Summary of TRIB3

TRIB3 causes insulin resistance. TRIB3 is induced by the transcription factor NF-kappaB. It disrupts insulin signaling by binding directly to Akt kinases and blocking their activation.


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The Function of TRIB3

Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. Binds to ATF4 and inhibits its transcriptional activation activity. Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. Interacts with MAPK kinases and regulates activation of MAP kinases. May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. Does not display kinase activity. Inhibits the transcriptional activity of DDIT3/CHOP and is involved in DDIT3/CHOP-dependent cell death during ER stress. Can inhibit APOBEC3A editing of nuclear DNA.

Protein names

Recommended name:

Tribbles homolog 3

Short name:

SINK

Alternative name(s):

TRB-3
Neuronal cell death-inducible putative kinase
p65-interacting inhibitor of NF-kappa-B

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Top Gene-Substance Interactions

TRIB3 Interacts with These Diseases

Substances That Increase TRIB3

Substances That Decrease TRIB3

Advanced Summary

Conditions with Increased Gene Activity

Conditions with Decreased Gene Activity

Technical