View source for Janus kinase

<StructureSection load='' size='350' side='right' scene='54/543313/Cv/1' caption='JAK2 kinase domain complex with inhibitor thienopyridine [[3tjc]]'>

== Function ==
'''Janus kinase''' or '''tyrosine-protein kinase JAK''' (JAK) are nonreceptor tyrosine kinases which transduces cytokine-mediated signals via the [[JAK-STAT pathway]]. The JAK-STAT pathway transmits signals through the cell membrane to DNA promoters thus causing transcription.  The name JAK is derived from Just Another Kinase.  JAK proteins contain 2 phosphate-transfer domains, one with kinase activity using a phosphotyrosine (PTyr) and the other a pseudokinase domain which negatively regulates the kinase domain.  JAK contains seven Janus homology domains named JH1-7.  JAK family members are JAK1, JAK2, JAK3 and TYK2<ref>PMID:9382798</ref>.<br />  '''JAK1''' and TYK2 are involved in signaling by members of type I and type II cytokine receptors.<br />  '''JAK2''' is involved in signaling by members of the interferon receptors (type II cytokines).<br />  '''JAK3''' is predominantly active in immune cells.  JAK3 is activated by cytokines whose receptors contain the common γ chain subunit (interleukin 2,4,7,9,15,21).<br />  '''TYK2''' is a component of type I and type III interferon signaling pathways. 

See [[Tyrosine kinase]]. 

== Relevance ==
Jak3 inhibitors are tested in treatment of autoimmune diseases and transplant rejection<ref>PMID:23532440</ref>.

== Disease ==
Mutations in Jak2 are associated with chronic myeloproliferative neoplasms, polycythemia vera, essential thrombocytosis and primary myelofibrosis<ref>PMID:19393837</ref>.  Mutations in Jak3 are associated with immune deficiency.

== Structural highlights ==
Jak2 containing <scene name='54/543313/Cv/5'>phosphotyrosine</scene> binds the <scene name='54/543313/Cv/6'>thienopyridine potent inhibitor</scene> in the ATP-binding pocket<ref>PMID:22087750</ref>. Water molecules shown as red spheres.

== 3D Structures of Janus kinase ==
[[Janus kinase 3D structures]]

</StructureSection>

== References ==
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