The CRKL adaptor protein transforms fibroblasts and functions in transformation by the BCR-ABL oncogene (Q24321680)

Ras protein signal transduction

GOA release 2020-03-11

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Journal of Biological Chemistry

GOA release 2020-03-11

author name string

K Senechal

series ordinal

1

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J Halpern

series ordinal

2

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C L Sawyers

series ordinal

3

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language of work or name

English

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publication date

20 September 1996

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published in

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volume

271

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issue

38

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page(s)

23255-61

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cites work

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c-Abl kinase regulates the protein binding activity of c-Crk

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Dominant negative MYC blocks transformation by ABL oncogenes

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A novel transforming protein (SHC) with an SH2 domain is implicated in mitogenic signal transduction

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An SH3-SH2-SH3 protein is required for p21Ras1 activation and binds to sevenless and Sos proteins in vitro

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A Drosophila SH2-SH3 adaptor protein implicated in coupling the sevenless tyrosine kinase to an activator of Ras guanine nucleotide exchange, Sos.

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

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Alternative signals to RAS for hematopoietic transformation by the BCR-ABL oncogene

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Specificity of receptor tyrosine kinase signaling: transient versus sustained extracellular signal-regulated kinase activation

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SH2 and SH3 domains as molecular adhesives: the interactions of Crk and Abl

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Evidence that SH2 domains promote processive phosphorylation by protein-tyrosine kinases

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Altered adhesive interactions with marrow stroma of haematopoietic progenitor cells in chronic myeloid leukaemia

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A novel viral oncogene with structural similarity to phospholipase C

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Acute leukaemia in bcr/abl transgenic mice

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C. elegans cell-signalling gene sem-5 encodes a protein with SH2 and SH3 domains

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Protein modules and signalling networks

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Direct demonstration of an intramolecular SH2-phosphotyrosine interaction in the Crk protein

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The molecular genetics of Philadelphia chromosome-positive leukemias

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In vitro transformation of immature hematopoietic cells by the P210 BCR/ABL oncogene product of the Philadelphia chromosome

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Induction of a chronic myelogenous leukemia-like syndrome in mice with v-abl and BCR/ABL.

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The Bcr-Abl leukemia oncogene activates Jun kinase and requires Jun for transformation

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Molecular cloning of human paxillin, a focal adhesion protein phosphorylated by P210BCR/ABL

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v-Crk modulation of growth factor-induced PC12 cell differentiation involves the Src homology 2 domain of v-Crk and sustained activation of the Ras/mitogen-activated protein kinase pathway

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Crkl is complexed with tyrosine-phosphorylated Cbl in Ph-positive leukemia

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CRKL links p210BCR/ABL with paxillin in chronic myelogenous leukemia cells

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Possible v-Crk-induced transformation through activation of Src kinases.

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Novel tyrosine kinase substrates from Rous sarcoma virus-transformed cells are present in the membrane skeleton

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Paxillin: a new vinculin-binding protein present in focal adhesions

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Coupling between p210bcr-abl and Shc and Grb2 adaptor proteins in hematopoietic cells permits growth factor receptor-independent link to ras activation pathway

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Negative regulation of p120GAP GTPase promoting activity by p210bcr/abl: implication for RAS-dependent Philadelphia chromosome positive cell growth

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Genetic requirement for Ras in the transformation of fibroblasts and hematopoietic cells by the Bcr-Abl oncogene

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The human GRB2 and Drosophila Drk genes can functionally replace the Caenorhabditis elegans cell signaling gene sem-5.

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Paxillin, a tyrosine phosphorylated focal adhesion-associated protein binds to the carboxyl terminal domain of focal adhesion kinase

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Abl protein-tyrosine kinase selects the Crk adapter as a substrate using SH3-binding sites

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Induction of chronic myelogenous leukemia in mice by the P210bcr/abl gene of the Philadelphia chromosome

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Differential complementation of Bcr-Abl point mutants with c-Myc

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Identification of a ten-amino acid proline-rich SH3 binding site

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BCR first exon sequences specifically activate the BCR/ABL tyrosine kinase oncogene of Philadelphia chromosome-positive human leukemias

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Activation of c-Src in cells bearing v-Crk and its suppression by Csk

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The SH2- and SH3-containing Nck protein transforms mammalian fibroblasts in the absence of elevated phosphotyrosine levels

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A 41-kilodalton protein is a potential substrate for the p210bcr-abl protein-tyrosine kinase in chronic myelogenous leukemia cells

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Two species of human CRK cDNA encode proteins with distinct biological activities

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SH1 domain autophosphorylation of P210 BCR/ABL is required for transformation but not growth factor independence

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Both the SH2 and SH3 domains of human CRK protein are required for neuronal differentiation of PC12 cells

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CRK protein binds to two guanine nucleotide-releasing proteins for the Ras family and modulates nerve growth factor-induced activation of Ras in PC12 cells

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

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Differential inhibition of signaling pathways by dominant-negative SH2/SH3 adapter proteins

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pp125FAK-dependent tyrosine phosphorylation of paxillin creates a high-affinity binding site for Crk

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7 January 2021

The product of the cbl oncogene forms stable complexes in vivo with endogenous Crk in a tyrosine phosphorylation-dependent manner

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7 January 2021

Inhibition of NIH 3T3 cell proliferation by a mutant ras protein with preferential affinity for GDP.

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7 January 2021

The BCR-ABL oncogene transforms Rat-1 cells and cooperates with v-myc

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Expression of raf oncogenes activates the PEA1 transcription factor motif

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Identifiers

DOI

10.1074/JBC.271.38.23255

1 reference

Consolidated OpenCitations Corpus – April 2017

3404642

3404642

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

1 reference