The microfibril-associated glycoproteins (MAGP1 and MAGP2) are small ECM proteins that associate with fibrillin to influence microfibril function.

A distinguishing feature of both MAGPs is their ability to interact with TGF尾 family growth factors, Notch and Notch ligands, integrins (MAGP2 specifically) and multiple elastic fiber proteins.

Inactivation of the MAGP1 gene in mice resulted in bone abnormalities, hematopoietic changes, increased fat deposition, diabetes, impaired wound repair, and a bleeding diathesis.

Inactivation of MAGP2 produced a neutropenia yet had minimal effects on bone or adipose homeostasis.

A common mechanism underlying all of the traits associated with MAGP knockout phenotypes is altered TGF尾 signaling.