Varaico: Literature-Extracted Genetic Variants

Gene:KIT
Variant:p.Y568F
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KIT

NM_000222.3:p.Y568F

Associated Papers

CRISPR/Cas9-engineering of HMC-1.2 cells renders a human mast cell line with a single D816V-KIT mutation: An improved preclinical model for research on mastocytosis.

Bandara G et al.

Frontiers in Immunology, 2023

XK-related protein 5 (XKR5) is a novel negative regulator of KIT/D816V-mediated transformation.

Sun J et al.

Oncogenesis, 2018

Activating c-KIT mutations confer oncogenic cooperativity and rescue RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors.

Wichmann C et al.

Leukemia, 2015

KIT-D816V oncogenic activity is controlled by the juxtamembrane docking site Y568-Y570.

Chaix A et al.

Oncogene, 2014

Src-like-adaptor protein (SLAP) differentially regulates normal and oncogenic c-Kit signaling.

Kazi JU et al.

Journal of Cell Science, 2014

The D816V mutation of c-Kit circumvents a requirement for Src family kinases in c-Kit signal transduction.

Sun J et al.

The Journal of Biological Chemistry, 2009

Direct binding of Cbl to Tyr568 and Tyr936 of the stem cell factor receptor/c-Kit is required for ligand-induced ubiquitination, internalization and degradation.

Masson K et al.

The Biochemical Journal, 2006

Identification of Tyr900 in the kinase domain of c-Kit as a Src-dependent phosphorylation site mediating interaction with c-Crk.

Lennartsson J et al.

Experimental Cell Research, 2003

Phosphorylation of Shc by Src family kinases is necessary for stem cell factor receptor/c-kit mediated activation of the Ras/MAP kinase pathway and c-fos induction.

Lennartsson J et al.

Oncogene, 1999

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Regarding the variants extracted from papers and shown text snippets from research papers, the following holds: "Some rights reserved. This work permits non-commercial use, distribution and reproduction in any medium, provided the original author and source are credited."