JAK2 Autophosphorylates in Response to Leptin

Stable Identifier
R-HSA-2586555
Type
Reaction [transition]
Species
Homo sapiens
Compartment
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As inferred from mouse, binding of Leptin (LEP) to the Leptin receptor (LEPR) causes a conformational change in LEPR that activates autophosphorylation of JAK2 at multiple tyrosine residues. Phosphorylated JAK2 has much higher kinase activity than unphosphorylated JAK2.

Literature References
PubMed ID Title Journal Year
10514492 The role of SOCS-3 in leptin signaling and leptin resistance

Bjørbaek, C, El-Haschimi, K, Frantz, JD, Flier, JS

J. Biol. Chem. 1999
Participants
Participates
Catalyst Activity

protein tyrosine kinase activity of LEP:LEPR:JAK2 [plasma membrane]

This event is regulated
Negatively by
Regulator
Summation

As inferred from mouse, the kinase inhibitory domain of SOCS3 interacts with the activation loop of jAK2 and inhibits the phosphorylation of JAK2.

Inferred From
Authored
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