Expression of death-associated protein kinase during tumour progression of human renal cell carcinomas: Hypermethylation-independent mechanisms of inactivation (original) (raw)

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Inhibition of MAPK Kinase Signaling Pathways Suppressed Renal Cell Carcinoma Growth and Angiogenesis In vivo

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Association of Protein Expression and Methylation of DAPK1 with Clinicopathological Features in Invasive Ductal Carcinoma Patients from Kashmir

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Note: Supplementary data for this article are available at Cancer Discovery

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612 PD-0332991, AN INHIBITOR OF CYCLIN-DEPENDENT KINASE 4/6, DEMONSTRATES INHIBITION OF PROLIFERATION IN RENAL CELL CARCINOMA AT NANOMOLAR CONCENTRATIONS AND MOLECULAR MARKERS PREDICT FOR SENSITIVITY

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Bidirectional signals transduced by DAPK–ERK interaction promote the apoptotic effect of DAPK

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Control of Death-associated Protein Kinase (DAPK) Activity by Phosphorylation and Proteasomal Degradation

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A Germ Line Mutation in the Death Domain of DAPK-1 Inactivates ERK-induced Apoptosis

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DAP-kinase is a Ca2+/calmodulin-dependent, cytoskeletal-associated protein kinase, with cell death-inducing functions that depend on its catalytic activity

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DOK4/IRS-5 expression is altered in clear cell renal cell carcinoma

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Autophosphorylation restrains the apoptotic activity of DRP-1 kinase by controlling dimerization and calmodulin binding

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The apoptosis associated tyrosine kinase gene is frequently hypermethylated in human cancer and is regulated by epigenetic mechanisms

Tanja Haag

Genes & cancer, 2014

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