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Human DLL4 Protein expressed in Human Cells - ABIN2002236
Dorsch, Zheng, Yowe, Rao, Wang, Shen, Murphy, Xiong, Shi, Gutierrez-Ramos, Fraser, Villeval: Ectopic expression of Delta4 impairs hematopoietic development and leads to lymphoproliferative disease. in Blood 2002
Show all 6 Pubmed References
TR3/Nur77 regulated the expression of DLL4 and Jagged1 in culture endothelial cells. DLL4 and Jagged1 play important roles in the angiogenic responses induced by TR3/Nur77.
Notch1 inactivation in keratinocytes is sufficient to cancel the repressive effects of the Dll4-Notch1 loop on wound healing in diabetes, thus making Notch1 signaling an attractive locally therapeutic target for the treatment of Diabetic foot ulcerations.
These data indicate that DLL4 represents a new prognostic biomarker for nonsmall cell lung cancer , and DLL4 overexpression inhibits cell proliferation and metastasis in vitro.
Study demonstrates that DLL4 is important in regulating the tumour growth of hepatitis B virus (HBV)-associated hepatocellular carcinoma as well as the neovascularization and suppression of HBV replication.
this study revealed that DLL4 has pathophysiological roles on the progression of esophagus cancer cells, including migration, invasion and apoptosis, which indicated that DLL4 may be considered as a potent therapeutic target for the treatment of malignant esophageal cancer.
The regulation of DLL4 by the LDB2 complex provides a novel mechanism of DLL4 transcriptional control that may be exploited to develop therapeutics for aberrant vascular remodeling.
Data show that Delta-like 4 (DLL4) and Jagged1 (JAG1) displayed equal potency in stimulating Notch target genes in HMEC-1 dermal microvascular endothelial cells but had opposing effects on sprouting angiogenesis in vitro.
epigenetic silencing and TP53 mutation have an effect on the expression of DLL4 in human cancer stem disorder
the Notch signaling and atherosclerosis relevant markers in lesions from femoral arteries of symptomatic peripheral artery disease patients, were characterized.
Data suggest that Numb acts as a Notch antagonist by controlling intracellular destination and stability of the Notch ligand Delta-like 4 (DLL4) through a post-endocytic sorting process; Numb negatively controls DLL4 plasma membrane recycling through well-documented recycling regulator protein AP1.
Results show that DLL4 is involved in SYNJ2BP-induced hepatocellular carcinoma (HCC) development though activating its pathway.
Positive Jagged1 and DLL4 expression is closely correlated with severe clinicopathological characteristics and poor prognosis in patients with gallbladder cancers.
We show that GIT1, which also contains an ANK domain, inhibits the Notch1-Dll4 signaling pathway by competing with Notch1 ANK domain for binding to RBP-J in stalk cells
Results provide evidence that DLL4 is associated with gastric cancer stem/progenitor cells (GCSPCs), and its expression impacts CSPC stemness characteristics associated with the Notch-1 pathway including self-renewal, differentiation, proliferation, and tumor formation.
The authors present novel structures of human ligands Jagged2 and Delta-like4 and human Notch2, together with functional assays, which suggest that ligand-mediated coupling of membrane recognition and Notch binding is likely to be critical in establishing the optimal context for Notch signalling.
Overexpression of DLL4 could significantly attenuate the cytotoxic effects of docetaxel in MCF-7 cells by increasing Bcl-2 expression, while decreasing Bax expression, apoptosis rate and DNA damage
In gastric epithelial cells co-cultured with Helicobacter pylori, the expression level of the ligand DLL4 was found to be significantly increased.
Low DLL4 abundance in tumour cells may predict the benefit from adjuvant gemcitabine therapy after PDAC resection.
Angiogenesis in Infantile haemangioma (IH) appears to be controlled by DLL4 within the endothelium in a VEGF-A isoform-dependent manner, and in perivascular cells in a VEGF-independent manner. The contribution of VEGF-A isoforms to disease progression also indicates that IH may be associated with altered splicing.
Dll4 modulates liver inflammatory response by down-regulating chemokine expression
repressed Dll4-Notch1 signaling pathway but not downregulation of VEGF-A expression are responsible for hyperoxia induced pervasive vessel regression.
this study shows that DLL4 induces epigenetic regulation of Treg cell differentiation and function in viral infection
Collectively, these data show that DLL4 preferentially activates NOTCH1 over NOTCH2, whereas DLL1 is equally effective in activating NOTCH1 and NOTCH2, establishing that the ectodomains dictate selective ligand function in vivo, and that features outside the known binding interface contribute to their differences.
anti-Dll4 antibody could inhibit the differentiation of Th17 cells in asthmatic mice.
Data suggest that endothelial specific Delta-like 4 (Dll4) overexpression appears as a promising anti-angiogenic modality that might improve cancer control.
Dll4 seems to promote Apc (Min/+) tumorigenesis.
Dll4-Notch1 signalling couples sprouting angiogenesis and artery formation.
Results suggest that Dll4 activation during differentiation sustained Treg cell phenotype and function to control respiratory syncytial virus infection.
DLL4 expression is not associated with the Pathogenesis of Non-Alcoholic Steatohepatitis.
The results demonstrate that the Vegf-Dll4/Notch feedback system normally operates to generate heterogeneity between endothelial cells driving blood vessel branching, whilst synchronization drives vessel expansion.
Cyclic AMP Response Element Binding Protein Mediates Pathological Retinal Neovascularization via Modulating DLL4-NOTCH1 Signaling
miRNA-30e targeted the 3'-UTR of Dll4 and downregulated Dll4 expression
Dll4/Notch signaling and HIF-1alpha are closely related to lymphangiogenesis in dry eye-induced lacrimal glands.
Dll4-induced Notch1 activity is required to specify the arterial programme in the aorta-gonad-mesonephros embryonic region.
Tumor promoting effect of low-dosage inhibition needs to be considered when implementing Delta-like 4 targeting therapies.
The heart defects in Dll4-/- embryos are consistent with primary defects in vessel patterning.
DLL4 is an efficient cis-inhibitor of Notch signaling during embryogenesis.
Tmem230a may have a modulatory role in vessel-network formation and growth, regulating endothelial cell number by Dll4/Notch pathway.
Thsd7a could regulate ISV angiogenesis via Notch-dll4 signaling. Thus, Thsd7a is a potent angioneurin involved in the development of both neural and vascular systems.
show that blood flow suppresses vascular Notch signalling via down-regulation of dll4
Microinjection of miR-30 mimics into zebrafish embryos resulted in suppression of dll4 and subsequent excessive sprouting of intersegmental vessels and reduction in dorsal aorta diameter.
Notch signalling pathway mutants Ectopic filopodia were also observed on the inter-somitic vessels of Notch signalling pathway mutants. Ectopic filopodia are not due to loss of dll4.
These studies imply critical roles for Dll4/Notch signaling in the formation and wiring of the lymphatic network.
Dll4-Notch signalling acts as an angiogenic ;off' switch by making endothelial cells unresponsive to Vegf.
Vegfc/Flt4 signalling is suppressed by Dll4 in developing zebrafish intersegmental arteries.
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.
delta-like protein 4
, delta 4
, delta ligand 4
, delta-like 4 homolog
, delta-like 4 protein
, drosophila Delta homolog 4
, notch ligand DLL4
, notch ligand delta-2