deacylase

de·ac·yl·ase

(dē-as'il-ās),
1. A member of the subclass of hydrolases (EC class 3), especially of that subclass of esterases, lipases, lactonases, and hydrolases (EC subclass 3.1).
2. Any enzyme catalyzing the hydrolytic cleavage of an acyl group (R-CO-) in an ester linkage; also includes enzymes cleaving amide linkages (EC subclass 3.5) and similar acyl compounds.

deacylase

/de·acyl·ase/ (de-as´il-ās) any hydrolase that catalyzes the cleavage of an acyl group in ester or amide linkage.

de·ac·yl·ase

(dē-as'il-ās)
1. A member of the subclass of hydrolases (EC class 3), especially of that subclass of esterases, lipases, lactonases, and hydrolases (EC subclass 3.1).
2. Any enzyme catalyzing the hydrolytic cleavage of an acyl group (R-CO-) in an ester linkage; also includes enzymes cleaving amide linkages (EC subclass 3.5) and similar acyl compounds.
References in periodicals archive ?
PIA biosynthesis is carried out by the proteins encoded by the ica gene operon: N-acetylglucosamine transferase (icaA and icaD), PIA deacylase (icaB), PIA exporter (icaC) and the regulatory gene (icaR) [12 13].
Miller, "3-O-deacylation of lipid A by PagL, a PhoP/PhoQ-regulated deacylase of Salmonella typhimurium, modulates signaling through Toll-like receptor 4," Journal of Biological Chemistry, vol.
52 1-phosphatidyl-D-myo-inositol deacylase + H20 = 1-acylglycerophosphoinositol + a carboxylate Phospholipase C 3.
Histone deacylase inhibitors: Induction of differentiation of ATRA-resistant APL with PLZF-RAR[alpha], using combination of pharmacological dose of ATRA and HDAC inhibitors (TSA or sodium phenylbutyrate) opened a new avenue in the treatment of not only APL but also AML1-ETO AML [36].
High expression of sphingomyelin deacylase is an important determinant of ceramide deficiency leading to barrier disruption in atopic dermatitis.
Filaggrin deficiency appears to lead to impaired barrier function and a reduction in the activity of one of the key enzymes involved in bilayer formation, sphingomyelin deacylase, leading to reduced ceramide levels and altered lipid packaging.
He produced evidence suggesting that the high levels of expression of SM deacylase in atopic dermatitis explains the mechanism of ceramide deficiency leading to barrier disruption which is strongly linked to atopic skin's vulnerability to irritants or allergens.
Although once disused or disappeared, the PLB is classified as a member of the deacylases of phospholipids in addition to PLA and LPL.