Ask about this productRelated genes to: TLE2 antibody
- Gene:
- TLE2 NIH gene
- Name:
- TLE family member 2, transcriptional corepressor
- Previous symbol:
- -
- Synonyms:
- ESG2, GRG2, ESG, FLJ41188
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-12-20
- Date modifiied:
- 2018-11-15
Related products to: TLE2 antibody
Related articles to: TLE2 antibody
- Human nephrogenesis is complete at 34-36 weeks gestation, with 60% of nephrons forming during the third trimester through lateral branch nephrogenesis (LBN). Currently, no mechanism exists for LBN as there are no late gestation human kidney transcriptional datasets. We hypothesized that an induced but dividing population of nephron progenitor cells (NPCs) would contribute to the amplification of nephrons in late gestation. We used the rhesus macaque, an established model of LBN, to help identify potential mechanisms. - Source: PubMed
Publication date: 2026/05/04
Thakkar KairaveeYarlagadda SunithaAlkhudairy LyanPotter AndrewThorner KonradChaturvedi PraneetCebrian CristinaMcCracken Kyle WSalomonis NathanKopan RaphaelSchuh Meredith P - : The Notch signaling pathway regulates cell fate, proliferation, and differentiation, and its dysregulation has been implicated in various cancers, including breast cancer. MicroRNAs (miRNAs) are critical post-transcriptional regulators that can modulate Notch pathway components. The aim of this study was to identify miRNAs that may potentially regulate the expression of Notch pathway-related genes across five molecular subtypes of breast cancer in Polish women. : Tumor and adjacent normal tissue samples were collected from 405 patients with five breast cancer subtypes: luminal A ( = 130), HER2-negative luminal B ( = 100), HER2-positive luminal B ( = 96), non-luminal HER2-positive ( = 36), and triple-negative breast cancer ( = 43). Gene expression was profiled using mRNA microarrays and validated with RT-qPCR and ELISA. Candidate regulatory miRNAs were identified by miRNA microarrays and confirmed using the miRDB database. : , , , , , , , , and were consistently dysregulated across all breast cancer subtypes. Overexpression of and may be driven by decreased levels of miR-145, miR-98, and miR-381. Conversely, downregulation of may be associated with elevated expression of miR-196a and miR-155. No regulatory miRNAs meeting the selection criteria were identified for , , , , , or . : The consistent alterations suggest the presence of a shared Notch-driven oncogenic signature in breast cancer, potentially driving cell proliferation, stemness, and resistance to therapy. These findings enhance our understanding of Notch signaling in breast cancer and propose novel miRNA-Notch interactions as candidate targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/12/12
Mitka-Krysiak ElżbietaKról-Jatręga KatarzynaOssowski PiotrZmarzły NikolaBereza KrzysztofOrdon PawełKulej WojciechSirek TomaszSirek AgataBoroń KacperBoroń MaciejBoroń DariuszGrabarek Beniamin Oskar - Current treatments for pancreatic ductal adenocarcinoma (PDAC) fall short of meeting clinical needs, highlighting the urgent need for a comprehensive understanding of PDAC progression, which involves not only biochemical signals but also essential biomechanical cues. Here, we used a CRISPR-Cas9 screen in an orthotopic xenograft model to explore PDAC dynamics. The RNA binding protein DEAD-box helicase 3X-linked (DDX3X) was identified as a pivotal oncogene and biomechanical checkpoint. Specifically, DDX3X up-regulation in PDAC promoted tumorigenesis and metastasis, primarily through the transcriptional repressor TLE family member 2 (TLE2). Dysregulation of DDX3X in the tumor destabilized TLE2 messenger RNA and therefore disrupted the interaction with KLF4 (KLF transcription factor 4), leading to increased expression of myosin light chain 9 (MYL9). This change remodeled F-actin, enhancing tumor cell traction forces and consequently facilitating tumor metastasis. Targeting the DDX3X-TLE2-MYL9 pathway considerably reduces PDAC progression. This research reveals a promising approach for treating PDAC by focusing on biomechanical cues. - Source: PubMed
Publication date: 2025/09/12
Wang YuanyangYang QianyiLin FengSong XiaoweiYang GangWen DahanYang YingyunWu BichengMeng YunmengZhang NingLu XiaomeiXiong ChunyangZhao WenLiang JunboZhang TaipingLiu Yuying - Prematurity is associated with low nephron endowment and an increased risk of chronic kidney disease. Human nephrogenesis is complete at 34-36 weeks gestation, with 60% of nephrons forming during the third trimester through lateral branch nephrogenesis (LBN). We hypothesized that a differentiated but dividing population of nephron progenitor cells (NPCs) would contribute to the amplification of nephrons in late gestation. Methods: Single-cell RNA-sequencing (scRNA-Seq) was performed on cortically-enriched fetal rhesus kidneys (n=9) from late second trimester and third trimester during LBN. This data was integrated with publicly available human scRNA-seq datasets from 8-18 weeks gestation kidneys (n=8) using state-of-the-art bioinformatics pipelines. Differentially expressed genes and ligand-receptor interactions were assessed and validated using RNAScope on human and rhesus archival tissue. - Source: PubMed
Publication date: 2025/08/22
Thakkar KairaveeYarlagadda SunithaAlkhudairy LyanPotter AndrewThorner KonradChaturvedi PraneetMcCracken Kyle WSalomonis NathanKopan RaphaelSchuh Meredith P - Here, we investigated the role of the canonical Wnt signaling pathway transcriptional regulators at the neuromuscular junction. Upon applying a denervation paradigm, the transcription levels of , , , , , and were significantly downregulated. A significant decrease in canonical Wnt signaling activity was observed using the denervation paradigm in Axin2-lacZ reporter mice. Alterations in the transcriptional profile of the myogenic lineage in response to agrin (AGRN) suggested that TLE3 and TLE4, family members of groucho transducin-like enhancer of split 3 (TLE3), transcriptional repressors known to antagonize T cell factor/lymphoid enhancer factor (TCF)-mediated target gene activation, could be important regulators of canonical Wnt signaling activity at the postsynapse. Knockouts of these genes using CRISPR/Cas9 gene editing in primary skeletal muscle stem cells, called satellite cells, led to decreased AGRN-dependent acetylcholine receptor (CHRN) clustering and reduced synaptic gene transcription upon differentiation of these cells. Overall, our findings demonstrate that TLE3 and TLE4 participate in diminishing canonical Wnt signaling activity, supporting transcription of synaptic genes and CHRN clustering at the neuromuscular junction. - Source: PubMed
Publication date: 2024/03/27
Gessler LeaHuraskin DanyilEiber NaneHashemolhosseini Said