TWIST1 Antibody - N-terminal region (ARP33423_P050)
- Known as:
- TWIST1 Antibody - N-terminal region (ARP33423_P050)
- Catalog number:
- arp33423_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- TWIST1 Antibody - N-terminal region (ARP33423_P050)
Related genes to: TWIST1 Antibody - N-terminal region (ARP33423_P050)
- Gene:
- TWIST1 NIH gene
- Name:
- twist family bHLH transcription factor 1
- Previous symbol:
- ACS3, BPES3, TWIST, CRS
- Synonyms:
- SCS, H-twist, BPES2, bHLHa38, CRS1
- Chromosome:
- 7p21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-01
- Date modifiied:
- 2016-10-05
Related products to: TWIST1 Antibody - N-terminal region (ARP33423_P050)
Related articles to: TWIST1 Antibody - N-terminal region (ARP33423_P050)
- Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality worldwide. Cigarette smoke extract (CSE) is a major environmental factor driving NSCLC progression, yet the underlying molecular mechanisms remain incompletely understood. Protein arginine methyltransferase 6 (PRMT6) is implicated in various malignancies, including NSCLC, and epithelial-mesenchymal transition (EMT) contributes to metastasis and poor prognosis in this disease. However, the role of PRMT6 in CSE-induced NSCLC progression has not been elucidated. - Source: PubMed
Zhang YanwenChang XiaojingCao JieZhang JingZhao Haiyan - Interleukin-6 (IL-6) and twist family bHLH transcription factor 1 (TWIST1) are critical regulators of cancer progression, including in pancreatic ductal adenocarcinoma (PDAC), but how they dynamically interact remains unclear. Therefore, this study aimed to elucidate the interaction between IL-6 and TWIST1 and explore the underlying mechanisms involved in PDAC progression. - Source: PubMed
Publication date: 2026/06/24
Yu MiaoHuang EnlaiSu MingxinTian ZhenfengLi YaqingLin XingyiHu BingrongChen YintingOu Guangsheng - Stromal cell states are altered in active Crohn's disease (CD), but their origin and phenotypic stability are unknown. Using single-cell spatial transcriptomics, RNA sequencing and ATAC sequencing of ~2,500,000 cells, we map 18 distinct stromal cell states within their cellular and cytokine signaling environments in human full-thickness CD bowel. Inflammatory fibroblasts (IFs) reside in immune cell-rich mucosal ulcers and are induced through combinatorial cytokine exposure suppressing submucosal universal fibroblast programs. The IF state is stabilized through transcription factor (TF) activity of GLI3, TWIST1, ETV4, PRDM1 and RELB, and does not spontaneously revert; however, histone deacetylase inhibition destabilizes the IF state, preventing IF secretome-induced epithelial transmigration and activation of neutrophils. The IF open chromatin configuration is distinct from that of fibrotic contractile stroma, which populate adjoining immune-depleted submucosal fibrotic niches. These findings show that microenvironments in pathological tissue niches shape open chromatin configuration of stromal states that are amenable to modulation by epigenetic modifiers. - Source: PubMed
Publication date: 2026/08/12
Koplev SimonSharma OsheenWoelfel SimonHuang NiPohin MathildeFeile AdrianWarschinke MariaArtero Mikel RezolaSuthakaran SharujanSarropoulos IoannisPett J PatrickNyman JuliaThomas TomPham DuyLi BinAttar MoustafaPakpoor JuliaMilosevic-Hutton KateEaston AlistairButler MattDunford JamesPhilpott MartinColes MarkBuckley Christopher DDendrou CalliopeShamiyah KhalidKretschmer LorenzDratva LisaIssa FadiHester JoannaRittscher JensWalsh AlissaTravis Simon PProgatzky FränzeUnger Lukas WBignell MarkBaker KatherineGeorge BruceAl-Mossawi HusseinKlenerman PaulMosig Alexander SOppermann UdoTeichmann Sarah APowrie Fiona MFriedrich Matthias - - Source: PubMed
- Genome-wide analyses of transcription factor (TF) motif binding sites have largely emphasized individual high-affinity sites, while overlooking the regulatory importance of locally repetitive motif clusters. Such clusters, including combinations of weak and strong binding sites, can collectively enhance TF occupancy and regulatory activity. Here we present Motif-Cluster, an open-source framework for motif-driven prioritization and visualization of TF binding clusters using sequence information alone. Motif-Cluster integrates a density-based clustering strategy with flexible modeling of binding-site gaps and affinity signals, enabling the identification and ranking of candidate regulatory regions without requiring experimental binding data. Through simulations and multiple real-data analyses, we show that combining gap distributions with binding affinity effectively balances cluster size and signal strength while reducing noise from weak sites. Application to ZNF410 successfully recovers the previously characterized binding clusters in the CHD4 promoter, which are conserved between human and mouse. Additional case studies involving PHB1, TWIST1, and EGR1 further demonstrate the general applicability of the method across diverse transcription factors. Motif-Cluster also provides intuitive visualization and reproducible workflows to facilitate interpretation of spatially dense motif patterns. Overall, Motif-Cluster offers a robust and flexible approach for prioritizing transcription factor regulatory regions from genome-wide motif scans, enabling biological discovery and guiding experimental design, particularly in settings where direct genome-wide binding assays are unavailable. - Source: PubMed
Publication date: 2026/08/05
Zhou MengyuanYao Qiuming