Varaico: Literature-Extracted Genetic Variants

Gene:BCR
Variant:p.Y177F
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BCR

NM_004327.4:p.Y177F

Associated Papers

Proteomic analysis reveals dual requirement for Grb2 and PLCγ1 interactions for BCR-FGFR1-Driven 8p11 cell proliferation.

Peiris MN et al.

Oncotarget, 2022

Critical individual roles of the BCR and FGFR1 kinase domains in BCR-FGFR1-driven stem cell leukemia/lymphoma syndrome.

Chong Y et al.

International Journal of Cancer, 2020

Breakpoint Cluster Region-Mediated Inflammation Is Dependent on Casein Kinase II.

Meng J et al.

Journal of Immunology (baltimore, Md. : 1950), 2016

BCR: a new target in resistance mediated by BCR/ABL-315I?

Haberbosch I et al.

Genes & Cancer, 2016

Regulation of dendritic arborization by BCR Rac1 GTPase-activating protein, a substrate of PTPRT.

Park AR et al.

Journal of Cell Science, 2012

Tyrosine kinase gene fusions in cancer: translating mechanisms into targeted therapies.

Medves S et al.

Journal of Cellular and Molecular Medicine, 2012

BCR-tyrosine 177 plays an essential role in Ras and Akt activation and in human hematopoietic progenitor transformation in chronic myelogenous leukemia.

Chu S et al.

Cancer Research, 2007

BCR/ABL kinase induces self-mutagenesis via reactive oxygen species to encode imatinib resistance.

Koptyra M et al.

Blood, 2006

Distinct stem cell myeloproliferative/T lymphoma syndromes induced by ZNF198-FGFR1 and BCR-FGFR1 fusion genes from 8p11 translocations.

Roumiantsev S et al.

Cancer Cell, 2004

Coexistence of phosphotyrosine-dependent and -independent interactions between Cbl and Bcr-Abl.

Gaston I et al.

Experimental Hematology, 2004

Bcr: a negative regulator of the Bcr-Abl oncoprotein in leukemia.

Arlinghaus RB

Oncogene, 2002

Critical role for Gab2 in transformation by BCR/ABL.

Sattler M et al.

Cancer Cell, 2002

Inhibition of the Bcr-Abl oncoprotein by Bcr requires phosphoserine 354.

Hawk N et al.

Cancer Research, 2002

Molecular cloning of Ian4: a BCR/ABL-induced gene that encodes an outer membrane mitochondrial protein with GTP-binding activity.

Dahéron L et al.

Nucleic Acids Research, 2001

Signal transducer and activator of transcription (STAT)5 activation by BCR/ABL is dependent on intact Src homology (SH)3 and SH2 domains of BCR/ABL and is required for leukemogenesis.

Nieborowska-Skorska M et al.

The Journal of Experimental Medicine, 1999

Expression of constitutively active Raf-1 in the mitochondria restores antiapoptotic and leukemogenic potential of a transformation-deficient BCR/ABL mutant.

Salomoni P et al.

The Journal of Experimental Medicine, 1998

Requirement of two specific tyrosine residues for the catalytic activity of Bcr serine/threonine kinase.

Wu Y et al.

Oncogene, 1998

Transformation of hematopoietic cells by BCR/ABL requires activation of a PI-3k/Akt-dependent pathway.

Skorski T et al.

The Embo Journal, 1997

Bcr phosphorylated on tyrosine 177 binds Grb2.

Ma G et al.

Oncogene, 1997

Tyrosine phosphorylation of p120cbl in BCR/abl transformed hematopoietic cells mediates enhanced association with phosphatidylinositol 3-kinase.

Jain SK et al.

Oncogene, 1997

Co-expression with BCR induces activation of the FES tyrosine kinase and phosphorylation of specific N-terminal BCR tyrosine residues.

Li J et al.

The Journal of Biological Chemistry, 1996

The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene.

Senechal K et al.

The Journal of Biological Chemistry, 1996

The dimerization property of glutathione S-transferase partially reactivates Bcr-Abl lacking the oligomerization domain.

Maru Y et al.

The Journal of Biological Chemistry, 1996

Inhibition of Bcr serine kinase by tyrosine phosphorylation.

Liu J et al.

Molecular and Cellular Biology, 1996

Structural and signaling requirements for BCR-ABL-mediated transformation and inhibition of apoptosis.

Cortez D et al.

Molecular and Cellular Biology, 1995

BCR-ABL-induced oncogenesis is mediated by direct interaction with the SH2 domain of the GRB-2 adaptor protein.

Pendergast AM et al.

Cell, 1993

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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."