|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for DLL4(NM_019074.2) Search again
Product ID:
HQP013577
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AOS6, delta4, hdelta2
Gene Description:
delta like canonical Notch ligand 4
Target Gene Accession:
NM_019074.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene is a homolog of the Drosophila delta gene. The delta gene family encodes Notch ligands that are characterized by a DSL domain, EGF repeats, and a transmembrane domain. [provided by RefSeq].
Gene References into function
- Ectopic expression of human Delta4 in mice by retroviral gene delivery impairs hematopoietic development and leads to lymphoproliferative disease.
- We show here that vascular endothelial growth factor but not basic fibroblast growth factor can induce gene expression of Notch1 and Dll4, in human arterial endothelial cells. The VEGF-induced specific signaling is mediated through VEGF receptors 1 and 2
- suppresses the self-renewal capacity and long-term growth of two myeloblastic leukemia cell lines
- upon transduction into cord blood CD34+ stem cells, DLL4 induced a 25-fold reduction in nucleated cell production by maintaining a higher proportion of cells in G0/G1 phase; specific retention of CD34+ cells throughout the culture was observed.
- DLL4 not associated with susceptibility to periodic catatonia in German patients from 15q15 linked families
- DLL4 expression is essential for tumor angiogenesis.
- DLL4 expression is associated with vascular differentiation in bladder cancer.
- CD34+ cord blood progenitors were exposed for 4 days to either immobilized Notch ligand Delta-4. Delta-4 priming led to an acceleration of T-cell development, including a completion of the TCR rearrangement.
- Dll4-triggered Notch signaling may mediate inflammatory responses in macrophages and promote inflammation.
- Notch1 ligand, Delta-like ligand-4, stimulates R-Ras-dependent alpha 5 beta 1 integrin-mediated adhesion, demonstrating the physiological relevance of this pathway.
- Dll4 expression acts as a switch from the proliferative phase of angiogenesis to the maturation and stabilisation phase by blocking endothelial cell proliferation and allowing induction of a more mature, differentiated phenotype.
- Overexpression of DLL4 is associated with breast cancer
- Endometrial Dll4 may enhance the development of the endometrial microvascular system and facilitate the implantation of blastocyst in a fertile cycle.
- integrated role of dll4 with interleukin-12 demonstrated that, together, both of these instructive signals direct the immune response toward a more competent, less pathogenic antiviral response.
- The effects of a soluble form of Delta4 (solD4) by exposing CD34+CD38(low) cells to S17 feeders engineered to express solD4 (solD4/S17), were assessed.
- Overexpression of Delta-like 4 Notch ligand regulates tumor angiogenesis, improves tumor vascular function, and promotes tumor growth
- Dll4 may contribute to vascular differentiation and inhibition of the angiogenic response by regulating multiple receptor pathways.
- Global intrinsic (conformational) disorder, in concert with local preorganization, may play a role in Notch signaling mediated by Delta-4.
- retrovirus-induced over-expression of Dll4 in tumor cells activates Notch signaling in cocultured endothelial cells and limits vascular endothelial growth factor-induced endothelial cell growth
- Escape of human T-cell acute lymphoblastic leukemia cells from dormancy is associated with increased Notch3 signaling in tumor cells