FAM60A disrupts Sin3/HDAC control of the Hippo signaling and promotes oncogenic YAP1 activation (2026)

DOI OpenAlex
Mitochondrial antioxidant enzyme (SOD2) at the crossroads of redox signaling and cancer progression (2026)

DOI OpenAlex
SUMOylation Protects Endothelial Cell-Expressed Leukocyte-Specific Protein 1 from Ubiquitination-Mediated Proteasomal Degradation and Facilitates Its Nuclear Export (2026)

DOI OpenAlex
Targeting <i>EZH2</i> Oncogenic Splicing: Decoding the Regulatory Network and Antisense Correction (2026)

DOI OpenAlex
SRSF6 and SRSF1 coordinately enhance the inclusion of human <i>MUSK</i> exon 10 to generate a Wnt-sensitive MuSK isoform (2025)

3 citations DOI OpenAlex
Beyond the Sin3/HDAC Complex: FAM60A emerges as a regulator of RNA Splicing (2024)

DOI OpenAlex
RNA Splicing in Cancer and Targeted Therapies (2023)

1 citation DOI OpenAlex
Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis (2023)

27 citations DOI OpenAlex

View all publications on OpenAlex →

Federal Grants 1 $376,670 total

NIH/National Institute of General Medical Sciences Contact PI Jul 2024 - Apr 2029

Decoding Mechanisms of Nonsense-mediated mRNA Decay through Alternative Splicing

National Institute of General Medical Sciences $376,670 R35

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