202213805ENSG00000106991ENSMUSG00000026814P17813Q96CG0Q63961NM_000118NM_001114753NM_001278138NM_001146348NM_001146350NM_007932NP_000109NP_001108225NP_001265067NP_001108225.1NP_001265067.1NP_001139820NP_001139822NP_031958Endoglin (ENG) is a type I membrane glycoprotein located on cell surfaces and is part of the TGF beta receptor complex.

[5] It has a crucial role in angiogenesis, therefore, making it an important protein for tumor growth, survival and metastasis of cancer cells to other locations in the body.

This, however, changes once neoangiogenesis begins and endothelial cells become active in places like tumor vessels, inflamed tissues, skin with psoriasis, vascular injury and during embryogenesis.

A soluble form of endoglin can be produced by the proteolytic cleaving action of metalloproteinase MMP-14 in the extracellular domain near the membrane.

[13] Together with a second intermolecular disulfide, involving cysteine 582,[16] this generates a molecular clamp that secures the ligand via interaction of two copies of OR1 with the knuckle regions of homodimeric BMP-9.

[13] In addition to rationalizing a large number of HHT1 mutations, the crystal structure of endoglin shows that the epitope of anti-ENG monoclonal antibody TRC105 overlaps with the binding site for BMP-9.

[16] The amino acid (aa) region 437–558 in the extracellular domain of endoglin will bind to TGF beta receptor II.

[16] Endoglin can also mediate F-actin dynamics, focal adhesions, microtubular structures, endocytic vesicular transport through its interaction with zyxin, ZRP-1, beta-arrestin and Tctex2beta, LK1, ALK5, TGF beta receptor II, and GIPC.

[21] In humans endoglin may be involved in the autosomal dominant disorder known as hereditary hemorrhagic telangiectasia (HHT) type 1.

[22] This condition leads to frequent nose bleeds, telangiectases on skin and mucosa and may cause arteriovenous malformations in different organs including brain, lung, and liver.

Some mutations that lead to this disorder are:[22] Endoglin levels have been found to be elevated in pregnant women who subsequently develop preeclampsia.

[25][26] Being able to target and efficiently reduce or halt neoangiogenesis in tumors would prevent metastasis of primary cancer cells into other areas of the body.

TGF beta can act as a tumor suppressor in the premalignant stage of the benign neoplasm by inhibiting its growth and inducing apoptosis.