Rabbit polyclonal to DLL1, Host Rabbit
- Known as:
- Rabbit pab DLL1, Host Rabbit
- Catalog number:
- YF-PA18503
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Rabbit polyclonal DLL1 Host
Related genes to: Rabbit polyclonal to DLL1, Host Rabbit
- 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
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guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody'F 4_80 Antigen (mouse) Host Rat'F 4_80 Antigen (mouse) Host Rat(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
A71915 98% C69H116N26O15S2 CAS:(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host Rabbit(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig(Arg8)-Vasopressin - Diluted Antiserum for RIA, Host: Guinea Pig Related articles to: Rabbit polyclonal to DLL1, Host Rabbit
- 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 - Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL) and several inflammatory disorders. Despite extensive research, the molecular mechanisms underlying HTLV-1 pathogenesis remain incompletely defined. Among host pathways hijacked by the virus, Notch signaling has emerged as a critical regulator of T-cell biology, immune evasion, and leukemogenesis. The Notch family, comprising four receptors (NOTCH1-4) and five ligands (Jagged1/2, DLL1/3/4), regulates key cellular processes, including proliferation, differentiation, and survival. Evidence suggests that HTLV-1 proteins, such as Tax and HBZ, directly or indirectly modulate Notch activity, leading to the constitutive activation of the Notch pathway and oncogenic transformation. Mutations in NOTCH1 and FBXW7 further stabilize the Notch intracellular domain (NICD), sustaining the transcription of proliferative and anti-apoptotic genes. Recent studies also highlight the involvement of JAG1 overexpression, H19/miR-675-mediated regulation, and crosstalk with PI3K and STAT3 signaling in maintaining Notch-driven leukemic phenotypes. Preclinical findings demonstrate that inhibition of Notch through γ-secretase inhibitors, restoration of FBXW7 function, or blockade of ligand-receptor interactions reduces ATLL cell growth and leukemia-initiating cell populations. However, clinical trials with selective Notch inhibitors show limited efficacy, underscoring the complexity of targeting this pathway. This mini-review provides an overview of Notch signaling in HTLV-1 infection, its contribution to ATLL pathogenesis, and therapeutic opportunities. Understanding the receptor-specific roles and molecular interactions within the Notch cascade may offer novel avenues for targeted interventions in HTLV-1-associated malignancies. - Source: PubMed
Publication date: 2026/05/27
Akbarin Mohammad MehdiFarjami ZahraÁlvarez Hugo Ramírez