DLL1 siRNA_Lentivectors
- Known as:
- DLL1 siRNA_Lentivectors
- Catalog number:
- i006190d
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- DLL1 siRNA_Lentivectors
Related genes to: DLL1 siRNA_Lentivectors
- 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 siRNA_Lentivectors
Related articles to: DLL1 siRNA_Lentivectors
- During transit in the genital tract until ejaculation, spermatozoa (SPZ) protein content and spatial distribution are remodeled through the cargo channeled by extracellular vesicles, namely epididymosomes (EpS), and the soluble luminal content. This remodeling confers the maturational competence for fertilization. This study evaluated the expression patterns of Notch components (NOTCH1-4, DLL1, 3 and 4, JAGGED1-2) in the bull genital tract tissues and their respective lumen, and their presence in EVs and SPZ, by immunocytochemistry and western blot. Results evidenced that NOTCH proteins are differentially expressed from the testis to the epididymis, the vas deferens and the accessory glands. In the testis, expression is mainly linked to acrosome biogenesis, while in post-testicular tissues is mainly localized in the adluminal cytoplasm of epithelial cells and the lumen. NOTCH1-3, DLL3 and JAGGED2 are released into the lumen via EVs, namely EpS, and are detected in SPZ of the corresponding genital tract segments. The spatial relationships support a model of region-specific acquisition of NOTCH proteins by SPZ through both testicular and EpS origins, with additional contributions from accessory glands at ejaculation. This prompts the involvement of NOTCH proteins in intercellular communication within the male reproductive tract, leading to SPZ maturation and competence for signaling in the female reproductive tract and during gamete interaction. - Source: PubMed
Publication date: 2026/07/10
Diniz PatríciaLeites InêsAlexandre-Pires GraçaTorres Ana CatarinaMateus LuísaLopes-da-Costa LuísSilva Elisabete - Mesenteric ischemia frequently causes bowel necrosis even after recirculation, known as reperfusion injury, and no effective therapy has been validated for preserving the intestine. Adipose-derived mesenchymal stem cell-conditioned medium (MSC-CM), a tissue engineering and regenerative therapy, has been suggested as a feasible acute-phase treatment for organ damages. This study aimed to elucidate the therapeutic effects of MSC-CM on intestinal tissue injuries by ischemia and reperfusion. Mice were categorized into three groups that underwent either 60-min mesenteric artery occlusion (ischemia group), 60-min reperfusion following 60-min occlusion (reperfusion group), or ischemia-reperfusion with the same duration following intravenous administration of 200-µL MSC-CM by retroorbital injection (MSC-CM group). The distal ileum was harvested, and immunofluorescence staining with caspase-3 and LGR5, an intestinal stem cell-specific marker, was performed for evaluating the injury location and type of cells protected by MSC-CM. Moreover, LGR5, Notch1, Jagged 1, Hes1, DLL1, DLL3, and DLL4 mRNA expressions were measured using quantitative polymerase chain reaction. Ischemia extensively damaged the epithelial layer, and reperfusion-induced cellular apoptosis at the epithelial layer. MSC-CM administration was associated with preservation of cells at the crypt base, which were identified as intestinal stem cells using double-immunofluorescence staining. The MSC-CM group demonstrated significantly higher LGR5 expression than the reperfusion and ischemia groups. Similarly, the MSC-CM group exhibited higher Notch1 and Jag1 expressions, whereas the reperfusion group showed a higher Notch1 expression. In conclusion, MSC-CM use was associated with preservation of the intestinal stem cells at the crypt of villi and higher Notch1 and Jag1 expressions. - Source: PubMed
Publication date: 2026/07/04
Yamamoto RyoSuzuki SayuriHomma KoichiroMaeshima KatsuyaKomura YasuoSasaki Junichi - Cell-based therapies hold great promise for treating late-stage retinal degenerative diseases. However, photoreceptor cell transplantation has been limited by poor cellular integration, suggesting that an ideal population of donor cells has not yet been defined. - Source: PubMed
Publication date: 2026/06/04
Yano Joseph JWei ZhangyongGajjar Krishna JBarati-Stec Kaidi TYang EmmaUyhazi Katherine E - 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