RGD Reference Report - Inhibitory receptor signaling via tyrosine phosphorylation of the adaptor Crk. - Rat Genome Database

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Inhibitory receptor signaling via tyrosine phosphorylation of the adaptor Crk.

Authors: Peterson, ME  Long, EO 
Citation: Peterson ME and Long EO, Immunity. 2008 Oct 17;29(4):578-88. doi: 10.1016/j.immuni.2008.07.014. Epub 2008 Oct 2.
RGD ID: 11568650
Pubmed: PMID:18835194   (View Abstract at PubMed)
PMCID: PMC2639764   (View Article at PubMed Central)
DOI: DOI:10.1016/j.immuni.2008.07.014   (Journal Full-text)

Many cellular responses, such as autoimmunity and cytotoxicity, are controlled by receptors with cytoplasmic immunoreceptor tyrosine-based inhibition motifs (ITIMs). Here, we showed that binding of inhibitory natural killer (NK) cell receptors to human leukocyte antigen (HLA) class I on target cells induced tyrosine phosphorylation of the adaptor Crk, concomitant with dephosphorylation of the guanine exchange factor Vav1. Furthermore, Crk dissociated from the guanine exchange factor C3G and bound to the tyrosine kinase c-Abl during inhibition. Membrane targeting of a tyrosine-mutated form of Crk could overcome inhibition of NK cell cytotoxicity, providing functional evidence that Crk phosphorylation contributes to inhibition. The specific phosphorylation of Crk and its dissociation from a signaling complex, observed here with two types of inhibitory receptors, expands the signaling potential of the large ITIM-receptor family and reveals an unsuspected component of the inhibitory mechanism.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
negative regulation of natural killer cell mediated cytotoxicity  IMP 11568650 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Crk  (CRK proto-oncogene, adaptor protein)


Additional Information