Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 1.14.11.68 extracted from

  • Na, J.; Lee, K.; Na, W.; Shin, J.; Lee, M.; Yune, T.; Lee, H.; Jung, H.; Kim, W.; Ju, B.
    Histone H3K27 demethylase JMJD3 in cooperation with NF-kappaB regulates keratinocyte wound healing (2016), J. Invest. Dermatol., 136, 847-858 .
No PubMed abstract available

Application

Application Comment Organism
medicine JMJD3 upregulation and NF-kappaB activation occur in the region of the wound edge during keratinocyte wound healing. JMJD3 interacts with NF-kappaB, resulting in increased expression of the inflammatory matrix metalloproteinase, and growth factor genes via demethylation of H3K27me3 at the gene promoters. Inactivation of JMJD3 or NF-kappaB results in aberrant keratinocyte wound healing Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens O15054
-
-

Source Tissue

Source Tissue Comment Organism Textmining
HaCaT cell
-
Homo sapiens
-
keratinocyte
-
Homo sapiens
-

General Information

General Information Comment Organism
physiological function JMJD3 upregulation and NF-kappaB activation occur in the region of the wound edge during keratinocyte wound healing. JMJD3 interacts with NF-kappaB, resulting in increased expression of the inflammatory matrix metalloproteinase, and growth factor genes via demethylation of H3K27me3 at the gene promoters. Inactivation of JMJD3 or NF-kappaB results in aberrant keratinocyte wound healing Homo sapiens