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)
- 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 - Insulin-like growth factor binding protein 2 (IGFBP2) has emerged as a multifarious and context-dependent oncoprotein that links several mechanisms in the tumor microenvironment (TME) including oncogenic signaling, extracellular matrix (ECM) remodeling, immune evasion, and therapy resistance. Beyond its established role in modulating IGF signaling, IGFBP2 exerts IGF-independent effects via its RGD integrin-binding motif and nuclear localization signal (NLS). By binding integrins (αvβ3, α5β1), IGFBP2 activates focal adhesion kinase (FAK), which then triggers PI3K/AKT signaling and MAPK/ERK signaling pathways, resulting in enhanced proliferation, migration, invasion, and angiogenesis. Nuclear translocation of IGFBP2, mediated by its NLS, enables direct regulation of gene expression, notably by upregulating epithelial-mesenchymal transition (EMT) transcription factors such as ZEB1, SNAI1, and TWIST1, and regulating immune checkpoint molecules. These actions reshape the TME by increasing angiogenesis, stromal stiffness, and tumor invasiveness. IGFBP2 further sustains survival signals under receptor tyrosine kinase inhibition, enhances tumor cell metabolic adaptation to hypoxia, and supports cancer stemness, all of which drive resistance to chemotherapy, radiotherapy, and immunotherapy. Overexpression of IGFBP2 in cancer is linked to increased tumor aggressiveness, unfavorable prognosis, and general resistance to therapy. Importantly, IGFBP2 functions are highly context-dependent, in some epithelial settings, IGFBP2 sequesters IGFs and dampens IGF-IR signaling, resulting suppression of downstream oncogenic pathways. This duality underscores IGFBP2's nuance and tumor-specific biology. Therapeutic strategies under development specifically target IGFBP2-integrin-mediated signaling and IGFBP2 nuclear activity. There are encouraging results in preclinical studies involving antisense oligonucleotides, monoclonal antibodies, and peptide inhibitors. As both a mediator of oncogenic adaptation and a clinical biomarker, IGFBP2 represents a vulnerability in the TME that may be targeted to improve, personalize, and combine cancer therapies. - Source: PubMed
Publication date: 2026/08/03
Das ProvasConley Shannon MarthaPanja PrasantaBhattacharya ReshamMukherjee Priyabrata - Metastatic dissemination is the principal cause of death in pancreatic ductal adenocarcinoma (PDAC), yet the molecular determinants that enable this process remain poorly understood. Here, we identify the axon guidance receptor UNC5B as a central regulator of PDAC metastasis. Using both genetically engineered KPCU and orthotopic mouse models, we demonstrate that loss of UNC5B completely abolishes metastatic spread, reduces tumor proliferative capacity, increases intratumoral necrosis, confining tumors to the pancreas with no invasion into adjacent tissues or lymph nodes and preserving epithelial morphology. Mechanistically, UNC5B drives epithelial-to-mesenchymal transition (EMT) and invasion through activation of the SRC-ZEB1 axis. Notably, UNC5B specifically engages ZEB1 to drive EMT, without altering other canonical EMT transcription factors such as SNAIL or TWIST1. Pharmacological degradation of exogenous UNC5B using a targeted protein degrader (degron) modulated EMT and invasive behavior in PDAC cells. Acute depletion of UNC5B resulted in a marked reduction in EMT scores, accompanied by decreased ZEB1 and SRC levels. Together, these findings identify UNC5B as a central molecular hub governing metastatic competence in PDAC by promoting EMT and invasion. - Source: PubMed
Publication date: 2026/08/01
Sadeqi Nezhad MuhammadHarris Chris RPrela OrjolaNarrow WadeBreitenbach MitchellWang LanJain ShubhrikaBecker Jennifer LBagci BuketHao YanshengHezel Aram FGerber Scott AMello StephanoWithers TracyCarpizo Darren R