Bcl2A1
- Known as:
- Bcl2A1
- Catalog number:
- 000230A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Bcl2A1
Related genes to: Bcl2A1
- 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
A1 Bfl-1 Primary Antibody, BCL2A1, Species: Human Recombinant Protein Source: Rabbit PolyclonalA1_Bfl-1 Polyclonal Antibody, Reactivity: H M R, Gene ID: 597, Synonyms: BCL2A1A1_Bfl-1 Polyclonal Antibody, Reactivity: H M R, Gene ID: 597, Synonyms: BCL2A1anti-Bcl-2 Related Protein Bfl-1 (Bcl2A1) , Rabbit polyclonal to Bcl-2 Related Protein Bfl-1 (Bcl2A1) , Isotype IgG, Host Rabbitanti-Bcl-2 Related Protein Bfl-1 (Bcl2A1) , Rabbit polyclonal to Bcl-2 Related Protein Bfl-1 (Bcl2A1) , Isotype IgG, Host Rabbitanti-BCL2A1anti-BCL2A1anti-BCL2A1 (C-Terminus)anti-BCL2A1 (C-Terminus)anti-BCL2A1 (N-Terminus)anti-BCL2A1 (N-Terminus)Anti-Bcl2A1 Antibodyanti-BCL2A1 type: Primary antibodies host: MouseAnti-BCL2A1(Bcl-2-related protein A1) AntibodyAntibodies: BCL2A1 HOST: Goat Clonality: pAb Related articles to: Bcl2A1
- Severe COVID-19 involves hyperinflammation and multiorgan pathology, but consistent gene signatures remain elusive. We aimed to identify consensus transcriptomic signatures and molecular mechanisms in severe COVID-19. We performed an integrative analysis of 39 studies spanning 11 tissue types, 1551 bulk RNA-seq samples, and over 2 million single cells. A vote-counting strategy combined with a systems-biology approach was applied to detect consensus differentially expressed genes (DEGs). Pathways related to interferon/TNF-α signaling, hypoxia response, and platelet activation were consistently enriched across data sets. Among consensus DEGs-such as IFITM3, BCL2A1, CAMK2D, and CCR1-RAB8B was prioritized for functional validation based on its recurrence in ~45% of tissues and its known role in vesicle trafficking, a process intimately linked to viral life cycles. Molecular dynamics simulations and in vitro assays in SARS-CoV-2-infected CaCo-2 cells demonstrated that RAB8B modulates VAMP-3 clustering and intracellular trafficking. Silencing of Rab8b-1 and Rab8b-2 reduced viral infection by 30% (p = 0.0302) and 76% (p < 0.001), respectively. This study defines robust consensus signatures and positions RAB8B as a critical host factor and potential therapeutic target in severe COVID-19. Further exploration of RAB8B inhibitors is warranted to explore therapeutic utility. An interactive database at https://covidatlas.sysbio.tools/. - Source: PubMed
Avila Jonathan PeñaPark PeterSingh YouvikaAmaral Paulo PCastro ÍcaroTen-Caten FelipeSchuch VivianeGonçalves André N AGiddaluru JeevanMorais Mauro César CafundóOgava Rodrigo L TLubiana Thiagode Castro Gabriel AmorosoAquino RodrigoDurão LuizMartins Júlia RaspanteJimenez LeandroCosta-Martins André GGonzalez-Dias PatríciaHirata Thiago Dominguez CrespoDias Thomaz LüscherPeixe Débora GuerraSimizo AdrianaE Silva Juan Carlo SantosVasconcelos Amanda PereiraRodrigues Marcelo BerçotCastelucci Bianca GVirgillio-da-Silva João VictorMenezes LarissaMoraes-Vieira Pedro MCabral-Marques OtavioNakaya Helder I - 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. We further evaluated the efficacy of BEZ235, a dual PI3K/mammalian target of rapamycin (mTOR) inhibitor, in both in vitro cell models and in vivo immunosuppressed mouse models. Results showed that C. parvum suppressed intrinsic apoptosis during 52-76 h 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) and ileal parasite burden by 60.3% (vs. 42.8% with paromomycin), and markedly alleviating intestinal epithelial damage and restoring villus‑crypt structure. 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: 2026/04/15
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