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Mohammad Rahman

TitleAssistant Professor
InstitutionUniversity of Arkansas for Medical Sciences
DepartmentBiochemistry & Molecular Biology, College of Medicine
Address325 S. Elm St.
Mail Slot # 516
Little Rock AR 72205
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    Collapse Overview 
    Collapse 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.

    Collapse Affiliation 
    Collapse member of
    American Association for Cancer Research (AACR)
    RNA Society
    Winthrop P. Rockefeller Cancer Institute

    Collapse Biography 
    Collapse education and training
    Nagoya University, Nagoya, JapanPhD2013Molecular Medicine
    Cold Spring Harbor Laboratory, New York, USAPostdoctoral Training2021Cancer Medicine

    Collapse Teaching 
    Collapse teaching overview
    1. GRAD BIOC 5106, Current Trends in Biomedical Science,
    Graduate Biochemistry Course, UAMS, Little Rock, AR, USA
    2. GRAD BIOC 5101, Biochemistry and Molecular Biology
    Graduate Biochemistry Course, UAMS, Little Rock, AR, USA

    Collapse Research 
    Collapse research activities and funding
    G1-55291-01     (Mohammad Rahman)Apr 1, 2022 - Mar 30, 2023
    UAMS Cancer Institute (Seeds of Science Pilot Award)
    Understanding and Targeting Aberrant Splicing in MDS-RS
    Role Description: To investigate the underlying mechanisms of aberrant splicing in myelodysplastic syndromes with ring sideroblasts and to develop tools to correct the aberrant splicing
    Role: Principal Investigator

    G1-55298-01     (Sayem Miah, Mohammad Rahman, Stephanie Byrum)Apr 1, 2022 - Mar 30, 2023
    UAMS Cancer Institute (Team of Science Pilot Award)
    Loss of FAM60A promotes HBB induced mammary gland tumorigenesis
    Role Description: To decipher the role of Fam60A in mammary epithelial cell transformation
    Role: Principal Investigator

    EYIA     (RAHMAN, MOHAMMAD)Jul 1, 2021 - Jun 30, 2023
    Edward P. Evans Foundation
    Understanding and Targeting Aberrant Splicing and NMD in MDS
    Role: Principal Investigator

    EYIA 2020     (RAHMAN, MOHAMMAD)Jul 1, 2021 - Jun 30, 2023
    Edward P. Evans Foundation
    Understanding and Targeting Aberrant Splicing and NMD in MDS
    Role: Principal Investigator

    G1-55002-01     (Mohammad Rahman)Jul 1, 2020 - Jun 30, 2023
    Edward P Evans Foundation
    Understanding and Targeting Aberrant Splicing and NMD in MDS
    Role Description: To investigate the underlying mechanisms of aberrant splicing and nonsense-mediated mRNA decay promoted by splicing factor mutations in myelodysplastic syndromes
    Role: Principal Investigator

    Collapse Bibliographic 
    Collapse additional bibliographic sources
    The links below are provided by the researcher to provide access to external online bibliographies that they keep independently from the Profiles System.
    Collapse selected publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions. Don't see publications published under other names? Login to add alternative names.
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    1. Wan L, Lin KT, Rahman MA, Ishigami Y, Wang Z, Jensen MA, Wilkinson JE, Park Y, Tuveson DA, Krainer AR. Splicing Factor SRSF1 Promotes Pancreatitis and KRASG12D-Mediated Pancreatic Cancer. Cancer Discov. 2023 Jul 07; 13(7):1678-1695. PMID: 37098965.
      View in: PubMed
    2. Nagar P, Islam MR, Rahman MA. Nonsense-Mediated mRNA Decay as a Mediator of Tumorigenesis. Genes (Basel). 2023 01 30; 14(2). PMID: 36833284.
      View in: PubMed
    3. Gao Y, Lin KT, Jiang T, Yang Y, Rahman MA, Gong S, Bai J, Wang L, Sun J, Sheng L, Krainer AR, Hua Y. Systematic characterization of short intronic splicing-regulatory elements in SMN2 pre-mRNA. Nucleic Acids Res. 2022 01 25; 50(2):731-749. PMID: 35018432.
      View in: PubMed
    4. Rahman MA, Nasrin F, Bhattacharjee S, Nandi S. Hallmarks of Splicing Defects in Cancer: Clinical Applications in the Era of Personalized Medicine. Cancers (Basel). 2020 May 28; 12(6). PMID: 32481522.
      View in: PubMed
    5. Rahman MA, Lin KT, Bradley RK, Abdel-Wahab O, Krainer AR. Recurrent SRSF2 mutations in MDS affect both splicing and NMD. Genes Dev. 2020 03 01; 34(5-6):413-427. PMID: 32001512.
      View in: PubMed
    6. Rahman MA, Krainer AR, Abdel-Wahab O. SnapShot: Splicing Alterations in Cancer. Cell. 2020 01 09; 180(1):208-208.e1. PMID: 31951519.
      View in: PubMed
    7. Yoshimi A, Lin KT, Wiseman DH, Rahman MA, Pastore A, Wang B, Lee SC, Micol JB, Zhang XJ, de Botton S, Penard-Lacronique V, Stein EM, Cho H, Miles RE, Inoue D, Albrecht TR, Somervaille TCP, Batta K, Amaral F, Simeoni F, Wilks DP, Cargo C, Intlekofer AM, Levine RL, Dvinge H, Bradley RK, Wagner EJ, Krainer AR, Abdel-Wahab O. Coordinated alterations in RNA splicing and epigenetic regulation drive leukaemogenesis. Nature. 2019 10; 574(7777):273-277. PMID: 31578525.
      View in: PubMed
    8. Feng H, Bao S, Rahman MA, Weyn-Vanhentenryck SM, Khan A, Wong J, Shah A, Flynn ED, Krainer AR, Zhang C. Modeling RNA-Binding Protein Specificity In?Vivo by Precisely Registering Protein-RNA Crosslink Sites. Mol Cell. 2019 06 20; 74(6):1189-1204.e6. PMID: 31226278.
      View in: PubMed
    9. Kim YJ, Rahman MA. NMD in diseases and potential therapies. Journal of Investigative Genomics. 2018; 5(1).
    10. Aznarez I, Nomakuchi TT, Tetenbaum-Novatt J, Rahman MA, Fregoso O, Rees H, Krainer AR. Mechanism of Nonsense-Mediated mRNA Decay Stimulation by Splicing Factor SRSF1. Cell Rep. 2018 05 15; 23(7):2186-2198. PMID: 29768215.
      View in: PubMed
    11. Rahman MA. Oncogenic Landscapes of Splicing-Factor Mutant MDS. Genomics & Gene Therapy International Journal. 2018; 2(1):000105.
    12. Nazim M, Nasrin F, Rahman MA. Coordinated regulation of alternative splicing and alternative polyadenylation. Journal of Genetics and Genetic Engineering. 2018; 2(3):26-34.
    13. Ahsan KB, Masuda A, Rahman MA, Takeda JI, Nazim M, Ohkawara B, Ito M, Ohno K. SRSF1 suppresses selection of intron-distal 5' splice site of DOK7 intron 4 to generate functional full-length Dok-7 protein. Sci Rep. 2017 09 05; 7(1):10446. PMID: 28874828.
      View in: PubMed
    14. Nazim M, Masuda A, Rahman MA, Nasrin F, Takeda JI, Ohe K, Ohkawara B, Ito M, Ohno K. Competitive regulation of alternative splicing and alternative polyadenylation by hnRNP H and CstF64 determines acetylcholinesterase isoforms. Nucleic Acids Res. 2017 02 17; 45(3):1455-1468. PMID: 28180311.
      View in: PubMed
    15. Rahman MA, Nasrin F. Human disease-causing mutations affecting RNA splicing and NMD. Journal of Investigative Genomics. 2016; 3(2).
    16. Shibata A, Okuno T, Rahman MA, Azuma Y, Takeda J, Masuda A, Selcen D, Engel AG, Ohno K. IntSplice: prediction of the splicing consequences of intronic single-nucleotide variations in the human genome. J Hum Genet. 2016 Jul; 61(7):633-40. PMID: 27009626.
      View in: PubMed
    17. Rahman MA, Ohno K. Splicing aberrations in congenital myasthenic syndromes. Journal of Investigative Genomics. 2015; 2(5).
    18. Rahman MA, Azuma Y, Nasrin F, Takeda J, Nazim M, Bin Ahsan K, Masuda A, Engel AG, Ohno K. SRSF1 and hnRNP H antagonistically regulate splicing of COLQ exon 16 in a congenital myasthenic syndrome. Sci Rep. 2015 Aug 18; 5:13208. PMID: 26282582.
      View in: PubMed
    19. Ohno K, Rahman MA, Nasrin F, Masuda A . Decoding abnormal splicing code in human diseases. Journal of Investigative Genomics. 2015; 2(1).
    20. Nasrin F, Rahman MA, Masuda A, Ohe K, Takeda J, Ohno K. HnRNP C, YB-1 and hnRNP L coordinately enhance skipping of human MUSK exon 10 to generate a Wnt-insensitive MuSK isoform. Sci Rep. 2014 Oct 30; 4:6841. PMID: 25354590.
      View in: PubMed
    21. Rahman MA, Masuda A, Ohe K, Ito M, Hutchinson DO, Mayeda A, Engel AG, Ohno K. HnRNP L and hnRNP LL antagonistically modulate PTB-mediated splicing suppression of CHRNA1 pre-mRNA. Sci Rep. 2013 Oct 14; 3:2931. PMID: 24121633.
      View in: PubMed
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