CBP-HSF2 structural and functional interplay in Rubinstein-Taybi neurodevelopmental disorder
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CBP-HSF2 structural and functional interplay in Rubinstein-Taybi neurodevelopmental disorder
Microdeletions and mutations of CREBBP (CBP) gene can cause
An aPKC Phosphorylation site on CBP Is Essential for It to Promote
A conserved PHD finger in the acetyltransferase domain of CBP and p300.
Heat Shock Factor 2 Protects against Proteotoxicity by Maintaining C
CBP/EP300-dependent acetylation and stabilization of HSF2 are compromised in Rubinstein-Taybi syndrome
CBP/EP300-dependent acetylation and stabilization of HSF2 are compromised in Rubinstein-Taybi syndrome
Targeted inactivation of the Hsf2 gene. ( A ) Schematic representation
Identification of p35 as a potential target gene for HSF2. (A) Western
CK2a 0 heterozygosity ameliorates biochemical and neurobiological
Proteomic analysis of 110A53T, A53T, and Hsp110 brains. (A) Synaptic
Stress pathways in neurodevelopmental disorders
CBP Regulates Differentiation, but Does Not Affect Survival or
Structures of HSF2 reveal mechanisms for differential regulation of human heat-shock factors
The CBP-KIX domain sequence and structure. (A) Alignment of selected
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