Dec 11, 2017 · Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts.

Jun 14, 2019 · We show that the cardio-protective N-terminal proteolytic fragment of HDAC4 is enhanced in vivo in patients with diabetes mellitus and mouse models, as well as in vitro under high-glucose and high–O-GlcNAc conditions.

Cardiac OE of HDAC4-NT (N-terminus) by intravenous injection of AAV9 with the cytomegalovirus (CMV)-enhanced myosin light chain promoter (Myl2) protected against the heart failure on TAC (Lehmann et al., 2018), suggesting that HDAC4-NT can promote cardiac function.

Histone deacetylase 4 (HDAC4) is a member of the HDAC class IIa family (HDAC-4, -5, -6, -7, and -10) that promotes chromatin condensation and represses transcription by acetylating lysine to inhibit histone–DNA, histone–histone, and other protein–DNA interactions.

Among class II HDACs, HDAC4 is implicated in controlling gene expression important for diverse cellular functions. Basic and clinical experimental evidence have well established that HDAC4 performs a wide variety of functions.

May 1, 2019 · Cardiomyocyte-specific HDAC4 knockout mice displayed exercise-induced cardiac dysfunction and impaired exercise capacity, both of which were attenuated by administration of an adeno-associated viral vector encoding HDAC4-NT (described in Section 3.1.3).

Exogenous administration of the histone deacetylation 4 (HDAC4) protein can effectively delay osteoarthritis (OA) progression. However, HDAC4 is unstable and easily degrades into N-terminal (HDAC4-NT) and C-terminal fragments, and the HDAC4-NT can exert biological effects, but little is known about …

Oct 10, 2011 · In this paper, we describe a novel mechanism whereby protein kinase A (PKA) overcomes CaMKII-mediated activation of MEF2 by regulated proteolysis of HDAC4. PKA induces the generation of an N-terminal HDAC4 cleavage product (HDAC4-NT).

O-GlcNAcylation of HDAC4 at serine (Ser)-642 induces the production of cardio-protective N-ter-minal fragment of HDAC4 and attenuates cardio-detrimental Ca2+/calmodulin–dependent protein kinase II–mediated phosphorylation of HDAC4 at Ser-632.

The stress-responsive epigenetic repressor histone deacetylase 4 (HDAC4) regulates cardiac gene expression. Here we show that the levels of an N-terminal proteolytically derived fragment of HDAC4, termed HDAC4-NT, are lower in failing mouse hearts than in healthy control hearts.