Rizwan Haq, Ph.D.

Affiliations: 
2003 University of Toronto, Toronto, ON, Canada 
Area:
Neuroscience Biology, Molecular Biology, Animal Physiology Biology
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"Rizwan Haq"
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Brent Zanke grad student 2003 University of Toronto
 (Mitogen -activated protein kinases: Characterization of a novel member and roles in senescence and erythropoietin signal transduction.)
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Publications

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Lauss M, Haq R, Cirenajwis H, et al. (2015) Genome-Wide DNA Methylation Analysis in Melanoma Reveals the Importance of CpG Methylation in MITF Regulation. The Journal of Investigative Dermatology. 135: 1820-8
Frederick DT, Salas Fragomeni RA, Schalck A, et al. (2014) Clinical profiling of BCL-2 family members in the setting of BRAF inhibition offers a rationale for targeting de novo resistance using BH3 mimetics. Plos One. 9: e101286
Konieczkowski DJ, Johannessen CM, Abudayyeh O, et al. (2014) A melanoma cell state distinction influences sensitivity to MAPK pathway inhibitors. Cancer Discovery. 4: 816-27
Haq R, Shoag J, Andreu-Perez P, et al. (2013) Oncogenic BRAF regulates oxidative metabolism via PGC1α and MITF. Cancer Cell. 23: 302-15
Haq R, Yokoyama S, Hawryluk EB, et al. (2013) BCL2A1 is a lineage-specific antiapoptotic melanoma oncogene that confers resistance to BRAF inhibition. Proceedings of the National Academy of Sciences of the United States of America. 110: 4321-6
Shoag J, Haq R, Zhang M, et al. (2013) PGC-1 coactivators regulate MITF and the tanning response. Molecular Cell. 49: 145-57
Li J, Song JS, Bell RJ, et al. (2012) YY1 regulates melanocyte development and function by cooperating with MITF. Plos Genetics. 8: e1002688
Yokoyama S, Woods SL, Boyle GM, et al. (2011) A novel recurrent mutation in MITF predisposes to familial and sporadic melanoma. Nature. 480: 99-103
Haq R, Brenton JD, Takahashi M, et al. (2002) Constitutive p38HOG mitogen-activated protein kinase activation induces permanent cell cycle arrest and senescence. Cancer Research. 62: 5076-82
Ho JM, Nguyen MH, Dierov JK, et al. (2002) TEL-JAK2 constitutively activates the extracellular signal-regulated kinase (ERK), stress-activated protein/Jun kinase (SAPK/JNK), and p38 signaling pathways. Blood. 100: 1438-48
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