Literature summary extracted from

Hutt, D.M.; Herman, D.; Rodrigues, A.P.; Noel, S.; Pilewski, J.M.; Matteson, J.; Hoch, B.; Kellner, W.; Kelly, J.W.; Schmidt, A.; Thomas, P.J.; Matsumura, Y.; Skach, W.R.; Gentzsch, M.; Riordan, J.R.; Sorscher, E.J.; Okiyoneda, T.; Yates, J.R.; Lukacs, G.L.; Frizzell, R.A.; Manning, G.; Gottesfeld, J.M.; Balc, B.a.l.c.h.
Reduced histone deacetylase 7 activity restores function to misfolded CFTR in cystic fibrosis (2010), Nat. Chem. Biol., 6, 25-33.

Inhibitors

EC Number	Inhibitors	Comment	Organism
3.5.1.98	MS-275	-	Homo sapiens
3.5.1.98	scriptaid	-	Homo sapiens
3.5.1.98	suberoylanilide hydroxamic acid	-	Homo sapiens
3.5.1.98	trichostatin A	-	Homo sapiens

EC Number	Organism	UniProt	Comment	Textmining
3.5.1.98	Homo sapiens	-	-	-

EC Number	Source Tissue	Comment	Organism	Textmining
3.5.1.98	airway epithelial cell	-	Homo sapiens	-
3.5.1.98	primary cell	-	Homo sapiens	-

EC Number	Synonyms	Comment	Organism
3.5.1.98	HDAC7	-	Homo sapiens
3.5.1.98	histone deacetylase 7	-	Homo sapiens

EC Number	General Information	Comment	Organism
3.5.1.98	malfunction	HDAC inhibition improves DELTAF508 cystic fibrosis transmembrane conductance regulator stability and trafficking, silencing of HDAC2 and HDAC3 causes a 2.5fold and 1.5fold increase in DELTAF508 cystic fibrosis transmembrane conductance regulator mRNA, respectively, as well as an about 5fold increase in total DELTAF508 protein. Silencing of HDAC1 induces a 1.4fold stimulation of iodide efflux. In contrast, silencing of HDAC7 exhibits a 3.6fold stimulation of cAMP-mediated iodide efflux comparable to 30°C efflux	Homo sapiens
3.5.1.98	physiological function	HDAC7 plays a central role in restoration of DELTAF508 cystic fibrosis transmembrane conductance regulator function	Homo sapiens