Recombinant human DLL4 protein
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(1 Publication)
Recombinant human DLL4 protein is a Human Fragment protein, in the 27 to 524 aa range, expressed in HEK 293 cells, with >95%, suitable for SDS-PAGE, FuncS.
View Alternative Names
UNQ1895/PRO4341, DLL4, Delta-like protein 4, Drosophila Delta homolog 4, Delta4
Reactivity data
Product details
Sequence info
Properties and storage information
Shipped at conditions
Appropriate long-term storage conditions
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
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.
Pathways
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.
Specifications
Form
Lyophilized
Additional notes
Purity is greater than 95% by SDS-PAGE gel and HPLC analyses.
General info
Function
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).
Target data
Publications (1)
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The Journal of experimental medicine 212:759-74 PubMed25918341
2015
Applications
Unspecified application
Species
Unspecified reactive species
Product promise
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