Last update 01 Nov 2024

BRPF2

Last update 01 Nov 2024

Basic Info

Synonyms

BR140-like, BR140-like protein, BRD1

+ [6]

Introduction

Scaffold subunit of various histone acetyltransferase (HAT) complexes, such as the MOZ/MORF and HBO1 complexes, that acts as a regulator of hematopoiesis (PubMed:16387653, PubMed:21753189, PubMed:21880731). Plays a key role in HBO1 complex by directing KAT7/HBO1 specificity towards histone H3 'Lys-14' acetylation (H3K14ac), thereby promoting erythroid differentiation (PubMed:21753189).

Drugs associated with BRPF2

CG-202

Target

BRPF2

Mechanism

BRPF2 inhibitors

Active Org.

Convergene LLC

Originator Org.

Convergene LLC

Active Indication

Hematologic Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NI-57

Target

BRPF1 x BRPF2

Mechanism

BRPF1 inhibitors [+1]

Active Org.

University College London

Originator Org.

University College London

Active Indication

Inflammation

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

[18F]PB006

Target

BRPF2

Mechanism

BRPF2 modulators

Active Org.

Harvard Medical School

Originator Org.

Harvard Medical School

Active Indication

Diagnostic agents

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with BRPF2

100 Translational Medicine associated with BRPF2

0 Patents (Medical) associated with BRPF2

293

Literatures (Medical) associated with BRPF2

11 Sep 2024·Journal of Agricultural and Food Chemistry

BLA1 Affects Leaf Angles by Altering Brassinosteroid Biosynthesis in Rice (Oryza sativa L.)

Article

Author: Zhang, Ying ; Jiang, Yaohuang ; Dong, Guojun ; Yu, Yanchun ; Ruan, Banpu ; Zhang, Yanli ; Chen, Fei ; Wu, Limin

Brassinosteroids (BRs) are crucial plant hormones influencing diverse developmental processes in rice. While several enzymes in BR biosynthesis have been identified, their regulatory mechanisms remain largely unknown. This study highlights a novel regulatory pathway wherein the CHD3 chromatin remodeler, BLA1, epigenetically modulates the expression of key BR biosynthesis genes, BRD1 and D2. Phenotypic analysis of bla1 mutants revealed significant alterations, such as increased leaf angles and longer mesocotyls, which were alleviated by BR synthesis inhibitors. Moreover, the bla1 mutants showed elevated BR levels that correlated with the significant upregulation of the expression levels of BRD1 and D2, particularly at the lamina joint sites. Mechanistically, the yeast one-hybrid and chromatin immunoprecipitation assays revealed specific binding of BLA1 to the promoter regions of BRD1 and D2, accompanied by a marked enrichment of the transcriptionally active histone modification, H3K4me3, on these loci in the bla1 mutant. Functional assessments of the brd1 and d2 mutants confirmed their reduced sensitivity to BR, further underscoring their critical regulatory roles in BR-mediated developmental processes. Our findings uncovered an epigenetic mechanism that governs BR biosynthesis and orchestrates the expression of BRD1 and D2 to modulate BR levels and influence rice growth and development.

19 Jul 2024·Medicine

The effect of overexpression of CyPA on gene expression in human umbilical vein endothelial cells

Article

Author: Zhou, XinRong ; Wang, Ning ; Yin, Mingyue ; Yang, Wenwen ; Li, Qiuju

The aim of this study is to screen the differentially expressed genes and genes with alternative splicing in PPIA overexpressing cells by transcriptome sequencing. Transcriptome sequencing was performed to identify differentially expressed genes and genes with altered alternative splicing in PPIA overexpressing cells and results were validated by real-time quantitative polymerase chain reaction. The biological function and pathways of those genes were further explored through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses. A total of 157 significantly upregulated genes and 171 significantly downregulated genes were identified in PPIA overexpressing cells, and the splicing pattern of LHPP, APH1A, BRD1, and ORAI3 was found to be altered. GO analyses showed that the most enriched GO terms of the 157 upregulated genes included extracellular region, protein binding, and metal ion, and the most enriched GO terms of the 171 downregulated genes included binding neuron projection, protein binding, and endoplasmic reticulum unfolded protein response. Kyoto Encyclopedia of Genes and Genomes analyses showed that the 157 upregulated genes were mainly enriched in gastric acid secretion, Mitogen-activated protein kinase signaling pathway, etc, and the 171 downregulated genes were mainly enriched in transcriptional misregulation in cancer, Tumor necrosis factor signaling pathway, etc. The overexpression of PPIA in human umbilical vein endothelial cells causes changes in the expression of downstream genes and induces alternative splicing in multiple genes. PPIA alters the expression or the alternative splicing pattern of downstream genes, leading to pathogenesis of vascular endothelial injury by high glucose mediated through CyPA.

01 May 2024·Clinical Genetics

Evidence for common mechanisms of pathology between SHANK3 and other genes of Phelan‐McDermid syndrome

Review

Author: Boccuto, Luigi ; Mitz, Andrew R ; Thurm, Audrey

AbstractChromosome 22q13.3 deletion (Phelan‐McDermid) syndrome (PMS, OMIM 606232) is a rare genetic condition that impacts neurodevelopment. PMS most commonly results from heterozygous contiguous gene deletions that include the SHANK3 gene or likely pathogenic variants of SHANK3 (PMS‐SHANK3 related). Rarely, chromosomal rearrangements that spare SHANK3 share the same general phenotype (PMS‐SHANK3 unrelated). Very recent human and model system studies of genes that likely contribute to the PMS phenotype point to overlap in gene functions associated with neurodevelopment, synaptic formation, stress/inflammation and regulation of gene expression. In this review of recent findings, we describe the functional overlaps between SHANK3 and six partner genes of 22q13.3 (PLXNB2, BRD1, CELSR1, PHF21B, SULT4A1, and TCF20), which suggest a model that explains the commonality between PMS‐SHANK3 related and PMS‐SHANK3 unrelated classes of PMS. These genes are likely not the only contributors to neurodevelopmental impairments in the region, but they are the best documented to date. The review provides evidence for the overlapping and likely synergistic contributions of these genes to the PMS phenotype.

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BRPF2

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