BTAF1
- Known as:
- BTAF1
- Catalog number:
- 002694A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BTAF1
Related genes to: BTAF1
- Gene:
- BTAF1 NIH gene
- Name:
- B-TFIID TATA-box binding protein associated factor 1
- Previous symbol:
- -
- Synonyms:
- TAFII170, TAF172, MOT1, TAF-172, TAF(II)170
- Chromosome:
- 10q23.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-03
- Date modifiied:
- 2016-10-05
Related products to: BTAF1
Related articles to: BTAF1
- This study aimed to explore whether Fufangteng Yixin Formula (FFTYXF) can ameliorate myocardial ischemia-reperfusion injury (MIRI) by regulating the gut microbiota and resultant metabolites. Wistar rats were given FFTYXF by gavage for 7 days, and MIRI rat model was established. Serum level of inflammatory markers was determined by ELISA, and heart function was evaluated by echocardiography. Myocardial histological changes and infarct size were examined by hematoxylin-eosin and triphenyltetrazolium chloride staining, respectively. 16S rRNA gene and metagenomics analyses were employed to explore gut microbiota, while untargeted metabolomics analysis was used to explore serum metabolites. FFTYXF pretreatment could significantly improve cardiac function, reduce infarct size, decrease level of inflammatory factors (TNF-α and IL-6) and inflammatory cells infiltration. At genus level, g__Oscillibacter and g__Rikenellaceae_RC9_gut_group were identified as key microbial bacteria in MIRI rat response to FFTYXF pretreatment. After FFTYXF pretreatment, the functional categories of gut microbiota were participated in fatty acid (FA) biosynthesis/metabolism, glycolysis _ gluconeogenesis and sphingolipid metabolism. Genes response to FFTYXF pretreatment in MIRI rats included K00023 (phbB), K00281 (GLDC, gcvP), K03879 (ND2), K07827 (KRAS) and K15192 (BTAF1), and they were mainly participated in carbon, butanoate, glyoxylate and dicarboxylate metabolism. Differential metabolites were also mainly participated in FA biosynthesis/metabolism, such as alpha-Linolenic acid, omega-3/omega-6 FA, and flavan-3-ol metabolic pathway. Abundance of g__Rikenellaceae_RC9_gut_group positively correlated with differential metabolites FAHFA 34:0, FAHFA 16:1/18:3, and FA 24:5. FFTYXF could alleviate MIRI by modulating gut microbial bacteria alteration and resultant metabolites, particularly short-chain FAs. - Source: PubMed
Publication date: 2026/07/28
Li FengyiZhao HaitaoLei YiluLuo JinweiChen BolingLi ChenglinZhao XuanJiang Huizhen - Chemotherapy is the primary mode of treatment for patients with advanced bladder cancer. However, because of their non-specificity, chemotherapy drugs induce many notable side effects in patients. Recent studies have shown that the expression of certain long non-coding RNAs (lncRNAs) is closely related to the sensitivity of tumors to chemotherapeutic drugs. Thus, lncRNAs can be exploited as markers of tumor chemotherapeutic sensitivity to improve the efficacy of chemotherapy. Here, we investigated the role of the lnc00892 in the response of bladder cancer cells to cisplatin. - Source: PubMed
Publication date: 2026/05/27
Chang YixinSun NingLiu YijieJin ZihuiZhang PeipeiWang SijiaChen JieLiu JiantingLin ZhenniLu YongyongHuang HaishanHuang ChuanshuJin Honglei - Age-associated hematopoietic stem cell (HSC) dysfunction is accompanied by dramatic transcription changes, but it remains unclear whether specific transcripts could orchestrate these HSC aging phenotypes. Here, we perform epigenetic profiling in male mice to investigate the regulatory mechanisms underlying the HSC aging transcriptome and screen for potential aging driver genes. We identify a looping structure formed between part of the Btaf1 gene and the whole Ide gene in old HSCs which is accompanied by overexpression of a shorter variant of Btaf1 (nBtaf1). Mechanistically, elevated expression of nBtaf1 drives the aging-associated overexpression of HSC and megakaryocyte progenitor (MkP) signature genes via regulating TBP binding at their promoters, which contributes to HSC expansion and elevated MkP production in aged mice. ShRNA-mediated knockdown of nBtaf1 restores a younger HSC transcriptome and specifically represses aging-associated HSC expansion and elevated MkP production. In summary, our data provide high resolution analysis of a dysregulated HSC aging epigenome and reveal a Btaf1 variant that drives HSC aging phenotypes in mice. - Source: PubMed
Publication date: 2026/03/18
Zong LePark BongsooCao YaqiangMa FeiTekin-Turhan FerdaKuribayashi WakakoZhao KejiBeerman Isabel - BTAF1, an ATP-dependent remodeler of the TBP-DNA complex, is frequently mutated in gastric cancer. However, its role in DNA repair and therapeutic relevance remains largely undefined. Here, we show that BTAF1 knockout leads to accumulation of double-strand breaks (DSBs) by impairing DNA end-resection process of homologous recombination (HR) repair, thereby sensitizing cells to genotoxic agents both in vitro and in vivo. Mechanistically, BTAF1 prevents ubiquitin-mediated degradation of MRE11, maintaining its protein stability, promoting DNA end resection and HR, and consequently enhancing cellular resistance to DNA-damaging stress. Notably, the interaction between BTAF1 and MRE11 is dynamically regulated by PARP1-mediated PARylation of BTAF1 during the DNA damage response. Loss of BTAF1 also increases chemosensitivity in gastric cancer xenograft and organoid models. Clinically, high BTAF1 expression correlates with poor prognosis in gastric cancer patients receiving neoadjuvant chemotherapy. Collectively, our findings identify BTAF1 as a critical regulator of HR repair through stabilization of MRE11 and propose BTAF1 as a potential biomarker for predicting response to genotoxic chemotherapy. BTAF1 is frequently mutated in gastric cancer, yet its role in DNA repair remains unclear. BTAF1 promotes homologous recombination and chemoresistance in gastric cancer by stabilizing MRE11. BTAF1 loss impairs DNA end resection, sensitizing cells to genotoxic agents. The BTAF1-MRE11 interaction is regulated by PARP1 mediated PARylation. - Source: PubMed
Publication date: 2026/03/17
Xie Juan-JuanLin Ji-LiangXiang Zhi-ChengQu Chun-HuaCai Xiao-XiaNie Run-CongLin PengYin Yi-XinDuan Jin-LingXie DanCai Mu-Yan - Meta-analysis of genome-wide association study data has implicated PDE4B in the pathogenesis of Alzheimer's disease (AD), the leading cause of senile dementia. PDE4B encodes one of four subtypes of cyclic adenosine monophosphate (cAMP)-specific phosphodiesterase-4 (PDE4A-D). To interrogate the involvement of PDE4B in the manifestation of AD-related phenotypes, the effects of a hypomorphic mutation (Pde4b) that decreases PDE4B's cAMP hydrolytic activity were evaluated in the App knock-in mouse model of AD using the Barnes maze test of spatial memory, C-2-deoxyglucose autoradiography, thioflavin-S staining of β-amyloid (Aβ) plaques, and inflammatory marker assay and transcriptomic analysis (RNA sequencing) of cerebral cortical tissue. At 12 months of age, App mice exhibited spatial memory and brain metabolism deficits, which were prevented by the hypomorphic PDE4B in App/Pde4b mice, without a decrease in Aβ plaque burden. RNA sequencing revealed that, among the 531 transcripts differentially expressed in App versus wild-type mice, only 13 transcripts from four genes - Ide, Btaf1, Padi2, and C1qb - were differentially expressed in App/Pde4b versus App mice, identifying their potential involvement in the protective effect of hypomorphic PDE4B. Our data demonstrate that spatial memory and cerebral glucose metabolism deficits exhibited by 12-month-old App mice are prevented by targeted inhibition of PDE4B. To our knowledge, this is the first demonstration of a protective effect of PDE4B subtype-specific inhibition in a preclinical model of AD. It thus identifies PDE4B as a key regulator of disease manifestation in the App model and a promising therapeutic target for AD. - Source: PubMed
Publication date: 2024/03/23
Armstrong PaulGüngör HüseyinAnongjanya PariyaTweedy ClareParkin EdwardJohnston JamieCarr Ian MDawson NeilClapcote Steven J