Literature summary for 3.5.1.98 extracted from

Icardi, L.; Lievens, S.; Mori, R.; Piessevaux, J.; De Cauwer, L.; De Bosscher, K.; Tavernier, J.
Opposed regulation of type I IFN-induced STAT3 and ISGF3 transcriptional activities by histone deacetylases (HDACS) 1 and 2 (2012), FASEB J., 26, 240-249.

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Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
HEK-293T cell	-	Homo sapiens	-

General Information

General Information	Comment	Organism
physiological function	simultaneous treatment with IFNalpha2 and inhibitor trichostatin A, as well as combined HDAC1/HDAC2 silencing, restores STAT3-dependent reporter gene and endogenous gene expression, strongly suggesting that HDAC1 and HDAC2 are directly involved in repressing IFNalpha2-activated STAT3. In contrast, HDAC1 and HDAC2 activities are required for ISGF3-dependent gene expression. HDAC1 and HDAC2 differentially modulate STAT activity in response to IFNalpha2, while they are required for the induction of ISGF3-responsive genes, they impair the transcription of STAT3-dependent genes	Homo sapiens

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Release 2023.1 (January 2023)