DLL1
- Known as:
- DLL1
- Catalog number:
- Y213259
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DLL1
Related genes to: DLL1
- Gene:
- DLL1 NIH gene
- Name:
- delta like canonical Notch ligand 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6q27
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2019-01-03
Related products to: DLL1
Related articles to: DLL1
- Ovarian cancer (OV) is a leading cause of cancer-related mortality, with cisplatin resistance being a major clinical challenge. This study investigates the role of the Notch ligand DLL1 in mediating ferroptosis resistance and its impact on cisplatin sensitivity in OV. - Source: PubMed
Publication date: 2026/06/17
Ye DanHuang GaotingYan XingchengSuntan LeziShen HaoranShen Jian - Identifying biological roles for glycosyltransferases is a continuing challenge and important for defining morbidities associated with congenital disorders of glycosylation. Here we investigate the consequences to intestinal development of conditionally deleting Lfng alone or Lfng, Mfng and Rfng together in a mixed or Eogt-null genetic background. Each Fringe transfers N-acetylglucosamine (GlcNAc) to fucose (Fuc) attached to Ser or Thr by POFUT1 in a consensus sequence found in certain epithelial growth factor-like (EGF) repeats. EOGT transfers GlcNAc directly to Ser/Thr in a separate consensus sequence of an EGF repeat. Notch receptors and Notch ligands contain the largest number of EGF repeats with consensus sites for these O-glycans. Conditional deletion of Pofut1 in mouse intestine causes similar developmental defects to deletion of Notch1 and Notch2 or Dll1 and Dll4. LFNG also contributes to optimal Notch signaling in mouse intestine. In this work, we generated Lfng[F/F]:Villin-Cre and Lfng[F/F]Mfng[-/-]Rfng[-/-]:Villin-Cre mice in which extension of O-Fuc on EGF repeats was respectively inhibited or prevented in intestinal epithelium. Conditional deletion of either Lfng alone or all three Fringe activities together led to defective intestinal development with a marked increase in goblet and Paneth cells, increased crypt width and reduced villus length. Unexpectedly, in mice globally lacking EOGT, conditional inactivation of the three Fringe genes did not lead to defective intestinal development. Thus, the absence of EOGT prevented disruption of development in Fringe-null intestine, identifying a novel role for EOGT in regulating intestinal development. - Source: PubMed
Publication date: 2026/06/09
Nauman MohdZhang JinghangStanley Pamela
- Source: PubMed
- The diagnosis of bacterial infections (BIs) in patients with acute-on-chronic liver failure (ACLF) remains a formidable clinical challenge, directly impacting mortality rates. Current biomarkers are often confounded by the profound systemic inflammation inherent to ACLF itself. The objective of this study was to evaluate the diagnostic and prognostic utility of serum Delta-like ligand 1 (DLL1) in ACLF patients with BIs. - Source: PubMed
Publication date: 2026/05/14
Huang JuanjunWang ZhiZhu WeiChen Jian - T-cell acute lymphoblastic leukemia (T-ALL) frequently involves the activation of NOTCH1 signaling. However, effective NOTCH-directed therapies remain elusive. We established and characterized a novel T-ALL cell line, TMD11, lacking NOTCH mutations but sensitive to γ-secretase inhibitors (GSIs), providing a tool for discovering novel molecular targeted therapies. - Source: PubMed
Itoh MaiTohda Shuji