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
- Osteosarcoma (OS) is highly invasive, metastatic, and lacks effective therapies, leading to poor prognosis. This study aims to dissect the core epigenetic features of OS from the perspective of chromatin accessibility to elucidate its pathogenesis and identify novel therapeutic targets. ATAC-seq was used to map the global chromatin accessibility profiles of OS tissues versus normal controls. We identified OS-specific aberrantly accessible chromatin regions and delineated enriched transcription factor binding motifs. Key transcription factors were validated by Western blotting and flow cytometry. Notably, in regions with enhanced accessibility, the binding probability of AP-1 family members (including Atf3, Fra1, Fra2, JunB, BATF, AP-1, Jun-AP1, Bach2, and CTCF) was significantly elevated. Further analysis indicates that JunB can inhibit apoptosis of OS cells and enhance their invasive ability, suggesting that it may be related to tumor progression. Overall, JunB, as a candidate molecule with potential research value, is worthy of further verification in subsequent in vivo models and clinical samples to determine its feasibility as an intervention target for OS. - Source: PubMed
Publication date: 2026/09/05
Ye FanHu Po - Foxp3 regulatory T (Treg) cells need to differentiate into effector Treg (eTreg) cells to maintain immune tolerance and tissue homeostasis. While several transcription factors such as Batf and JunB have been reported to be essential for eTreg differentiation and function, the underlying epigenetic mechanism remains unclear. Here, we show that the histone variant H3.3 is enriched in tissue Tregs compared to splenic Tregs and its chaperone Hira is a critical regulator of Treg effector program. Treg specific-deletion of resulted in reduced eTreg population, impaired suppressive function and multi-organ inflammation in mice. Mechanistically, Hira-dependent H3.3 deposition establishes a permissive epigenetic environment by enhancing chromatin accessibility, facilitating H3K36me3 and preventing H3K27me3 modifications on loci of genes enriched for AP-1 family binding motifs and associated with Treg effector function. Furthermore, overexpression of Batf in -deficient Treg cells largely ameliorates their regulatory defects. Together, our findings reveal a previously unreported epigenetic mechanism critical for Treg effector differentiation and function. - Source: PubMed
Publication date: 2026/08/19
Cao XiangxiangLv MengjieLv ZhihanZheng ShutingTan XinyiDing JiyuLiang WeiLi GuohongZhou XuyuZhu Mingzhao - Mugwort () is a predominant aeroallergen for allergic rhinitis (AR) in northern China. However, the molecular changes linking local nasal mucosal inflammation with systemic alterations remain incompletely understood. This study aimed to explore the cross-level regulatory network in a mouse model of mugwort-induced AR by combining nasal mucosal transcriptomics and serum metabolomics. - Source: PubMed
Publication date: 2026/07/08
Chi JiaoniChen LinJin YuxuanSun Jin-LyuXu Yajie - Large B-cell lymphoma with IRF4 rearrangement (LBCL-IRF4) predominantly affects children and young adults (CAYA) and presents as localized disease with excellent prognosis. Although most tumors harbor IRF4 rearrangements (IRF4-R), the existence of cryptic rearrangements has been suggested. Whether IRF4-R LBCL in adults represents the same biological entity remains unclear. To address this question, 35 CAYA patients diagnosed with LBCL-IRF4 and 7 adult (>40-year-old) LBCL with IRF4-R were investigated by an integrative molecular approach. Targeted sequencing structural variant analysis (SV-NGS) confirmed the IRF4-R in 84% of investigated cases. In CAYA, an enrichment (55% vs 29% in adults) of translocations involving IGH, with a breakpoint cluster 3' to IRF4 (EXOC2) was observed, including a cryptic insertion of IGHM-IGHJ5 into IRF4 locus. Novel translocations, IRF4::MIR142 in two CAYA (7%) and IRF4::BATF in one adult, were discovered. Whole-exome sequencing analysis identified unreported mutations in LBCL-IRF4 as YY1 and ZC3H12A (11% each). The high incidence of mutations affecting the B-cell receptor/NF-KB pathways in LBCL-IRF4 was confirmed in cases with diffuse component only. None of the CAYA tumors were classified by LymphGen tool. Adult IRF4-R LBCL showed higher levels of genetic complexity and a distinct mutational profile with mutations on KMT2D and DTX1 (43% each), and MYD88-L265P (29%), and were predicted as EZB or MCD (29% each). These differential genetic features were in line with different clinical presentations (extranodal involvement and advanced stage). In conclusion, IRF4-R architecture and mutational profile differ according to age, supporting that not all cases should be classified as LBCL-IRF4. - Source: PubMed
Publication date: 2026/07/16
Colmenero AriadnaFrauenfeld LeonieMato SaraSalmerón-Villalobos JuliaArredondo-Prats VicenteRamis-Zaldivar Joan EnricMontaner AnnaCastrejon-de-Anta NataliaGonzalez-Farre BlancaGarcia NoeliaVerdu-Amorós JaimeAndres MaraAndión MaitaneAzorín DanielCelis VerónicaRodríguez-Pinilla Socorro MariaAliste Santos CarlosHsi EricGheorghe GabrielaMariani Rachel AngelicaSchafernak Kristian TShestakova AnnaMenon MadhuLlamas Gutierrez FranciscoHebeda Konnie MBhavsar Tapan MahendraLópez-Guillermo ArmandoJaffe Elaine SQuintanilla-Martinez LeticiaCampo ElíasNadeu FerranBalagué OlgaSalaverria Itziar - Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) is a late-onset neurodegenerative disorder caused by FMR1 premutation CGG repeat expansions (55-200 repeats). The epigenetic landscape of the FXTAS brain remains uncharacterized. We performed genome-wide DNA methylation profiling of postmortem prefrontal cortex tissue to identify differentially methylated positions (DMPs) and candidate genes, and sought protein-level support for a neuroinflammatory signal. - Source: PubMed
Publication date: 2026/07/10
Lozano ReymundoLin XiaoHagerman RandiCerdeño Verónica MartínezPinto Dalila