Polyclonal Rabbit BATF Antibody
- Known as:
- Polyclonal Rabbit BATF Antibody
- Catalog number:
- KA0384
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit BATF Antibody
Related genes to: Polyclonal Rabbit BATF Antibody
- 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: Polyclonal Rabbit BATF Antibody
Related articles to: Polyclonal Rabbit BATF Antibody
- Cardiovascular disease (CVD) is a major cause of morbidity/mortality in juvenile-onset systemic lupus erythematosus (JSLE), yet no reliable tools exist to stratify CVD-risk. - Source: PubMed
Publication date: 2026/03/26
Peng JunjieDönnes PierreMcDonnell ThomasArdoin Stacy PSchanberg Laura ELewandowski Laura BJury Elizabeth CRobinson George ACiurtin Coziana - Individuals with inborn errors of immunity often mount suboptimal responses to vaccination, yet the molecular determinants underlying their variable responses to mRNA vaccines remain poorly defined. The present study aimed to identify baseline immune transcriptional signatures predictive of humoral responses to the BNT162b2 (Comirnaty) mRNA vaccine in individuals with inborn errors of immunity. Twenty-one SARS-CoV-2-naïve participants with diverse inborn errors of immunity were stratified as high or low responders to the BNT162b2 vaccine based on anti-SARS-CoV-2 spike IgG titers at day 28 post-vaccination. Although vaccine-induced T cell responses were broadly comparable, low responders had significantly lower frequencies of switched memory B cells ( = .014). Transcriptional profiling revealed 41 differentially expressed genes between groups at baseline. Activated memory B cells and peripheral T follicular helper cells from high responders exhibited greater induction of activation and memory-related genes, including NFKB1, CD69, TIGIT, CD40L, and BATF, indicating greater intrinsic readiness to support coordinated antibody production. These findings demonstrate that distinct pre-vaccination gene expression patterns within specific immune subsets are associated with differential humoral responses to mRNA vaccination in individuals with inborn errors of immunity. More broadly, the study highlights that baseline molecular immune features substantially influence vaccine efficacy and suggests that pre-vaccination transcriptional profiling may enable more personalized vaccination strategies for individuals with impaired immunity. - Source: PubMed
Publication date: 2026/04/24
Palma PaoloEmili ElenaPighi ChiaraColantoni NicoleMorrocchi ElenaPascucci Giuseppe RubensRivalta BeatriceRotulo Gioacchino AndreaRossetti ChiaraSantilli VeronicaZangari PaolaManno Emma ConcettaSanna MarcoFinocchi AndreaCancrini CaterinaCicalese Maria PiaCenciarelli SabinaCirillo EmiliaGiardino GiulianaMoschese VivianaAmodio DonatoCotugno Nicola - CD8 T lymphocytes differentiate from effector to memory cells after antigen clearance, with prolonged IL-2 production characterizing functional cytotoxic T lymphocytes (CTLs). To identify transcription factors associated with sustained IL-2 production, we compared influenza virus-specific and cytomegalovirus-specific CTLs, identifying Basic Leucine Zipper ATF-Like Transcription Factor 3 (BATF3) as a key candidate. BATF3 overexpression significantly enhanced cell proliferation in both virus-specific CTLs and CD19 chimeric antigen receptor T (CAR-T) cells while reducing cytokine production. Among AP-1 transcription factor family members, BATF and BATF3 demonstrated similar functions during effector phase expansion, but BATF3 exhibited distinct roles in promoting memory cell formation. ATAC-seq analysis revealed that BATF3 overexpression dynamically regulates chromatin accessibility, affecting diverse cellular processes including cytoskeletal organization, metabolic pathways, and survival signaling. BATF and BATF3 showed comparable kinetics until peak expansion, but BATF3 specifically facilitated the transition from effector to memory phase, up-regulating memory-associated genes while down-regulating exhaustion markers. These findings establish BATF3 as a master regulator of CD8 T-cell fate determination through chromatin remodeling, offering therapeutic targets for enhancing CAR-T cell persistence in immunotherapy. - Source: PubMed
Publication date: 2026/04/13
Umemura KojiKojima YasuhiroJulamanee JakrawadeeOkuno YusukeTakeuchi YukiOhara FumiyaKuwano ShihomiAdachi YoshitakaHanajiri RyoTerakura SeitaroKiyoi Hitoshi - A wealth of noncoding regulatory elements has been described across mammalian cell types, yet determining their functional role remains a challenge. Regulatory control of gene expression is critical during active processes such as the adaptive immune response. Upon antigen presentation, a naive CD4+ T cell undergoes major transcriptional and structural reorganization necessary for establishment of subset identity and immune function. In this study, we systematically measure the regulatory potential of candidate regulatory elements associated with open chromatin across five mouse CD4+ T cell subsets. Using ATAC-STARR-seq, we found that approximately one quarter of open chromatin regions demonstrate regulatory activity. Most exhibit shared functional potential across subsets, though we identify enhancers with activity that is restricted to specific cellular contexts. To distinguish regulatory potential from endogenous function, we performed CRISPR-based epigenome editing screens at noncoding regions of Th17 cells and identified a set of core elements essential for subset polarization. Integrating Region Capture Micro-C, we resolved precise 3D chromatin topologies that explain functional regulatory networks via physical contacts. We characterize examples of active regulatory hubs formed through multiple CTCF-independent interactions organized in a hierarchical architecture. Furthermore, we discover a critical enhancer that operates via these contacts. Using targeted perturbations, we disrupt local chromatin topology and gene expression with profound consequence to downstream Th17 cell phenotypes. We confirm the physiological necessity of these functional enhancers , demonstrating the importance of noncoding elements for Th17 cell identity. Together, this work reveals how DNA sequence and chromatin cooperate to shape the regulatory logic of Th17 cells, with implications for cis-regulatory principles beyond the immune system. - Source: PubMed
Publication date: 2026/04/08
Siklenka KeithZhang ChuangchuangLi LiqingParker MorganMehta NarenBarrera AlejandroVenukuttan RevathyCrawford Gregory EGersbach Charles ACiofani MariaReddy Timothy E - CAR-T cell therapies are revolutionizing the treatment of refractory or relapsed hematological malignancies, but many patients do not achieve durable responses, and these therapies remain ineffective against solid tumors. Therapeutic failure is closely associated with a poor persistence of CAR-T cells in patients, highlighting the need to identify strategies promoting in vivo expansion. Although numerous gene-editing strategies have been proposed, comparative studies to identify the most effective ones are still lacking. Here, using a focused CRISPR-knockout library targeting 50 selected gene candidates, we developed a competitive screening that revealed ZC3H12A, SOCS1, PTPN2, and CDKN2A as the most robust targets to improve persistence of EGFR CAR-T cells in human lung tumor-bearing mice. Surprisingly, disruption of other genes previously reported to improve CAR-T cell efficacy in other preclinical models-MED12, PRDM1, and BATF-had a detrimental effect in this context. These results suggest that some gene-editing strategies can yield beneficial, neutral, or even deleterious effects on CAR-T cell persistence, depending on specific conditions. Altogether, these findings highlight the importance of performing context-specific evaluations of genetic modifications to accelerate the clinical translation of the most promising editing strategies for optimizing CAR-T cell therapies. - Source: PubMed
Publication date: 2026/04/04
Fumagalli MattiaAn DongjieSimula LucaCombe CamilleAziez LisaSimoni YannickAlves-Guerra Marie-ClotildeValentini AndreaMarchais MaudeVermare AnaïsMoraly JosquinManni SimonaQuadraccia Maria CeciliaQuintarelli ConcettaDe Angelis BiagioBercovici NadègeDonnadieu EmmanuelPendino Frédéric