Recombinant human DLL4 protein (Fc Chimera Active) is a Human Fragment protein, in the 1 to 529 aa range, expressed in HEK 293, with >=95% purity, < 0.01 EU/µg endotoxin level and suitable for SDS-PAGE, FuncS.
Application | Reactivity | Dilution info | Notes |
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Application SDS-PAGE | Reactivity Reacts | Dilution info - | Notes - |
Application FuncS | Reactivity Reacts | Dilution info - | Notes - |
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Involved in the Notch signaling pathway as Notch ligand (PubMed:11134954). Activates NOTCH1 and NOTCH4. Involved in angiogenesis; negatively regulates endothelial cell proliferation and migration and angiogenic sprouting (PubMed:20616313). Essential for retinal progenitor proliferation. Required for suppressing rod fates in late retinal progenitors as well as for proper generation of other retinal cell types (By similarity). During spinal cord neurogenesis, inhibits V2a interneuron fate (PubMed:17728344).
UNQ1895/PRO4341, DLL4, Delta-like protein 4, Drosophila Delta homolog 4, Delta4
Recombinant human DLL4 protein (Fc Chimera Active) is a Human Fragment protein, in the 1 to 529 aa range, expressed in HEK 293, with >=95% purity, < 0.01 EU/µg endotoxin level and suitable for SDS-PAGE, FuncS.
Constituents: PBS, 0.5% Trehalose
Purified using affinity chromatography.
Involved in the Notch signaling pathway as Notch ligand (PubMed:11134954). Activates NOTCH1 and NOTCH4. Involved in angiogenesis; negatively regulates endothelial cell proliferation and migration and angiogenic sprouting (PubMed:20616313). Essential for retinal progenitor proliferation. Required for suppressing rod fates in late retinal progenitors as well as for proper generation of other retinal cell types (By similarity). During spinal cord neurogenesis, inhibits V2a interneuron fate (PubMed:17728344).
This product is an active protein and may elicit a biological response in vivo, handle with caution.
ab108557 interacts with Human Notch1 (as confirmed by Flow Cytometry).
DLL4 also known as Delta-like ligand 4 is a member of the Delta/Serrate/Lag-2 family. This target is a single-pass type I membrane protein with a molecular weight of approximately 65 kDa. It features prominently in the vascular endothelium where it impacts angiogenic activity. DLL4 acts as a ligand for Notch receptors initiating a signaling cascade important to cell fate decisions. DLL4 expression occurs mainly on the arterial endothelium and the tumor vasculature highlighting its significance in angiogenesis.
DLL4 engages in precise regulation of angiogenesis and vascular development. It participates in the Notch signaling pathway playing an integral role in controlling endothelial cell proliferation differentiation and migration. DLL4 does not operate in isolation; instead it functions as part of the Notch receptor-ligand complex. This relationship effectively regulates the sprouting of new blood vessels ensuring proper vascular patterning and functional blood supply.
DLL4 links directly to the Notch signaling and VEGF (vascular endothelial growth factor) pathways both of which play critical roles in vascular development and homeostasis. Through the Notch pathway DLL4 interacts with Notch1 and Notch4 receptors facilitating communication that inhibits endothelial cell proliferation distinguishing it from other pro-angiogenic factors. Its relationship with the VEGF pathway allows DLL4 to modulate angiogenic processes balancing vessel sprouting by opposing excessive VEGF-induced activities.
Aberrations of DLL4 influence cancer and cardiovascular diseases. Overexpression and dysregulation of DLL4 have been observed in various cancers where it contributes to tumor angiogenesis promoting the growth and spread of cancer cells. In cardiovascular disorders dysfunctional DLL4 signaling impacts vascular development which can lead to fatal arteriovenous malformations. In these conditions DLL4 interacts with proteins like Notch1 and VEGF underlining its critical involvement in pathological angiogenesis and vessel formation.
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Terms & Conditions.
Interaction of Human Notch1 with Human DLL4.
HEK293 cells transfected with a Human Notch1 or a Human GITR ligand expressing vector were incubated with 25 μg/ml of Human GITR-Fc or ab108557. Cells were stained with anti-Human IgG (Fc specific) FITC conjugate for DLL4-Fc binding.
Induction of Hes-1 with the treatment of recombinant Human DLL4-Fc (ab108557).
A Mouse preadpipocyte cell line, 3T3L-1, was stimulated with 5 μg/ml of Human DLL4-Fc as in indicated time points and each cell lysate was prepared and subjected to western blot by using anti-Mouse Hes1 or GAPDH.
M: Marker.
Lane 1: hDLL4-Fc, 0 min.
Lane 2: hDLL4-Fc, 10 min.
Lane 3: hDLL4-Fc, 30 min.
Lane 4: hDLL4-Fc, 1 hr.
Lane 5: hDLL4-Fc, 2 hr.
Lane 6: hDLL4-Fc, 4 hr.
Lane 7: hDLL4-Fc, 8 hr.
Lane 8: hDLL4-Fc, 24 hr.
Adipogenesis inhibition of 3T3L-1 cells.
3T3L-1 cells (mouse pre-adipocyte cells) were maintained in DMEM, supplemented with 10% fetal bovine serum
and penicillin-streptomycin. For differentiation of 3T3L-1 cells, 3T3L-1 cells were cultured in adipogenic medium
which was growth medium supplemented with 1 μM Dexamethasone, 0.5 mM IBMX, 10 μg/ml lnsulin (day 0).
Medium was changed every 2 days. Staining with Oil Red O was typically performed on day 7. Cells were
washed twice with PBS, fixed with 3.7% formalin, and stained with 0.5% filtered Oil Red O in propylene glycol.
For negative controls, mouse TNF-α (20 ng/ml) was added. Recombinant Human DLL4-Fc (ab108557) (5 μg/ml) dissolved in
DPBS was added to the differentiation medium. These plates were then used to differentiate 3T3L-1 cells.
Adipogenesis inhibition of MSCs.
MSCs (Mesenchymal stem cells) were maintained in DMEM, supplemented with 10% fetal bovine serum, penicilinstreptomycin and glutamine. For differentiation of MSCs, MSCs were cultured in adipogenic medium which was
growth medium supplemented with 1 μM Dexamethasone, 0.5mM IBMX, 10 μg/m lnsulin, 100 μM Indomethacin (day 1). Medium was changed every 3 days. Staining with Oil Red O was typically performed on day 30. For negative controls, TNF-α (20 ng/ml) was added. To immobilize Notch ligands on the plastic surface of the culture plates, plates were incubated with a solution of ab108557 (5 μg/ml) or mCD137-Fc (5 μg/ml) in PBS for 2 hours at 37°C. Plates were then used to differentiate MSCs.
Adipogenesis inhibition of 3T3L-1 cells.
50 μg of cell lysates derived from hDLL4-Fc (ab108557) or non-treated 3T3L-1 cells, which had been either differentiated or undifferentiated, and were subjected to Western blot by using a Mouse adiponectin antibody.
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