Mouse Anti-GDF2 Recombinant Antibody (4D2) (V2LY-1225-LY996)

growth differentiation factor 2

Potent circulating inhibitor of angiogenesis. Signals through the type I activin receptor ACVRL1 but not other Alks. Signaling through SMAD1 in endothelial cells requires TGF-beta coreceptor endoglin/ENG.

Activin receptor signaling pathway Source: BHF-UCL
Angiogenesis Source: UniProtKB
Blood vessel morphogenesis Source: DFLAT
BMP signaling pathway Source: BHF-UCL
Branching involved in blood vessel morphogenesis Source: DFLAT
Cartilage development Source: DFLAT
Cellular iron ion homeostasis Source: DFLAT
Cellular response to BMP stimulus Source: BHF-UCL
Negative regulation of angiogenesis Source: DFLAT
Negative regulation of blood vessel endothelial cell migration Source: DFLAT
Negative regulation of cell growth Source: BHF-UCL
Negative regulation of DNA biosynthetic process Source: BHF-UCL
Negative regulation of DNA replication Source: DFLAT
Negative regulation of endothelial cell migration Source: BHF-UCL
Negative regulation of endothelial cell proliferation Source: DFLAT
Ossification Source: DFLAT
Osteoblast differentiation Source: Ensembl
Pathway-restricted SMAD protein phosphorylation Source: BHF-UCL
Positive regulation of angiogenesis Source: DFLAT
Positive regulation of BMP signaling pathway Source: Ensembl
Positive regulation of cartilage development Source: Ensembl
Positive regulation of endothelial cell differentiation Source: Ensembl
Positive regulation of endothelial cell proliferation Source: DFLAT
Positive regulation of interleukin-8 production Source: BHF-UCL
Positive regulation of pathway-restricted SMAD protein phosphorylation Source: BHF-UCL
Positive regulation of transcription, DNA-templated Source: BHF-UCL
Positive regulation of transcription by RNA polymerase II Source: BHF-UCL
SMAD protein signal transduction Source: GO_Central
Vasculogenesis Source: Ensembl

Secreted

Telangiectasia, hereditary hemorrhagic, 5 (HHT5):
A multisystemic vascular dysplasia leading to dilation of permanent blood vessels and arteriovenous malformations of skin, mucosa, and viscera. The disease is characterized by recurrent epistaxis and gastro-intestinal hemorrhage. Visceral involvement includes arteriovenous malformations of the lung, liver, and brain.

A reversible disulfide bond can be formed between the two subunits in the homodimer; this has no effect on GDF2 activity.