Volume 270,
Number 2,
Issue of January 13, 1995 pp. 765-769
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
GH3 Pituitary
Tumor Cells Contain Heteromeric Type I and Type II Receptor Complexes
for Transforming Growth Factor 
and Activin-A
(Received for publication, August 15,
1994; and in revised form, November 1, 1994)
Aristidis
Moustakas
,
Toru
Takumi
,
Herbert Y.
Lin
, ,
Harvey F.
Lodish
Transforming growth factors 
(TGF-s) and activins
induce and inhibins block secretion of follicle-stimulating hormone by
rat GH3 pituitary tumor cells. Cheifetz et al. (Cheifetz, S.,
Ling, N., Guillemin, R., and Massagué, J.(1988) J. Biol. Chem. 263, 17225-17228) reported that GH3 cells
express a 
50-kDa surface protein, termed the type IV TGF-
receptor, that directly binds all of these peptide hormones. Here we
show that GH3 cells express the previously identified type I and type
II receptors for TGF- and activin-A. Immunoprecipitation of
affinity-labeled surface binding proteins with antisera specific to
known receptors demonstrated independent heteromeric complexes of
TGF- types I and II receptors and of activin types I and II
receptors. As judged by ligand-binding and cross-linking analysis,
TGF- binding to the TGF- receptors is not inhibited by
activin-A and activin-A binding to its receptors is not inhibited by
TGF-. Screening of a cDNA library from GH3 cells for potential
receptor serine-threonine kinases yielded the known types I and II
TGF- and activin receptors. The presumed common intracellular
signaling pathway for TGF- and activin in GH3 cells appears to be
mediated by distinct cell-surface receptors.
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