BCAT1 antibody (clone AT3C8)
- Known as:
- BCAT1 (anti-) (clonality AT3C8)
- Catalog number:
- ATGA0359
- Product Quantity:
- 50ul
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- BCAT1 antibody (clone AT3C8)
Related genes to: BCAT1 antibody (clone AT3C8)
- Gene:
- BCAT1 NIH gene
- Name:
- branched chain amino acid transaminase 1
- Previous symbol:
- BCT1
- Synonyms:
- -
- Chromosome:
- 12p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-03-07
Related products to: BCAT1 antibody (clone AT3C8)
Related articles to: BCAT1 antibody (clone AT3C8)
- Fibrosis remains a major driver of organ dysfunction, yet the metabolic programs that sustain extracellular matrix production are incompletely understood. In this issue of the JCI, Takizawa and colleagues identified branched-chain amino acid transaminase 1 (BCAT1) as a crucial metabolic regulator of fibroblast activation and fibrosis in a model of cardiac fibrosis. Their observations were corroborated by analyses of datasets from patients with heart failure with preserved ejection fraction and metabolic dysfunction-associated steatohepatitis. They report that by coupling mechanical and TGF-β signaling to a proline biosynthesis and utilization program, BCAT1 enhanced collagen production in activated cardiac fibroblasts. These findings place branched-chain amino acid metabolism as a pivotal contributor to fibroblast activation and highlight BCAT1 as a promising therapeutic target for fibrotic disease. - Source: PubMed
Publication date: 2026/09/01
Ronfini MarcoElrod John W - Branched-chain amino acid (BCAA) transaminase 1 (BCAT1), the rate-limiting enzyme in BCAA metabolism, serves a pivotal role in tumor progression. Astragaloside IV (AS-IV) exhibits potential antitumor properties; however, whether AS-IV suppresses breast cancer migration by modulating BCAA metabolism via BCAT1 remains to be elucidated. The present study aimed to investigate whether AS-IV inhibits the invasion and migration of MDA-MB-231 triple-negative breast cancer (TNBC) cells by targeting BCAT1-mediated BCAA metabolic reprogramming. The present study used network pharmacology to predict AS-IV targets against breast cancer invasion, followed by BCAT1 knockdown and overexpression in MDA-MB-231 cells. Using molecular docking, cellular thermal shift assay, wound healing, Transwell, western blotting, quantitative PCR and liquid chromatography-mass spectrometry metabolomics, the present study systematically evaluated: i) AS-IV-BCAT1 direct binding and protein stability; ii) BCAA metabolic flux regulation via the branched-chain α-ketoacid dehydrogenase kinase (BCKDK)/branched-chain α-ketoacid dehydrogenase (BCKDH) axis; and iii) functional impacts on breast cancer cell migration and invasion. Network pharmacology predicted BCAT1 as a key potential target of AS-IV, with significant enrichment of the BCAA metabolic pathway. The results of the present study suggested that AS-IV binds to and stabilizes BCAT1 , an effect that is associated with reduced migration and invasion of MDA-MB-231 cells. It also promotes BCAA degradation via the BCKDK/BCKDH axis, lowering intracellular BCAA levels and suppressing malignancy. Notably, AS-IV maintained dose-dependent inhibition even with BCAT1 knockdown or overexpression, albeit with reduced efficacy. In conclusion, the present study suggested that AS-IV suppresses MDA-MB-231 cell invasion and migration by targeting BCAT1-mediated BCAA metabolism. These findings support further evaluation of AS-IV in TNBC and highlight BCAA metabolism as a potential intervention point in future research. - Source: PubMed
Publication date: 2026/08/03
Liu Yi-TingZhang LuSun Xiao-Dong - Primary cutaneous T-lymphomas (CTCL), particularly in their early stages, frequently present with clinical and histopathologic features that overlap with atopic dermatitis (AD) and psoriasis, contributing to diagnostic delay and ineffective, or even deleterious, treatment approaches. Thus, minimally invasive molecular tests capable of distinguishing CTCL from benign inflammatory dermatoses are urgently needed. - Source: PubMed
Publication date: 2026/08/07
Fleischli AbigailBar JonathanManson MeredithNg Brandon DMeledathu ShannonBurnett AmeliaChefitz GabriellaEstrada Yeriel DGour DigpalCices AhuvaCorrea da Rosa JoelBrunner Patrick MGuttman-Yassky Emma - Global sperm concentration has declined by over 50% in the past five decades, with environmental pollutants identified as a critical driving factor. This review focuses on testicular-level evidence regarding the effects of microplastics, bisphenol compounds, and air pollution on male reproductive health, with an emphasis on spermatogenic and testicular somatic cell mechanisms. Microplastics have been detected in human testicular tissue, with a causal pathway established linking gut microbiota dysbiosis, immune activation, and blood-testis barrier disruption. Bisphenol A substitutes show comparable or greater reproductive toxicity than BPA, with BCAT1-mediated ferroptosis identified as a novel testicular injury mechanism. For air pollution, spermatogenesis stage I (70-90 days prior to semen collection) has been pinpointed as the critical PM2.5 exposure vulnerability window, with metal constituents of traffic-derived PM2.5 as the primary toxicity drivers. Future research should prioritize prospective cohort studies and clinical intervention trials targeting these emerging mechanistic pathways. - Source: PubMed
Publication date: 2026/08/04
Guo AndongLu YiGuo YeLi Hongjun - Myofibroblasts are the cells responsible for collagen production, leading to tissue fibrosis. Because 20.5% of the total amino acids in collagen are proline, myofibroblasts must acquire a well-developed proline-producing mechanism during their differentiation. However, the detailed mechanism for myofibroblasts to acquire and keep the developed proline biosynthesis machinery remains obscure. Here, we show that branched-chain amino acid (BCAA) transaminase 1 (Bcat1) was upregulated in a substantial subset of Periostin (Postn)-expressing protomyofibroblast-like fibroblasts, which are transitional cells en route to fully differentiated myofibroblasts, as well as in myofibroblasts in the fibrotic hearts and livers of mice and humans, and promoted the production of proline. The production of BCAA by BCAT1 promoted SMAD3 phosphorylation via HDAC5 phosphorylation at Ser488, thereby enhancing SMAD3-dependent transcription of the proline biosynthesis-related genes Aldh18a1, Pycr1, and Eprs in protomyofibroblast-like fibroblasts and myofibroblasts. In BCAT1-deficient mice, expression of proline biosynthesis-related genes was significantly attenuated in their hearts after myocardial infarction (MI), resulting in decreased cardiac fibrosis. Moreover, mice with MI that were treated with a BCAT1 inhibitor had reduced cardiac fibrosis. Our results identified a BCAT1-mediated pathway that promoted collagen production via proline biosynthesis regulation in protomyofibroblast-like fibroblasts and myofibroblasts, which may provide a therapeutic target for cardiac fibrosis. - Source: PubMed
Publication date: 2026/07/16
Takizawa NoburoHironaka TakanoriWatanabe HayatoSuetsugu HarunaYoshioka KeisukeHorii YumaNagata YuriMatoba HiroakiKosako HidetakaHamase KenjiHirai GoNakaya Michio