BATF
- Known as:
- BATF
- Catalog number:
- 002426A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BATF
Related genes to: BATF
- Gene:
- BATF NIH gene
- Name:
- basic leucine zipper ATF-like transcription factor
- Previous symbol:
- -
- Synonyms:
- B-ATF, SFA-2, BATF1
- Chromosome:
- 14q24.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-15
- Date modifiied:
- 2016-10-05
Related products to: BATF
Related articles to: BATF
- The Kaposi's sarcoma-associated herpesvirus oncoprotein vIRF3 is essential for primary effusion lymphoma (PEL) cell survival and cooperates with cellular interferon regulatory factor 4 (IRF4) to activate super-enhancers (SEs) controlling MYC and IRF4. However, the DNA sequence requirements for this cooperation are unknown. Using reporter assays, we mapped vIRF3/IRF4 responsiveness within the IRF4-SE to an ∼83-bp element activated by vIRF3 alone and cooperatively by vIRF3 and IRF4. vIRF3-dependent activation required an AP-1 motif, whereas cooperation with IRF4 required IRF4 DNA binding and IRF-related motifs outside canonical AP-1-IRF composite elements (AICEs). These motifs were necessary but insufficient outside their native sequence context, indicating a requirement for extended flanking sequences. DNA pulldowns revealed distinct motif requirements for vIRF3 and IRF4 association with the IRF4-SE. A distal MYC-SE required a similarly extended region containing a functional AICE2 motif, with vIRF3 activity depending primarily on its AP-1 half-site. Motif requirements were preserved in integrated reporter assays. BATF promoted vIRF3/IRF4-dependent activation preferentially in integrated reporters and was required to maintain vIRF3 and IRF4 occupancy at the endogenous MYC-SE. These findings define context-dependent DNA and cofactor requirements through which vIRF3 co-opts IRF4-regulated oncogenic enhancers in PEL. - Source: PubMed
Liang ZiyanMagdongon Christine BMa Haocong KatherineHaynes Maureen ELu JingyiBartom Elizabeth TGottwein Eva - Persistent plasma cell responses in systemic lupus erythematosus (SLE) sustain autoantibody production and immune complex formation, contributing to macrophage activation and renal inflammation. We investigated P2Y12 expression in plasma cell-related populations and evaluated the effects of ticagrelor on humoral and macrophage inflammatory responses in SLE. - Source: PubMed
Publication date: 2026/09/26
Lin JingjingLai JiayuanXu JiaxiangLin YichengYan QingLin RongfangMa Wenjuan - Brief psychotherapies have been shown to improve clinical symptoms within a limited number of sessions without compromising treatment quality. - Source: PubMed
Publication date: 2026/09/08
Marques Manoel Victor FernandesNunes Emerson Arcoverdede Oliveira Rodrigo CostaCoelho Nicole Leite GalvãoSilva Glauco FranciscoVilar Mariana Dantas de CarvalhoPiuvezam Grasiela - Immune tolerance after transplantation reduces immunosuppression-related complications and improves the overall survival rates. The unique tolerogenic microenvironment of the liver enables a proportion of liver transplantation (LT) recipients to develop tolerance with intact liver function. However, the underlying immunological mechanisms remain unclear. - Source: PubMed
Publication date: 2026/09/23
Liu YongboWang BingranSun DiZhou AiweiCai ZimengZhou TaoYang SenPan QiGao YunmuSong JiaqiZong ZhipengXiao WanglongLiu HongyuanYang TaihuaZhao ZhicongLuo YiZhang JianjunFang JianchenZhan ZhenzhenLu LinrongLiu YuanXia Qiang - Regulatory T (T) cells in mice can lose lineage identity and acquire proinflammatory functions, but whether human T cells are similarly susceptible to cytokine-driven destabilization remains unclear. Here we established an in vitro model of human T cell destabilization defined by silencing of the lineage-specifying transcription factor FOXP3, loss of suppressive function and acquisition of proinflammatory activity. Single-cell chromatin accessibility and transcriptomic profiling revealed a genome-wide increase in accessibility at AP-1-binding sites, including a putative regulatory element distal to IRF4. Increased accessibility at this element correlated with increased IRF4 expression during T cell destabilization, and its excision conferred resistance to inflammatory cytokine-induced reprogramming. Conversely, forced expression of IRF4 together with BATF promoted T cell destabilization. These data identify a distal IRF4 regulatory element as a critical node enabling heightened AP-1-IRF4 cooperative activity to drive T cell destabilization, with implications for the design of more stable and effective T cell-based therapies. - Source: PubMed
Publication date: 2026/09/21
Ho PatrickVu AlexanderLeung JoeyRosenthal WendyNtranos VasilisBluestone Jeffrey ATang Qizhi