High impact information on Dok3

• Here, we demonstrate that Dok-3 suppresses B-cell activation by way of its interaction with SHIP-1, rather than Csk [1].
• Together, these data elucidate the mechanism by which Dok-3 inhibits B-cell activation [1].
• Dok-3 is a Dok-related adaptor expressed in B cells and macrophages [1].
• Herein, we report the identification of Dok-3, a novel adapter molecule belonging to the Dok family [2].
• Our studies show that Dok-3 is highly expressed in several hemopoietic cell types, including B cells and macrophages [2].

Biological context of Dok3

• This phosphorylation induces the binding of Dok-3 to at least two inhibitory molecules, the 5' inositol phosphatase SHIP and the protein tyrosine kinase Csk [2].

Anatomical context of Dok3

• Finally, overexpression of DOKL in NIH 3T3 cells inhibits the transforming activity of v-Abl [3].
• The DOKL gene is predominantly expressed in bone marrow, spleen, and lung, although low-level expression of the RNA can also be detected in other tissues [3].

Associations of Dok3 with chemical compounds

• DOKL is phosphorylated by the Abl tyrosine kinase in vivo [3].

Other interactions of Dok3

• Overexpression of DOKL, but not p62(dok), suppresses v-Abl-induced mitogen-activated protein (MAP) kinase activation but has no effect on constitutively activated Ras- and epidermal growth factor-induced MAP kinase activation [3].
• In the absence of Dok-3, the localization of the inhibitory phosphatase SHIP-1 to the plasma membrane is intact while its phosphorylation is compromised, suggesting that Dok-3 could function to facilitate or sustain the activation of SHIP-1 [4].

References