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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Forkhead box H1

FoxH1, FAST-1, FAST-2
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: FasT, Smad2, NODAL, SFRP1, CAN
Papers on FoxH1
High Frequency of Normal Response during GH Stimulation Tests in Patients with Ectopic Posterior Pituitary Gland: A Source of False-Negative Diagnosis of Pituitary Insufficiency.
Longui et al., São Paulo, Brazil. In Horm Res Paediatr, Feb 2016
AIMS: To report false-negative normal growth hormone (GH) peak response in patients with ectopic posterior pituitary gland (EPP) identified with a simplified magnetic resonance imaging (FAST1-MRI).
The activation of the TLR2/p38 pathway by sodium butyrate in bovine mammary epithelial cells is involved in the reduction of Staphylococcus aureus internalization.
López-Meza et al., Nicolás Romero, Mexico. In Mol Immunol, Dec 2015
Additionally, bMECs that were treated with 0.5mM NaB (24h) showed activation of 8 transcriptional factors (AP-1, E2F-1, FAST-1, MEF-1, EGR, PPAR, ER and CBF), which were partially reverted when the bMECs were S. aureus-challenged.
Pou5f3.2-induced proliferative state of embryonic cells during gastrulation of Xenopus laevis embryo.
Kinoshita et al., Japan. In Dev Growth Differ, Dec 2015
Reporter analyses showed that one of the conserved regions contained an enhancer region, which had several Smad2/3 and FoxH1 binding motifs.
Characterization and genomic structure of Dnah9, and its roles in nodal signaling pathways in the Japanese flounder (Paralichthys olivaceus).
Qi et al., Qingdao, China. In Fish Physiol Biochem, Oct 2015
The transcription factor binding site of FAST-1 (SMAD interacting protein) was identified in the transcription region of Dnah9 by the promoter analysis, which might format the complexes of SMADs, FAST-1 and the transcription region of Dnah9 served as a bridge of Dnah9 and nodal signaling.
Nmnat1-Rbp7 Is a Conserved Fusion-Protein That Combines NAD+ Catalysis of Nmnat1 with Subcellular Localization of Rbp7.
Meyer et al., Innsbruck, Austria. In Plos One, 2014
We find that early embryonic rbp7a expression is negatively regulated by the Nodal/FoxH1-signaling pathway and we show that Nodal/FoxH1 activity has the opposite effect on aldh1a2, which encodes the major enzyme for early embryonic retinoic acid production.
Reprogramming barriers and enhancers: strategies to enhance the efficiency and kinetics of induced pluripotency.
Ebrahimi, Yazd, Iran. In Cell Regen (lond), 2014
Different strategies have been applied for enhancing reprogramming efficiency, including depletion/inhibition of barriers (p53, p21, p57, p16(Ink4a)/p19(Arf), Mbd3, etc.), overexpression of enhancing genes (e.g., FOXH1, C/EBP alpha, UTF1, and GLIS1), and administration of certain cytokines and small molecules.
Benzyl isothiocyanate inhibits breast cancer cell tumorigenesis via repression of the FoxH1-Mediated Wnt/β-catenin pathway.
Huang et al., Chengdu, China. In Int J Clin Exp Med, 2014
In the present study, we found that the overexpression of FOXH1 in breast cancers tissues and cells, and FOXH1 significantly promoted cell proliferation, invasion and tumorigenesis in vitro.
Icatibant for the treatment of hereditary angioedema.
Lundquist et al., United States. In Ann Pharmacother, 2013
Icatibant was compared to placebo in 2 clinical trials (FAST-1 and FAST-3) and to tranexamic acid in the FAST-2 trial.
HEB and E2A function as SMAD/FOXH1 cofactors.
Baker et al., Stanford, United States. In Genes Dev, 2011
HEB and E2A-bind the SCA motif at regions overlapping SMAD2/3 and FOXH1
Nodal-dependent mesendoderm specification requires the combinatorial activities of FoxH1 and Eomesodermin.
Burdine et al., Princeton, United States. In Plos Genet, 2011
Axial mesoderm induction is differentially disrupted in FoxH1 mutants. FoxH1 mutants respond differently to Activin-like signaling.
Etiopathogenetic advances and management of holoprosencephaly: from bench to bedside.
Bona et al., Novara, Italy. In Panminerva Med, 2010
Genetic causes are responsible for about 20% of cases: they are chromosomal abnormalities and gene mutations: up to date, nine genes (SHH, ZIC2, SIX3, TGIF, PATCHED1, TDGF1/CRIPTO, FAST1, GLI2 and DHCR) are definitely associated with HPE, but many others candidate gene are under investigation.
Forkhead box H1 (FOXH1) sequence variants in ventricular septal defect.
Ma et al., In Int J Cardiol, 2010
Four genetic variants are found in FOXH1 that are associated with ventricular septal defects in Chinese patients.
Icatibant, a new bradykinin-receptor antagonist, in hereditary angioedema.
Fan et al., Milano, Italy. In N Engl J Med, 2010
RESULTS: A total of 56 and 74 patients underwent randomization in the FAST-1 and FAST-2 trials, respectively.
Foxh1 and Foxa2 are not required for formation of the midgut and hindgut definitive endoderm.
Hoodless et al., Vancouver, Canada. In Dev Biol, 2010
Formation of midgut and hindgut definitive endoderm is unaffected by loss of Foxh1 or Foxa2.
PKA-mediated stabilization of FoxH1 negatively regulates ERalpha activity.
Yeo et al., Seoul, South Korea. In Mol Cells, 2009
Results suggest that PKA can negatively regulate ERalpha, at least in part, through FoxH1.
Holoprosencephaly: clinical, anatomic, and molecular dimensions.
Cohen, Halifax, Canada. In Birth Defects Res A Clin Mol Teratol, 2006
Holoprosencephaly is addressed under the following headings: alobar, semilobar, and lobar holoprosencephaly; arrhinencephaly; agenesis of the corpus callosum; pituitary abnormalities; hindbrain abnormalities; syntelencephaly; aprosencephaly/atelencephaly; neural tube defects; facial anomalies; median cleft lip; minor facial anomalies; single maxillary central incisor; holoprosencephaly-like phenotype; epidemiology; genetic causes of holoprosencephaly; teratogenic causes of holoprosencephaly; SHH mutations; ZIC2 mutations; SIX3 mutations; TGIF mutations; PTCH mutations; GLI2 mutations; FAST1 mutations; TDGF1 mutations; and DHCR7 mutations.
Human FOX gene family (Review).
Katoh et al., Japan. In Int J Oncol, 2004
Human Forkhead-box (FOX) gene family consists of at least 43 members, including FOXA1, FOXA2, FOXA3, FOXB1, FOXC1, FOXC2, FOXD1, FOXD2, FOXD3, FOXD4, FOXD5 (FOXD4L1), FOXD6 (FOXD4L3), FOXE1, FOXE2, FOXE3, FOXF1, FOXF2, FOXG1 (FOXG1B), FOXH1, FOXI1, FOXJ1, FOXJ2, FOXJ3, FOXK1, FOXK2, FOXL1, FOXL2, FOXM1, FOXN1, FOXN2 (HTLF), FOXN3 (CHES1), FOXN4, FOXN5 (FOXR1), FOXN6 (FOXR2), FOXO1 (FOXO1A), FOXO2 (FOXO6), FOXO3 (FOXO3A), FOXO4 (MLLT7), FOXP1, FOXP2, FOXP3, FOXP4, and FOXQ1.
Inhibition of excess nodal signaling during mouse gastrulation by the transcriptional corepressor DRAP1.
Shen et al., United States. In Science, 2003
Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity.
Nodal signaling in vertebrate development.
Schier, New York City, United States. In Annu Rev Cell Dev Biol, 2002
Nodal signaling activates a canonical TGFss pathway involving activin receptors, Smad2 transcription factors, and FoxH1 coactivators.
Smad4 and FAST-1 in the assembly of activin-responsive factor.
Whitman et al., Boston, United States. In Nature, 1997
The principal DNA-binding component of ARF is FAST-1, a transcription factor with a novel winged-helix structure.
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