Brpf3
- Known as:
- Brpf3
- Catalog number:
- 051618A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Brpf3
Related genes to: Brpf3
- Gene:
- BRPF3 NIH gene
- Name:
- bromodomain and PHD finger containing 3
- Previous symbol:
- -
- Synonyms:
- KIAA1286
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-12-14
- Date modifiied:
- 2015-11-11
Related products to: Brpf3
Related articles to: Brpf3
- GC-rich sequences affect DNA replication, recombination and repair, as well as RNA transcription in vivo. Such sequences may also impede site-directed mutagenesis in vitro. P3a site-directed mutagenesis is a highly efficient method, but it has not been tested with plasmids possessing GC-rich sequences. Here we report that it is very efficient with a BRPF3 expression vector but unsuccessful with that for KAT2B. Because two GC-rich regions located within the synthetic CAG promoter and the KAT2B coding region may form guanine (G)-quadruplexes and hinder plasmid denaturation during PCR, we developed P3b site-specific mutagenesis, achieving an average efficiency of 97.5% in engineering ten KAT2B mutants. Importantly, deletion mutagenesis revealed that either of the two GC-rich regions is sufficient for rendering the plasmid incompatible with P3a mutagenesis. Consistent with this, only P3b mutagenesis worked efficiently with several widely used sgRNA/Cas9 expression vectors, which contain the CAG promoter, and with an expression vector for CDK13, which possesses an intrinsically disordered domain encoded by a GC-rich DNA fragment. Thus, this study highlights serious challenges posed by GC-rich sequences to site-directed mutagenesis and provides an effective remedy to address such challenges. The findings support that G-quadruplex formation is one mechanism whereby such sequences impede regular PCR-based mutagenesis methods. - Source: PubMed
Publication date: 2025/12/18
Varela-Castillo PaulinaZhou EthanRazavi ArezousadatEbrahimi ElhamYang Xiang-Jiao - Cardiac fibrosis is characterized by an elevated amount of extracellular matrix (ECM) within the heart. However, the persistence of cardiac fibrosis ultimately diminishes contractility and precipitates cardiac dysfunction. Circular RNAs (circRNAs) are emerging as important regulators of cardiac fibrosis. Here, we elucidate the functional role of a specific circular RNA CELF1 in cardiac fibrosis and delineate a novel feedback loop mechanism. Functionally, circ-CELF1 was involved in enhancing fibrosis-related markers' expression and promoting the proliferation of cardiac fibroblasts (CFs), thereby exacerbating cardiac fibrosis. Mechanistically, circ-CELF1 reduced the ubiquitination-degradation rate of BRPF3, leading to an elevation of BRPF3 protein levels. Additionally, BRPF3 acted as a modular scaffold for the recruitment of histone acetyltransferase KAT7 to facilitate the induction of H3K14 acetylation within the promoters of the gene. Thus, the transcription of was dramatically activated, thereby inhibiting the subsequent response of their downstream target gene expression to promote cardiac fibrosis. Moreover, further promoted pre-mRNA transcription and back-splicing, thereby establishing a feedback loop for circ-CELF1 production. Consequently, a novel feedback loop involving CELF1/circ-CELF1/BRPF3/KAT7 was established, suggesting that circ-CELF1 may serve as a potential novel therapeutic target for cardiac fibrosis. - Source: PubMed
Publication date: 2025/07/29
Jiang YuanZhang BowenZhang BoSong XinhuaWang XiangyuZeng WeiZuo LiyangLiu XinqiDong ZhengCheng WenzhengQiao YangJin SaidiJi DongniGuo XiaofeiZhang RongGong XieyangSun LihuaXuan LinaAlexandrovna Berezhnova TatjanaGuan XiaoxiangZhang MingyuYang BaofengXu Chaoqian - Lung cancer is one of the most commonly diagnosed cancers. N-methyladenosine (mA) modification has a profound impact on RNA translation, splicing, transportation, and stability. - Source: PubMed
Publication date: 2025/03/25
Han XiaominMa QiangChang RuyiXin SiyuanZhang GuojunWang RuilongWang Yukun - Currently, the treatment and prevention of migraine remain highly challenging. Mendelian randomization (MR) has been widely used to explore novel therapeutic targets. Therefore, we performed a systematic druggable genome-wide MR to explore the potential therapeutic targets for migraine. - Source: PubMed
Publication date: 2024/06/12
Zhang ChengchengHe YiweiLiu Lu - PARP inhibitors (PARPi) kill cancer cells by stalling DNA replication and preventing DNA repair, resulting in a critical accumulation of DNA damage. Resistance to PARPi is a growing clinical problem in the treatment of high grade serous ovarian carcinoma (HGSOC). Acetylation of histone H3 lysine 14 (H3K14ac) and associated histone acetyltransferases (HATs) and epigenetic readers have known functions in DNA repair and replication. Our objectives are to examine their expression and activities in the context of PARPi-resistant HGSOC, and to determine if targeting H3K14ac or associated proteins has therapeutic potential. Using mass spectrometry profiling of histone modifications, we observed increased H3K14ac enrichment in PARPi-resistant HGSOC cells relative to isogenic PARPi-sensitive lines. By reverse-transcriptase quantitative PCR and RNA-seq, we also observed altered expression of numerous HATs in PARPi-resistant HGSOC cells and a PARPi-resistant PDX model. Knockdown of HATs only modestly altered PARPi response, although knockdown and inhibition of PCAF significantly increased resistance. Pharmacologic inhibition of HBO1 depleted H3K14ac but did not affect PARPi response. However, knockdown and inhibition of BRPF3, a bromodomain and PHD-finger containing protein that is known to interact in a complex with HBO1, did reduce PARPi resistance. This study demonstrates that depletion of H3K14ac does not affect PARPi response in HGSOC. Our data suggest that the bromodomain function of HAT proteins, such as PCAF, or accessory proteins, such as BRPF3, may play a more direct role compared to direct HATs function in PARPi response. - Source: PubMed
Publication date: 2023/07/26
Bitler Benjamin GBailey Courtney AYamamoto Tomomi MMcMellen AlexandraKim HyunminWatson Zachary L