Brent Zanke

Affiliations: 
University of Toronto, Toronto, ON, Canada 
Area:
Neuroscience Biology, Molecular Biology, Animal Physiology Biology
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"Brent Zanke"
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Publications

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Yee KW, Moore SJ, Midmer M, et al. (2003) NKIAMRE, a novel conserved CDC2-related kinase with features of both mitogen-activated protein kinases and cyclin-dependent kinases. Biochemical and Biophysical Research Communications. 308: 784-92
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
Haq R, Halupa A, Beattie BK, et al. (2002) Regulation of erythropoietin-induced STAT serine phosphorylation by distinct mitogen-activated protein kinases. The Journal of Biological Chemistry. 277: 17359-66
Gronda M, Arab S, Iafrate B, et al. (2001) Hematopoietic protein tyrosine phosphatase suppresses extracellular stimulus-regulated kinase activation Molecular and Cellular Biology. 21: 6851-6858
Haq R, Randall S, Midmer M, et al. (2001) NKIATRE is a novel conserved cdc2-related kinase. Genomics. 71: 131-41
Jones NL, Islur A, Haq R, et al. (2000) Escherichia coli Shiga toxins induce apoptosis in epithelial cells that is regulated by the Bcl-2 family. American Journal of Physiology. Gastrointestinal and Liver Physiology. 278: G811-9
Midmer M, Haq R, Squire JA, et al. (1999) Identification of NKIAMRE, the human homologue to the mitogen-activated protein kinase-/cyclin-dependent kinase-related protein kinase NKIATRE, and its loss in leukemic blasts with chromosome arm 5q deletion Cancer Research. 59: 4069-4074
Haq R, Zanke B. (1998) Inhibition of apoptotic signaling pathways in cancer cells as a mechanism of chemotherapy resistance. Cancer Metastasis Reviews. 17: 233-9
Zanke BW, Lee C, Arab S, et al. (1998) Death of tumor cells after intracellular acidification is dependent on stress-activated protein kinases (SAPK/JNK) pathway activation and cannot be inhibited by Bcl-2 expression or interleukin 1β-converting enzyme inhibition Cancer Research. 58: 2801-2808
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