BACH2 antibody - middle region (ARP33233_P050)
- Known as:
- BACH2 (anti-) - middle region (ARP33233_P050)
- Catalog number:
- arp33233_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- BACH2 antibody - middle region (ARP33233_P050)
Related genes to: BACH2 antibody - middle region (ARP33233_P050)
- Gene:
- BACH2 NIH gene
- Name:
- BTB domain and CNC homolog 2
- Previous symbol:
- -
- Synonyms:
- BTBD25
- Chromosome:
- 6q15
- Locus Type:
- gene with protein product
- Date approved:
- 2001-04-27
- Date modifiied:
- 2016-01-28
Related products to: BACH2 antibody - middle region (ARP33233_P050)
Related articles to: BACH2 antibody - middle region (ARP33233_P050)
- 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 - In ∼10% of asthma patients, symptoms remain uncontrolled despite maximal treatment, representing an unmet clinical need. The causal variants, genes and pathways underlying genetic risk factors have not been fully elucidated, and it is unclear whether there are unique genetic risk factors for this asthma subtype. - Source: PubMed
Publication date: 2026/09/01
Piga Noemi NPortelli Michael AShrine NickChen JingPacker RichardColey KayeshaWilliams Alexander TBatini ChiaraJohn CatherineLutz Sharon MVoorhies Kirsten RLevin Albert MZounemat-Kermani NazaninGern James EGold Diane RHartert Tina VJackson Daniel JJohnson Christine CKhurana Hershey Gurjit KMiller Rachel LSeroogy Christine MZoratti Edward MSin Don Dvan den Berge MaartenBossé YohanHall Robert JShaw DominickPogson Zara E KFogarty AndrewHeaney Liam GMansur Adel HChaudhuri RekhaThomson Neil CHolloway John WChung Kian FanBlakey John DWain Louise VOber CaroleWu Ann CAdcock Ian MHall Ian PBrightling Christopher ELassi GlendaSayers IanFawcett Katherine A - Hashimoto thyroiditis (HT) is a prevalent autoimmune thyroid disease characterized by lymphocytic infiltration and autoantibody production. Our previous findings showed that enhancer of zeste homolog 2 (EZH2) and BACH transcriptional regulator 2 (BACH2) are upregulated in HT thyroid tissues. However, the role of EZH2 in B-cell-mediated autoimmunity remains unclear. - Source: PubMed
Yi ShengguoLi XinnanCao YediLu GuizhiZhang JixinZhang YangYu NanHuang YouyuanQu ChenxueZhang JunqingGao Ying - To explore the function and molecular mechanism of BACH2 in septic lung injury induced by lipopolysaccharide (LPS). We established LPS-induced septic lung injury models in mice and human bronchial epithelial BEAS-2B cells. By overexpressing/knocking down BACH2 and knocking down Nrf2, combined with pathological staining, molecular biology and cell experiment techniques, we detected the levels of lung tissue injury, inflammation and pulmonary fibrosis, and verified the regulatory relationship between BACH2 and Nrf2. In the lung tissues of mice with LPS-induced septic lung injury, the expression level of BACH2 was decreased in a time-dependent pattern. Overexpression of BACH2 significantly alleviated LPS-induced pathological injury of mouse lung tissues, inhibited neutrophil infiltration, and reduced the release of inflammatory cytokines and the degree of pulmonary fibrosis. BACH2 could directly bind to the -2000 ~ -1800 bp region of the Nrf2 promoter and upregulate its expression, and knockdown of Nrf2 completely reversed the lung protective effect of BACH2. BACH2 exerts anti-inflammatory and anti-fibrotic effects by directly binding to and activating the Nrf2 signaling pathway, thereby ameliorating LPS-induced septic lung injury. The BACH2/Nrf2 axis may serve as a candidate molecular target for further preclinical research on septic lung injury treatment. - Source: PubMed
Publication date: 2026/08/29
Wang LihuiJi XiaoliangDong ShiminLu Qinglong - Identification of the origin of pathogenic immune cells is crucial for therapeutic interventions and diagnosis but pseudotime methods struggle to trace immune cells accurately. Current trajectory inference methods for B cell development and response in health and disease either ignore or underutilize antigen receptor sequence information, limiting their ability to resolve developmental pathways, particularly for pathogenic populations. Widely used methods such as Monocle 3 reconstruct developmental paths from transcriptomic similarity alone, discarding the features from immune receptors. Dandelion has combined the immune receptor features with transcriptomics but it struggles to simulate the trajectory path of B cells. Here we present ClonoTrace, a computational framework that integrates BCR sequence features with transcriptomic trajectory inference through gated fusion of multimodal embeddings. In fetal B cell development and germinal centre development, ClonoTrace demonstrates closer concordance with the canonical reference ordering than Monocle 3 and Dandelion. Applied to systemic lupus erythematosus, ClonoTrace indicates a memory B cell extrafollicular maturation route alongside the naïve B cell route, accompanied by induction of ZEB2 with a concomitant decline of BACH2 along the trajectory, as a candidate alternative route to pathogenic double negative 2 B cells (DN2) in systemic lupus erythematosus (SLE) patients. In healthy ageing, ClonoTrace resolved three candidate age-related B cell maturation routes, from naïve, IgM memory and switched-memory B cells, each passing through a DN2-associated transcriptional state that is ordered before age-associated B cells along the inferred trajectory. ClonoTrace's fate probability algorithm indicated that IgM memory B cell to ABC transition as the leading candidate age-associated transition, which may be distinct from SLE DN2 maturation. ClonoTrace provides a generalizable framework for receptor-informed trajectory inference, describing candidate developmental routes of pathogenic B cell populations in autoimmunity and ageing. - Source: PubMed
Publication date: 2026/08/28
Lou HantaoZhang MeihanZhang BoLu QianjinZheng JianqingCao Xuetao