Antagonism of Activin by Follistatin

Stable Identifier
Homo sapiens
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Both Follistatin (FST) and Follistatin-like-3 (FSTL3) irreversibly bind Activin dimers and prevent Activin from interacting with its receptor (reviewed in Schneyer et al. 2004, Xia and Schneyer 2009). Though functionally similar in vitro, FST and FSTL3 do not function identically in vivo. Mice lacking FST die shortly after birth due to defects in muscle and bone (Matzuk et al. 1995); mice lacking FSTL3 are viable but have altered glucose metabolism (Mukherjee et al. 2007).

Literature References
PubMed ID Title Journal Year
17229845 FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults

Mahan, A, Xia, Y, Thomas, MK, Rosen, ED, Schneyer, AL, Mukherjee, A, Raher, MJ, Sidis, Y, Bloch, KD

Proc. Natl. Acad. Sci. U.S.A. 2007
7885475 Multiple defects and perinatal death in mice deficient in follistatin

Bradley, A, Roop, DR, Matzuk, MM, Vogel, H, Sellheyer, K, Lu, N

Nature 1995
19273500 The biology of activin: recent advances in structure, regulation and function

Xia, Y, Schneyer, AL

J. Endocrinol. 2009
15451564 Differential actions of follistatin and follistatin-like 3

Xia, Y, Schneyer, A, Saito, S, Lin, HY, Sidis, Y, Keutmann, H, del Re, E

Mol. Cell. Endocrinol. 2004
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