TLE3 antibody (N-terminal)
- Known as:
- TLE3 (anti-) (N-terminal)
- Catalog number:
- 20r-3004
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- TLE3 antibody (N-terminal)
Related genes to: TLE3 antibody (N-terminal)
- Gene:
- TLE3 NIH gene
- Name:
- TLE family member 3, transcriptional corepressor
- Previous symbol:
- -
- Synonyms:
- ESG, ESG3, KIAA1547, HsT18976, GRG3
- Chromosome:
- 15q23
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-13
- Date modifiied:
- 2018-11-15
Related products to: TLE3 antibody (N-terminal)
Related articles to: TLE3 antibody (N-terminal)
- The roles of translational control in the immune system are incompletely understood. Using a CRISPR/Cas9-mediated functional screen of RNA helicases in an in vitro system of plasma cell differentiation, we identify in this study DHX29 as a critical regulator of this process. Mice with B-cell-specific deletion of Dhx29 exhibit severely impaired germinal center B-cell formation, plasma cell differentiation, and antibody production. Mechanistically, DHX29 promotes translation of Tcf3 and Tle3 mRNAs via binding to their 5' untranslated regions (UTRs). In the absence of DHX29, B cells exhibit normal proliferation but fail to undergo class switch to IgG1 and differentiation into plasma cells, resulting in impaired antibody production. Ectopic expression of TCF3 and TLE3 largely restores plasma cell differentiation of Dhx29-deficient B cells. Our study provides insights into the functional importance of translational control in the immune system by unraveling critical roles of the RNA helicase DHX29 in the translation of key transcription factors controlling germinal center response and plasma cell differentiation. - Source: PubMed
Publication date: 2026/05/26
Zhao JiayiHe XiaoyuHong PeichengLin LianghuaDu YingChen PengdaZhang LixiaoLeng JialeMa LihuiXie JunLin XinyongAdilijiang AbidanWang JiazhenHong YazhenXiao ZhengtaoLiu Wen-HsienXiao Changchun - Keloids are pathological scars. There is a genetic predisposition for keloids, and the molecular events associated with keloid need to be profiled. - Source: PubMed
Publication date: 2026/04/22
Sun NanaLiu BoZeng NiWen YangCai YuanXu GuangchaoLiu JieLiu Jianguo - To integrate multiscale embedded gene co-expression network analysis (MEGENA) and Mendelian randomisation (MR) to identify new pathogenic factors associated with breast cancer (BC). - Source: PubMed
Wang YangXie RuiZhang HuimingGe Zhicheng - Hybridization effectively enhances breeding efficiency and significantly boosts sheep productivity. However, the epigenetic mechanisms underlying the superior production performance of crossbreds remain largely elusive. In this study, Hu sheep were crossbred with Suffolk rams used as the paternal line. We integrated RNA-seq, ATAC-seq, and CUT&Tag (H3K4me3, H3K4me1, H3K27ac, and H3K27me3) techniques to characterize epigenetic regulatory differences in the longissimus dorsi muscle between Hu sheep (HU) and crossbred progeny (SH). Phenotypic and transcriptomic analyses revealed that SH crossbred sheep exhibited superior growth performance ( < 0.05), and the upregulated genes in the Apelin signaling pathway were significantly correlated with eye muscle area ( < 0.05). Utilizing a Hidden Markov Model, we annotated 15 distinct chromatin states in both HU and SH sheep, systematically characterizing the dynamic epigenomic landscapes across the two breeds. In contrast to SH sheep, the genome of HU sheep exhibited enrichment of repressive chromatin modifications typified by H3K27me3. Strong active enhancers (EnhA) were significantly enriched within upregulated genes in SH. A total of 1862 SH-specific and 691 HU-specific EnhA elements were characterized in this study. Motif analysis revealed that SH-specific EnhA were enriched for myogenic MEF2 family motifs ( < 0.05), which promote muscle and vascular development. By integrating multi-omics data, we constructed a putative regulatory network potentially modulated by SH-specific enhancers, identifying , , and as the core hub genes. Collectively, this study provides a robust data resource, identifying candidate genes and regulatory elements associated with crossbreeding-related muscle phenotypes. - Source: PubMed
Publication date: 2026/04/04
Cheng JiangboXu DanTian HuibinZhang XiaoxueZhao LimingZhang RunanWang JianlinXiao JinyuLi FadiWang WeiminZhang Deyin - The transcriptional corepressor Tle (transducin-like enhancer of split) proteins interact with transcription factors such as TCF-1 and Runx3 to regulate transcriptional programmes during cellular development and differentiation; however, their roles in CD8+ T cell differentiation, particularly under conditions of chronic antigen stimulation, remain poorly defined. Here, we demonstrated that overexpression of Tle1, Tle3, and Tle4 improves the proliferation of antigen-specific effector CD8+ T cells during both acute and chronic viral infections. Notably, overexpression of Tle3 and Tle4, but not Tle1, augmented secondary responses of memory CD8+ T cells in the context of acute viral infection. Tle1-overexpressing CD8+ T cells displayed enhanced TCR signal strength, accompanied by elevated expression of immunoinhibitory receptors such as PD-1 and LAG-3. Transcriptome analyses and genome-wide binding profiles suggested that Tle1 and Tle3 cooperate with multiple transcription factors, including members of the Ets, AP-1, and Runx families, to drive expression of genes involved in the activation and maintenance of antigen-specific CD8+ T cell responses. Notably, Tle1 overexpression improves cytotoxic T lymphocyte (CTL) responses to PD-1/PD-L1 blockade during chronic viral infection. Tle1 was found to enhance TCR signalling and the expression of immunoinhibitory receptors through repression of TCF-1, whereas its effect on effector CD8+ T cell proliferation occurred independently of TCF-1. These findings revealed the regulatory roles of Tle proteins in orchestrating transcription factor networks that govern CD8+ T cell differentiation during viral infections. - Source: PubMed
Publication date: 2026/03/11
Shiga RyotaroFujisawa SotaroTanabe YamatoKurachi JunkoKoura MikiTamai ToshikatsuKurachi Makoto