Dr. Mamduh Khateb is a postdoctoral fellow in the Laboratory of Muscle Stem Cells & Gene Regulation at NIAMS (NIH). Before his current postdoctoral fellowship at the NIH, he completed postdoctoral research in embryonic stem cells and gene regulation at the Technion-Israel Institute of Technology. Dr. Khateb finished his Ph.D. studies in the Technion, where he became interested in investigating the gene regulation during hematopoiesis lineage. In particular, he focused on the Interferon Regulatory Factor 8 (IRF8) gene that plays an important role in monocytes, macrophages, and dendritic cell generation. During his Ph.D. studies, Dr. Khateb was an assistant teacher for students in undergraduate studies. 

Research Statement

Cell fate specification is a key process enabling the formation of multicellular organisms. Totipotent embryonic stem cells (ESC) remodel their epigenome to acquire particular cell fates and form different tissues. The transitions of the epigenetic landscape accompanying the acquisition of the myogenic lineage starting from ESC are largely unknown. I am interested in defining the epigenetic changes occurring during myogenic lineage specification and providing insight into molecular mechanisms of early muscle fate acquisition. More specifically, I am interested in identifying the regulatory element(s) regulating the Muscle Stem Cells (MuSC) regulator, PAX7.

Scientific Publications

The Third Intron of IRF8 Is a Cell-Type-Specific Chromatin Priming Element during Mouse Embryonal Stem Cell Differentiation.

Khateb M, Azriel A, Levi BZ
J Mol Biol.
2019 Jan 18;
doi: 10.1016/j.jmb.2018.11.022
PMID: 30502383

The Third Intron of the Interferon Regulatory Factor-8 Is an Initiator of Repressed Chromatin Restricting Its Expression in Non-Immune Cells.

Khateb M, Fourier N, Barnea-Yizhar O, Ram S, Kovalev E, Azriel A, Rand U, Nakayama M, Hauser H, Gepstein L, Levi BZ
PLoS One.
doi: 10.1371/journal.pone.0156812
PMID: 27257682

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism.

Khateb M, Ruimi N, Khamisie H, Najajreh Y, Mian A, Metodieva A, Ruthardt M, Mahajna J
BMC Cancer.
2012 Nov 27;
doi: 10.1186/1471-2407-12-563
PMID: 23186157

Allosteric inhibition enhances the efficacy of ABL kinase inhibitors to target unmutated BCR-ABL and BCR-ABL-T315I.

Mian AA, Metodieva A, Badura S, Khateb M, Ruimi N, Najajreh Y, Ottmann OG, Mahajna J, Ruthardt M
BMC Cancer.
2012 Sep 17;
doi: 10.1186/1471-2407-12-411
PMID: 22985168
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