描述：
Delta-like protein 4 (DLL4) is a type I membrane protein belonging to the Delta/Serrate/
Lag2 (DSL) family of Notch ligands. Notch signaling is an evolutionarily conserved pathway
that controls cell fate and is required in multiple developmental processes including vascular
development , hematopoiesis, somatogenesis, myogenesis, and neurogenesis. Dysregulation
in the Notch pathway is associated with various human diseases. In mammals, four Notch
homologs (Notch 1 to 4) and five ligands (DLL 1, 3 and 4, Jagged 1 and 2) have been identified.
Notch ligands are transmembrane proteins with a DSL motif necessary for Notch binding,
tandem EGF repeats, a transmembrane region and a short intracellular domain (ICD). Notch
ligands are categorized into two subfamilies based on the presence of an extracellular
cysteine-rich domain and insertions that interrupt some EGF repeats in the Jagged but not
the Delta ligand family. Interactions of Notch receptors with their ligands result in reciprocal
regulated intramembrane proteolysis (RIP). RIP is a mechanism for transmembrane signal
transduction that involves the sequential processing by a disintegrin metalloprotease (ADAM)
and then by presenilin/ γ secretase, resulting in shedding of the extracellular domains and the
generation of the soluble ICD signaling fragments, respectively. The Notch ICD translocates to
the nucleus and interacts with transcriptional coactivators, resulting in the transcription of
target genes. The ICDs of the Notch ligands have also been shown to translocate to the nucleus
where they may have a signaling function. DLL4 is expressed highly and selectively within the
arterial endothelium and has been shown to function as a ligand for Notch 1 and Notch 4.
Human and mouse DLL4 share 86% amino acid sequence identity.
原厂资料：
Delta-like protein 4 (DLL4) is a type I membrane protein belonging to the Delta/Serrate/
Lag2 (DSL) family of Notch ligands. Notch signaling is an evolutionarily conserved pathway
that controls cell fate and is required in multiple developmental processes including vascular
development , hematopoiesis, somatogenesis, myogenesis, and neurogenesis. Dysregulation
in the Notch pathway is associated with various human diseases. In mammals, four Notch
homologs (Notch 1 to 4) and five ligands (DLL 1, 3 and 4, Jagged 1 and 2) have been identified.
Notch ligands are transmembrane proteins with a DSL motif necessary for Notch binding,
tandem EGF repeats, a transmembrane region and a short intracellular domain (ICD). Notch
ligands are categorized into two subfamilies based on the presence of an extracellular
cysteine-rich domain and insertions that interrupt some EGF repeats in the Jagged but not
the Delta ligand family. Interactions of Notch receptors with their ligands result in reciprocal
regulated intramembrane proteolysis (RIP). RIP is a mechanism for transmembrane signal
transduction that involves the sequential processing by a disintegrin metalloprotease (ADAM)
and then by presenilin/ γ secretase, resulting in shedding of the extracellular domains and the
generation of the soluble ICD signaling fragments, respectively. The Notch ICD translocates to
the nucleus and interacts with transcriptional coactivators, resulting in the transcription of
target genes. The ICDs of the Notch ligands have also been shown to translocate to the nucleus
where they may have a signaling function. DLL4 is expressed highly and selectively within the
arterial endothelium and has been shown to function as a ligand for Notch 1 and Notch 4.
Human and mouse DLL4 share 86% amino acid sequence identity.
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