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BLK Kinase  Protéine

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Hôte d’expression: Baculovirus-Insect Cells  
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BLK Kinase Voies apparentées

BLK Kinase Produits apparentés

BLK Kinase Produits apparentés

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BLK Kinase Récapitulatif et informations sur les protéines

BLK Kinase Fond

Résumé du gène: This BLK gene encodes a nonreceptor tyrosine-kinase of the src family of proto-oncogenes that are typically involved in cell proliferation and differentiation. B Lymphoid Tyrosine Kinase protein has a role in B-cell receptor signaling and B-cell development. BLK protein also stimulates insulin synthesis and secretion in response to glucose and enhances the expression of several pancreatic beta-cell transcription factors. [provided by RefSeq, Aug 2010]
General information above from NCBI
Activité catalytique: ATP + a [protein]-L-tyrosine = ADP + a [protein]-L-tyrosine phosphate.
Régulation enzymatique: Antibody-mediated surface engagement of the B- cell antigen receptor (BCR) which results in the phosphorylation of BLK on tyrosine residues, stimulates the enzymatic activity (By similarity).
Structure de sous-unités: Interacts with CBL (via SH2 domain). Interacts with CD79A and CD79B (via SH2 domain) (By similarity).
Localisation subcellulaire: Cell membrane; Lipid-anchor (By similarity). Note=Present and active in lipid rafts. Membrane location is required for the phosphorylation of CD79A and CD79B (By similarity).
Spécificité tissulaire: Expressed in lymphatic organs, pancreatic islets, Leydig cells, striate ducts of salivary glands and hair follicles.
Induction: Expression is under the control of NF-kappa-B as well as the B-cell specific transcription factors PAX5 and EBF1.
Post-traductionnel: Phosphorylated on tyrosine residues after antibody-mediated surface engagement of the B-cell antigen receptor (BCR) (By similarity).
Ubiquitination of activated BLK by the UBE3A ubiquitin protein ligase leads to its degradation by the ubiquitin- proteasome pathway (By similarity).
Implication dans la maladie: Maturity-onset diabetes of the young 11 (MODY11) [MIM:613375]: A form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease. Note=The disease is caused by mutations affecting the gene represented in this entry.
Similarité de séquence: Belongs to the protein kinase superfamily. Tyr protein kinase family. SRC subfamily.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
Contains 1 SH3 domain.C
General information above from UniProt

Tyrosine-protein kinase Blk, also known as B lymphocyte kinase, p55-Blk and BLK, is a member of the protein kinase superfamily, Tyr protein kinase family and SRC subfamily. BLK / p55-Blk is expressed in lymphatic organs, pancreatic islets, Leydig cells, striate ducts of salivary glands and hair follicles. BLK / p55-Blk is a src-family protein tyrosine kinase specifically expressed in B-lineage cells of mice. The early onset of Blk expression during B-cell development in the bone marrow and the high expression levels of Blk in mature B cells suggest a possible important role of Blk in B-cell physiology. It is a modulator of beta-cells function, acting through the up-regulation of PDX1 and NKX6-1 and consequent stimulation of insulin secretion in response to glucose. Defects in BLK are a cause of maturity-onset diabetes of the young type 11 which is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.

BLK Kinase Autre dénomination

MODY11, [homo-sapiens]
BLK,MGC10442,MODY11, [human]
Blk,p55-Blk, [mouse]

BLK Kinase Études apparentées

  • Dymecki,S.M. et al., 1992, J Biol Chem. 267 (7):4815-23.
  • Drebin J.A. et al., 1995, Oncogene 10:477-86.
  • Islam K.B.et al., 1995, J. Immunol. 154:1265-72.
  • Texido,G. et al., 2000, Mol Cell Biol. 20 (4):1227-33.
  • Borowiec M. et al., 2009, Proc. Natl. Acad. Sci. USA. 106: 14460-5.
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