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Loss of Histone H3 K79 Methyltransferase Dot1l Facilitates Kidney Fibrosis by Upregulating Endothelin 1 through Histone Deacetylase 2.

Long ZhangLihe ChenChao GaoEnuo ChenAndrea R LightleLlewellyn FoulkeBihong ZhaoPaul J HigginsWenzheng Zhang
Published in: Journal of the American Society of Nephrology : JASN (2019)
Our study confirms Dot1l to be a genetic and epigenetic modifier of kidney fibrosis, reveals a new mechanism regulating Edn1 transcription by Dot1a and HDAC2, and reinforces endothelin 1 as a therapeutic target of kidney fibrosis.
Keyphrases
  • histone deacetylase
  • dna methylation
  • gene expression
  • genome wide
  • liver fibrosis
  • transcription factor
  • copy number