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Literature summary for 1.14.11.67 extracted from

  • Vasconez, A.E.; Janetzko, P.; Oo, J.A.; Pflueger-Mueller, B.; Ratiu, C.; Gu, L.; Helin, K.; Geisslinger, G.; Fleming, I.; Schroeder, K.; Fork, C.; Brandes, R.P.; Leisegang, M.S.
    The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3UTR of soluble epoxide hydrolase (2019), Acta Physiol. (Oxf.), 225, e13168 .
    View publication on PubMed
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Organism

Organism UniProt Comment Textmining
Mus musculus Q80Y84
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Synonyms

Synonyms Comment Organism
JARID1B
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 Mus musculus
KDM5B
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 Mus musculus

General Information

General Information Comment Organism
physiological function knockout or inhibition of Jarid1b prevents the development of endothelial dysfunction in response to angiotensin AngII, accompanied by a loss of the inflammatory response to AngII. AngII induces the soluble epoxide hydrolase (sEH). Knockout or inhibition of Jarid1b prevents the AngII-mediated sEH induction. Jarid1b maintains the length of the 3'-untranslated region of the sEH mRNA, thereby increasing its stability and thus sEH protein expression Mus musculus