Interleukin-1 receptor-associated kinase: Difference between revisions

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*IRAK4
*IRAK4


**[[2nru]], [[2nry]], [[2oib]], [[2o8y]] – hIRAK4 kinase domain - human<br />
**[[2nru]], [[2nry]], [[2oib]], [[2o8y]], [[4rmz]] – hIRAK4 kinase domain - human<br />
**[[4u97]], [[4u9a]] - hIRAK4 kinase domain (mutant)<br />
**[[4u97]], [[4u9a]] - hIRAK4 kinase domain (mutant)<br />
**[[1wh4]] – mIRAK4 DEATH domain – mouse – NMR<br />
**[[1wh4]] – mIRAK4 DEATH domain – mouse – NMR<br />
**[[2a9i]] - mIRAK4 DEATH domain<br />
**[[2a9i]] - mIRAK4 DEATH domain<br />
**[[2oic]], [[4xs2]] - hIRAK4 kinase domain + staurosporine<br />
**[[2oic]], [[4xs2]] - hIRAK4 kinase domain + staurosporine<br />
**[[4y73]], [[4yo6]], [[4yp8]], [[4ztl]], [[4ztm]], [[4ztn]] - hIRAK4 kinase domain + inhibitor<br />
**[[4y73]], [[4yo6]], [[4yp8]], [[4ztl]], [[4ztm]], [[4ztn]], [[5kx7]], [[5kx8]], [[5t1s]], [[5t1t]], [[5uiq]], [[5uir]], [[5uis]], [[5uit]], [[5uiu]]  - hIRAK4 kinase domain + inhibitor<br />
**[[2oid]] - hIRAK4 kinase domain + AMPPNP<br />
**[[2oid]] - hIRAK4 kinase domain + AMPPNP<br />
 
**[[3mop]] - hIRAK4 DEATH domain + hIRAK2 DEATH domain + MYD88<br />
}}
}}
== References ==
== References ==

Revision as of 11:57, 22 June 2017

Function

Interleukin-1 receptor-associated kinase (IRAK) is a kinase involved in signaling innate immune responses from Toll-like receptors and interleukin-1 receptor-related proteins[1].

Relevance

IRAK4 is involved in early recognition of pathogens and the initiation of inflammation when fighting infection.

Disease

IRAK4 deficiency is a disorder which causes recurrent bacterial infections.

Mouse IRAK4 death domain complex with Mn+2 ion , 2a9i

Drag the structure with the mouse to rotate

3D structures of IRAK43D structures of IRAK4

Updated on 22-June-2017

ReferencesReferences

  1. Cao Z, Henzel WJ, Gao X. IRAK: a kinase associated with the interleukin-1 receptor. Science. 1996 Feb 23;271(5252):1128-31. PMID:8599092

Proteopedia Page Contributors and Editors (what is this?)Proteopedia Page Contributors and Editors (what is this?)

Michal Harel, Alexander Berchansky, Jaime Prilusky