G beta-gamma complex and PIP3 recruit BTK to membrane

Stable Identifier
Reaction [binding]
Homo sapiens
Locations in the PathwayBrowser
SVG |   | PPTX  | SBGN
Click the image above or here to open this reaction in the Pathway Browser
The layout of this reaction may differ from that in the pathway view due to the constraints in pathway layout

G-Protein Coupled Receptors (GPCR) sense extracellular signals and activate different Guanine nucleotide binding proteins (G-proteins) that have alpha, beta and gamma subunits. Upon activation, the alpha subunit of G-proteins dissociates from beta-gamma and the both are then free to regulate downstream effectors. G-protein beta-gamma complex, along with phosphatidylinositol 3,4,5-trisphosphate (PIP3), recruits the non-receptor Tyrosine-protein kinase BTK to the cell membrane. This recruitment involves binding of the G-protein beta-gamma complex to the pleckstrin homology/Tec-homology module of Btk. Here, BTK is activated and subsequently released to the cytoplasm. Physiologically, BTK plays a key role in B lymphocyte development, differentiation and signalling.

Literature References
PubMed ID Title Journal Year
11698416 G Protein beta gamma subunits act on the catalytic domain to stimulate Bruton's agammaglobulinemia tyrosine kinase

Huang, XY, Lowry, WE

J. Biol. Chem. 2002
7567982 Activation of Tsk and Btk tyrosine kinases by G protein beta gamma subunits

Huang, XY, Wan, Y, Langhans-Rajasekaran, SA

Proc. Natl. Acad. Sci. U.S.A. 1995
Orthologous Events
Cite Us!