Dok1 promotes adipocyte hypertrophy, state scientists of the Kobe University in Japan. The protein antagonises the inhibitory effect of ERK on peroxisome proliferator-activated receptor (PPAR)-γ and may predispose the individual to diet-induced obesity.

The study showed that Dok1 regulates adiposity. Mice on a high-fat diet expressed Dok1 stronger in their white adipose tissue. Adipocytes without this adapter were smaller and did not respond as strongly to the dietary manipulation. Dok1-deficient mice were leaner and exhibited enhanced glucose tolerance and insulin sensitivity in comparison to wild-type mice. In a different experiment the scientists looked at embryonic fibroblasts from Dok1-deficient mice. They were impaired in their adipogenic differentiation. This defect was accompanied by an increased activity of the protein kinase ERK and a consecutive increase in the phosphorylation of PPAR-γ on Ser112. When this site is mutated, the development of the lean phenotype is blocked because Dok1 remains absent. Insulin receptor substrate (IRS)-1 and IRS-2 have dominant roles in the action of insulin1, but other substrates of the insulin receptor kinase, such as Gab1, c-Cbl, SH2-B and APS, are also physiologically relevant. The protein downstream of tyrosine kinases-1 (Dok1) is known to function as a multi-site adapter molecule in insulin signalling.

Related antibodies on antibodies-online.com:

Dok1

Adipocytes

Insulin

Gab1

c-Cbl

SH2-B

APS

PPAR-γ

ERK

Fibroblasts

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