JAK2 Autophosphorylates in Response to Leptin

Stable Identifier
R-HSA-2586555
Type
Reaction [transition]
Species
Homo sapiens
Compartment
plasma membrane, cytosol
ReviewStatus
5/5
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JAK2 Autophosphorylates in Response to Leptin
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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. As inferred from mouse, the kinase inhibitory domain of SOCS3 interacts with the activation loop of jAK2 and inhibits the phosphorylation of 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
Input
Output
Participates
as an event of
Catalyst Activity

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

Physical Entity
LEP:LEPR:JAK2 [plasma membrane] (Homo sapiens)
Activity
protein tyrosine kinase activity (GO:0004713)
This event is regulated
Negatively by
Regulator
LEP:p-LEPR:p-JAK2:SOCS3 [plasma membrane] (Homo sapiens)
Inferred From
Jak2 Autophosphorylates in Response to Leptin (Mus musculus)
Authored
May, B  (2012-11-15)
Reviewed
Scherer, T  (2013-08-31)
Gonzalez-Perez, RR  (2013-10-26)
Created
May, B  (2012-11-15)
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