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These results indicate that Smad4 acts as a tumor suppressor by activating FOXH1, and then suppressing the expression of estrogen receptor, in addition to tumor migration and invasion.
HEB and E2A-bind the SCA motif at regions overlapping SMAD2/3 and FOXH1
Four genetic variants are found in FOXH1 that are associated with ventricular septal defects in Chinese patients.
Results suggest that PKA can negatively regulate ERalpha, at least in part, through FoxH1.
This work suggests that FAST-1 may participate in the vascular smooth muscle response to injury and may represent a potential molecular target for modulating the progression of cardiac allograft vasculopathy.
Smad-binding peptide aptamer FOXH1 can be developed to selectively inhibit TGF-beta-induced gene expression.
These results demonstrate for a functional role for TGF-beta ligands in regulation of mammalian Mixl1, identify FoxH1 as an essential co-activator, and implicate Nodal as the embryonic regulator of Mixl1 in mesendoderm morphogenesis.
FoxH1 has a role in androgen receptor-mediated transactivation
Reduced NODAL signaling via mutation of several pathway members including FOXH1 is linked to heart defects and holoprosencephaly.
that FAST2 is expressed in a cell-specific manner during ovarian follicle development
The finding that Foxh1-Grg-mediated repression is not essential for Nodal expression during mouse embryogenesis suggests that other regulators compensate for the loss of repressive regulatory input that is mediated by Grg interactions.
Formation of midgut and hindgut definitive endoderm is unaffected by loss of Foxh1 or Foxa2.
A conserved intronic enhancer (ASE), containing binding sites for the fork head transcription factor Foxh1, modulates dynamic patterns of Nodal expression during early mouse development.
Foxh1 and Nkx2-5 functionally interact and are essential for development of the anterior heart field and its derivatives
As goosecoid is itself induced in a Foxh1-dependent manner, we propose that Foxh1 initiates positive and negative transcriptional circuits to refine cell fate decisions during gastrulation
Foxh1 initiates a transcriptional regulatory network within the developing anterior neuroectoderm.
Nodal-dependent gene expression is suppressed by FoxH1, but enhanced by a FoxH1 EH1 mutant, indicating that the EH1 motif is necessary for repression. Grg4 occupancy of the Xnr1 enhancer is dependent on the FoxH1 EH1 motif. Nodal-activated Smad2 physically displaces Grg4 from FoxH1. FoxH1 mediates both activation and repression of Nodal gene expression.
we identify a previously unappreciated role for the Nodal-transcription factor FoxH1 in mediating cell responsiveness to Bmp further linking the control of these two pathways in the heart
Axial mesoderm induction is differentially disrupted in FoxH1 mutants. FoxH1 mutants respond differently to Activin-like signaling.
These results and the association of FoxH1 and Mixer/Bon with phosphorylated Smad2 support a role for these factors as components of the Nodal signaling pathway.
flk1 is a direct target of FoxH1; FoxH1 is involved in vessel formation in zebrafish.
to an essential role for maternal FoxH1 and downstream keratins during gastrulation that is epistatic to Nodal signaling
FOXH1 encodes a human homolog of Xenopus forkhead activin signal transducer-1. FOXH1 protein binds SMAD2 and activates an activin response element via binding the DNA motif TGT(G/T)(T/G)ATT.
forkhead box H1
, forkhead activin signal transducer 1
, forkhead box protein H1
, forkhead box protein H1-like
, TGF-beta/activin signal transducer
, forkhead activin signal transducer 2
, forkhead activin signal transducer-1
, FAST1 transcription factor
, uncle freddy