Bcl2A1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- Bcl2A1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100159
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Bcl2A1 antibody Polyclonal Antibodies Primary antibodies
Related genes to: Bcl2A1 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- BCL2A1 NIH gene
- Name:
- BCL2 related protein A1
- Previous symbol:
- HBPA1
- Synonyms:
- GRS, BFL1, BCL2L5, ACC-1, ACC-2, ACC2, ACC1
- Chromosome:
- 15q25.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-08
- Date modifiied:
- 2016-10-05
Related products to: Bcl2A1 antibody Polyclonal Antibodies Primary antibodies
Related articles to: Bcl2A1 antibody Polyclonal Antibodies Primary antibodies
- Cryptosporidium parvum (C. parvum) is a zoonotic protozoan that causes cryptosporidiosis, primarily characterized by watery diarrhea. To clarify the molecular mechanisms of C. parvum-mediated host cell apoptosis regulation and identify potential therapeutics, we examined apoptosis rates, caspase activation, and apoptosis-related protein expression in infected NCM460 cells, along with the involvement of the phosphatidylinositol 3-kinase-nuclear factor kappa B (PI3K-NF-κB) signaling pathway, and evaluated the efficacy of BEZ235, a dual PI3K/mammalian target of rapamycin (mTOR) inhibitor. Results showed that C. parvum suppressed intrinsic apoptosis during 52-76 hours post-infection (hpi) by inhibiting caspase-3 and caspase-9 activation and upregulating anti-apoptotic proteins c-MYB and BCL2A1; RNA interference-mediated knockdown of either c-MYB and BCL2A1 significant reversed this anti-apoptotic effect. Mechanistically, C. parvum infection robustly activated the PI3K-NF-κB axis between 40 and 76 hpi, as evidenced by increased AKT phosphorylation (p-AKT) and enhanced nuclear translocation of NF-κB subunit p65. BEZ235 treatment effectively suppressed PI3K-NF-κB activation, downregulated c-MYB and BCL2A1 expression, and restored apoptosis in infected cells. In a murine model of C. parvum infection, oral BEZ235 (15 mg/kg/day) exhibited superior therapeutic efficacy to paromomycin (50 mg/kg/day), reducing fecal oocyst shedding by 61.4% (vs. 42.9% with paromomycin), ileal parasite burden by 60.3% (vs. 42.8% with paromomycin), and markedly alleviating intestinal epithelial damage. These findings deepen our understanding of the intracellular survival strategy of C. parvum and highlight BEZ235 as a promising candidate for cryptosporidiosis treatment. - Source: PubMed
Publication date: 2026/04/14
Zhou ShashaSun TiancongQi WanxiangLi QiuxiangMi RongshengHuang YanGong HaiyanChen Zhaoguo - SLC25A10, the mitochondrial dicarboxylate carrier, plays a crucial role in mitochondrial metabolism and protects against liver lipotoxicity. Moreover, its frequent amplification or mutation in cancers, particularly hepatocellular carcinoma (HCC), correlates with a poor prognosis. This study aimed to investigate the role of SLC25A10 in chemotherapy resistance in HCC and elucidate the underlying mechanisms. In this study, we found that hypoxia increased SLC25A10 expression with a preferential shift toward isoform 3 in HCC. This isoform interacts with the nuclear transporter IPO7 to translocate into the nucleus, where it binds to transcription factor CEBPB. This interaction upregulates the transcription of the anti-apoptotic gene BCL2A1, thereby enhancing HCC cell resistance to the chemotherapeutic agent, etoposide. Notably, disruption of the SLC25A10 isoform 3-IPO7 interaction significantly sensitized HCC tumors to etoposide in vivo, suggesting that targeting this interaction could be a promising therapeutic strategy to improve chemotherapy efficacy in HCC. This study reveals a novel nuclear function of the mitochondrial dicarboxylate carrier SLC25A10 in transcriptional regulation under hypoxic conditions, distinct from its canonical mitochondrial role. These findings expand our understanding of SLC25A10 biology and uncover a previously unrecognized mechanism that drives hypoxia-induced chemoresistance in HCC. Our findings suggest that SLC25A10 is a potential therapeutic target to overcome drug resistance in HCC. - Source: PubMed
Publication date: 2026/04/09
Liu DanDong ShuangCheng SiweiLin YuanyuanChen ShengGao JiaxinBi BoLi NaMi JunXiong Wujun - Rheumatoid arthritis (RA) has complex pathological mechanisms, and mitochondria are critical to its occurrence and development while the specific mechanisms remain unclear. This study aimed to identify key mitochondria-related genes in RA via machine learning, validate them by two-sample Mendelian randomization (MR), and provide novel therapeutic target clues. - Source: PubMed
Publication date: 2026/03/27
Luo XiaolinDong ZhuqingSong YuansongHu JianweiLiao ShijieDing Xiaofei - Variants in (which encodes the p65 subunit of NF-κB) can cause a monogenic autoinflammatory disease with clinical manifestations that range from mucocutaneous lesions (Behçet's disease-like) to systemic inflammation. However, the diversity of the phenotype and its penetrance are uncertain. - Source: PubMed
Publication date: 2026/02/18
Hou LingYin LuZhao ChengguangDu Yue - Immune checkpoint inhibitors (ICIs) can cause immune-related adverse events (irAEs), with acute interstitial nephritis (ICI-AIN) being the most common irAE. While the exact mechanism remains unclear, upregulation of interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) pathways has been implicated. This study used a humanized chimeric PD-1/PD-L1 mouse model to assess renal effects of ICIs, alone or combined with pro-inflammatory cytokines, and to test if selective TNF-α blockade could prevent ICI-AIN. Mice were randomly divided into four experimental groups: Control, ICI-Only, ICI-Cytokines (ICI-Cyt), and ICI-Block (ICI-TNF-α blockade). Renal function and cytokine profiles were assessed, while kidney tissue was analyzed using microscopy and single-cell RNA sequencing. Histology revealed increased renal infiltration of CD4⁺/CD8⁺ T cells in ICI-treated groups and decreased TNF-α expression following TNF-α blockade. Additionally, kidney tissue ELISA demonstrated reduced IFN-γ levels following TNF-α blockade. Plasma IL-6, MCP-1, and TNF-α were lower in ICI-Block mice. Single-cell RNA sequencing revealed shifts in immune cell populations and genes of interest including: Bcl2a1, Icos, Il18r1, Ccr2, and Jaml. This humanized model replicates ICI-AIN key features, revealing a synergistic role of ICIs and pro-inflammatory cytokines. TNF-α blockade demonstrated protective effects, supporting its potential role in mitigating the risk of ICI-AIN. - Source: PubMed
Publication date: 2026/03/05
Cuenca Narvaez Victor DNava Chavez CoraimaAl Refai OmarJacobs Johanna E JGutierrez Luis EZhang SongLi XiaoyanHirdler Jacob BRomero Michael FHerrmann JoergLi XiaogangDong HaidongEirin AlfonsoHerrmann Sandra M