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Golam Mohi

Golam Mohi

Professor, Biochemistry and Molecular Genetics

Primary Location
PO Box 800733
1340 JPA Pinn Hall Room 6023A
Charlottesville, VA 22908
Primary Phone Number
434.924.5657
Fax Number
434.924.5069
Email
[email protected]

Bio & Overview

My laboratory focuses on understanding the molecular and epigenetic mechanisms involved in the regulation of normal hematopoiesis and hematologic malignancies. The ultimate goal of our research is to identify new therapeutic targets and develop novel therapeutic strategies for treatment of leukemia. JAK2, a member of the Janus family of non-receptor protein tyrosine kinases, is activated in response to a variety of cytokines. A somatic JAK2V617F mutation has been found in a majority of patients with myeloproliferative neoplasms (MPNs). One of the major interests in our lab is to study the role of the JAK/STAT signaling in the pathogenesis of MPNs. We are also investigating the interaction of epigenetic modulators with the JAK2 mutation in MPNs using state-of-the-art techniques and genetically engineered animal models. Current research projects in my laboratory are focused in the following areas: (1) Elucidation of the role of oncogenic JAK2 mutation in the pathogenesis of myeloproliferative neoplasms. (2) Investigation of the role of tyrosine phosphatases (e.g, PTPN1, PTPN11) in myeloid neoplasms. (3) Investigation of the role of RNA splicing factor mutations in myeloid neoplasms. (4) Investigation of the effects of epigenetic modifier mutations in myeloid malignancies. (5) Identification of new therapeutic targets and therapies for triple negative breast cancer.

Academic Information

Department
Biochemistry and Molecular Genetics
Academic Title
Professor

Primary Education

  • PhD, Molecular Cell Biology, University of Tokyo, 2001
  • Postdoc, Cancer Biology, Harvard Medical School, 2005

Other Affiliations

  • Mentor, Biochemistry and Molecular Genetics
  • MSTP
  • BIMS

Research Interests

Cell signaling, stem cell biology, molecular and epigenetic mechanisms of blood and breast cancers

Research Disciplines

  • Biochemistry
  • Cancer Biology
  • Epigenetics
  • Experimental Pathology
  • Genetics
  • Molecular Biology
  • Molecular Pharmacology

Research Opportunities

  • Biochemistry
  • Cancer Biology
  • Epigenetics
  • Experimental Pathology
  • Genetics
  • Molecular Biology
  • Molecular Pharmacology

PhD Programs

  • Biochemistry & Molecular Genetics
  • Experimental Pathology

Selected Publications

2023

Yang, Y., Abbas, S., Sayem, M. A., Dutta, A., & Mohi, G. (2023). SRSF2 mutation reduces polycythemia and impairs hematopoietic progenitor functions in JAK2V617F-driven myeloproliferative neoplasm. BLOOD CANCER JOURNAL, 13(1). doi:10.1038/s41408-023-00947-y

2022

Rahman, M. F. -U., Yang, Y., Le, B. T., Dutta, A., Posyniak, J., Faughnan, P., . . . Mohi, G. (2022). Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm. NATURE COMMUNICATIONS, 13(1). doi:10.1038/s41467-022-32928-3

2021

Dutta, A., Nath, D., Yang, Y., Le, B. T., Rahman, M. F. -U., Faughnan, P., . . . Mohi, G. (2022). Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models. LEUKEMIA, 36(3), 746-759. doi:10.1038/s41375-021-01464-2

Dutta, A., Nath, D., Yang, Y., Le, B. T., & Mohi, G. (2021). CDK6 Is a Therapeutic Target in Myelofibrosis. CANCER RESEARCH, 81(16), 4332-4345. doi:10.1158/0008-5472.CAN-21-0590

Dutta, A., Yang, Y., Le, B. T., Zhang, Y., Abdel-Wahab, O., Zang, C., & Mohi, G. (2021). U2af1 is required for survival and function of hematopoietic stem/progenitor cells. LEUKEMIA, 35(8), 2382-2398. doi:10.1038/s41375-020-01116-x

2019

Sano, S., Wang, Y., Yura, Y., Sano, M., Oshima, K., Yang, Y., . . . Walsh, K. (2019). JAK2V617F-Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure. JACC-BASIC TO TRANSLATIONAL SCIENCE, 4(6), 684-697. doi:10.1016/j.jacbts.2019.05.013

2017

Dutta, A., Hutchison, R. E., & Mohi, G. (2017). Hmga2 promotes the development of myelofibrosis in Jak2V617F knockin mice by enhancing TGF-β1 and Cxcl12 pathways. BLOOD, 130(7), 920-932. doi:10.1182/blood-2016-12-757344

Jobe, F., Patel, B., Kuzmanovic, T., Makishima, H., Yang, Y., Przychodzen, B., . . . Mohi, G. (2017). Deletion of Ptpn1 induces myeloproliferative neoplasm. LEUKEMIA, 31(5), 1229-1234. doi:10.1038/leu.2017.31

2016

Dutta, A., Yan, D., Hutchison, R. E., & Mohi, G. (2018). STAT3 mutations are not sufficient to induce large granular lymphocytic leukaemia in mice. BRITISH JOURNAL OF HAEMATOLOGY, 180(6), 911-915. doi:10.1111/bjh.14487

Yang, Y., Akada, H., Nath, D., Hutchison, R. E., & Mohi, G. (2016). Loss of Ezh2 cooperates with Jak2V617F in the development of myelofibrosis in a mouse model of myeloproliferative neoplasm. BLOOD, 127(26), 3410-3423. doi:10.1182/blood-2015-11-679431

Gu, S., Chan, W. W., Mohi, G., Rosenbaum, J., Sayad, A., Lu, Z., . . . Van Etten, R. A. (2016). Distinct GAB2 signaling pathways are essential for myeloid and lymphoid transformation and leukemogenesis by BCR-ABL1. BLOOD, 127(14), 1803-1813. doi:10.1182/blood-2015-06-653006

2015

Yan, D., Jobe, F., Hutchison, R. E., & Mohi, G. (2015). Deletion of Stat3 enhances myeloid cell expansion and increases the severity of myeloproliferative neoplasms in Jak2V617F knock-in mice. LEUKEMIA, 29(10), 2050-2061. doi:10.1038/leu.2015.116

2014

Akada, H., Akada, S., Hutchison, R. E., Sakamoto, K., Wagner, K. -U., & Mohi, G. (2014). Critical Role of Jak2 in the Maintenance and Function of Adult Hematopoietic Stem Cells. STEM CELLS, 32(7), 1878-1889. doi:10.1002/stem.1711

Akada, H., Akada, S., Hutchison, R. E., & Mohi, G. (2014). Loss of wild-type Jak2 allele enhances myeloid cell expansion and accelerates myelofibrosis in Jak2V617F knock-in mice. LEUKEMIA, 28(8), 1627-1635. doi:10.1038/leu.2014.52

2012

Yan, D., Hutchison, R. E., & Mohi, G. (2012). Tyrosine 201 is required for constitutive activation of JAK2V617F and efficient induction of myeloproliferative disease in mice. BLOOD, 120(9), 1888-1898. doi:10.1182/blood-2011-09-380808

Akada, H., Akada, S., Gajra, A., Bair, A., Graziano, S., Hutchison, R. E., & Mohi, G. (2012). Efficacy of vorinostat in a murine model of polycythemia vera. BLOOD, 119(16), 3779-3789. doi:10.1182/blood-2011-02-336743

Akada, H., Akada, S., Hutchison, R. E., & Mohi, G. (2012). Erythroid lineage-restricted expression of Jak2V617F is sufficient to induce a myeloproliferative disease in mice. HAEMATOLOGICA-THE HEMATOLOGY JOURNAL, 97(9), 1389-1393. doi:10.3324/haematol.2011.059113

2011

Yan, D., Hutchison, R. E., & Mohi, G. (2012). Critical requirement for Stat5 in a mouse model of polycythemia vera. BLOOD, 119(15), 3539-3549. doi:10.1182/blood-2011-03-345215

Zou, H., Yan, D., & Mohi, G. (2011). Differential biological activity of disease-associated JAK2 mutants. FEBS LETTERS, 585(7), 1007-1013. doi:10.1016/j.febslet.2011.02.032