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FSHB — SMAD3

Text-mined interactions from Literome

Suszko et al., Mol Endocrinol 2003 : Transfection of Smad3 , but not the highly related Smad2, led to a ligand independent stimulation of the FSHbeta promoter activity
Bernard et al., Mol Endocrinol 2004 : Because SMAD7 functions by preventing access of SMAD2 and SMAD3 to ALK4, these data suggested that both activins and ALK4 require SMAD2 and/or SMAD3 to affect FSHbeta transcription ... Transient transfection of SMAD3 , but not SMADs 1, 2, 4, 5, or 8, stimulated endogenous FSHbeta mRNA levels ... To assess more directly roles for both SMAD2 and SMAD3 in activin stimulated FSHbeta expression, RNA interference was used to decrease endogenous SMAD protein levels in LbetaT2 cells
Gregory et al., Mol Endocrinol 2005 (MAP Kinase Signaling System) : Overexpression of SMAD3 ( mediator of decapentaplegic related protein 3 ), but not of SMAD2, increased transcriptional activation of the rat ( r ) FSHbeta gene promoter, which was further enhanced by the combined overexpression of SMAD3 and 4 ( 3+4 )
Suszko et al., Mol Endocrinol 2005 : We investigated whether these structural features contribute to differential FSH(beta) transactivation by Smad2 and Smad3
Bernard et al., Reproductive biology and endocrinology : RB&E 2006 : Transfection of both ALK4 ( TD ) and ALK7 ( TD ) stimulated Smad2/3 phosphorylation, and the effects of both receptors on Fshb promoter activity were inhibited by depletion of endogenous Smad3 protein levels
McGillivray et al., Endocrinology 2007 : In addition, the glucocorticoid receptor and Smad3 are sufficient to confer a striking synergy with glucocorticoids on the mouse FSHbeta promoter
Thackray et al., Endocrinology 2008 : Disruption of Smad binding to the promoter with a Smad protein lacking the DNA binding domain or an FSHbeta promoter containing mutated activin-response elements prevents the synergistic enhancement of FSHbeta transcription
Lamba et al., Endocrinology 2008 : Both PITX1 and PITX2C interacted with Smad3 ( an effector of the activin signaling cascade in these cells ) in coprecipitation experiments, and the PITX binding site mutation greatly inhibited Smad2/3/4 stimulated Fshb transcription