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Hepatocyte nuclear factor 4, alpha

TCF, HNF4alpha, HNF-4, MODY, hepatocyte nuclear factor 4alpha
The protein encoded by this gene is a nuclear transcription factor which binds DNA as a homodimer. The encoded protein controls the expression of several genes, including hepatocyte nuclear factor 1 alpha, a transcription factor which regulates the expression of several hepatic genes. This gene may play a role in development of the liver, kidney, and intestines. Mutations in this gene have been associated with monogenic autosomal dominant non-insulin-dependent diabetes mellitus type I. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, TCF4, V1a, HAD, c-Myc
Papers using TCF antibodies
Inhibition of the anti-apoptotic PI(3)K/Akt/Bad pathway by stress
Wang Cun-Yu et al., In The Journal of Cell Biology, 1997
... For stable transfection, Rat-1/Wnt-1 cells were cotransfected with pcDNA3-flag-DN-Tcf-4, encoding the dominant-negative mutant (DN) of Tcf-4, or control empty vector and pBabe vector, containing a puromycin selectable marker, with Superfect (QIAGEN), according to the manufacturer's ...
Papers on TCF
A novel kinase regulates dietary restriction-mediated longevity in Caenorhabditis elegans.
Mukhopadhyay et al., New Delhi, India. In Aging Cell, Aug 2014
This DR-like state results in upregulation of beta-oxidation genes through the nuclear hormone receptor NHR-49, a HNF-4 homolog, resulting in depletion of stored fat.
Modulating and measuring Wingless signalling.
Vincent, London, United Kingdom. In Methods, Jul 2014
Various reporters have been devised by placing TCF-binding sites or DNA fragments from known target genes upstream of luciferase-coding sequences.
Wnt-independent role of β-catenin in thyroid cell proliferation and differentiation.
Santisteban et al., Madrid, Spain. In Mol Endocrinol, May 2014
This effect takes place in a Wnt-independent manner because TSH and IGF-1, through the activation of protein kinase A and protein kinase B/Akt, phosphorylate β-catenin at S552 and S675, which results in β-catenin release from E-cadherin at the adherens junctions.
TERT promoter mutations in cancer development.
Kumar et al., Heidelberg, Germany. In Curr Opin Genet Dev, Feb 2014
The newly described germline and recurrent somatic mutations in melanoma and other cancers in the TERT promoter that create de novo E-twenty six/ternary complex factors (Ets/TCF) binding sites, provide an insight into the possible cause of tumor-specific increased TERT expression.
Wnt signaling pathway in non-small cell lung cancer.
Stewart, Ottawa, Canada. In J Natl Cancer Inst, Jan 2014
Overexpression of Wnt-1, -2, -3, and -5a and of Wnt-pathway components Frizzled-8, Dishevelled, Porcupine, and TCF-4 is common in resected NSCLC and is associated with poor prognosis.
Integrative ChIP-seq/microarray analysis identifies a CTNNB1 target signature enriched in intestinal stem cells and colon cancer.
Dai et al., Irvine, United States. In Plos One, Dec 2013
Mutations in APC or CTNNB1 are highly frequent in colon cancer and cause aberrant stabilization of CTNNB1, which activates the transcription of Wnt target genes by binding to chromatin via the TCF/LEF transcription factors.
Noncanonical Wnt5a enhances Wnt/β-catenin signaling during osteoblastogenesis.
Kobayashi et al., Matsumoto, Japan. In Sci Rep, Dec 2013
Pretreatment of ST2 cells, a stromal cell line, with Wnt5a enhanced canonical Wnt ligand-induced Tcf/Lef transcription activity.
Assessing the phenotypic effects in the general population of rare variants in genes for a dominant Mendelian form of diabetes.
Altshuler et al., Cambridge, United States. In Nat Genet, Nov 2013
We sequenced seven genes for maturity-onset diabetes of the young (MODY) in well-phenotyped population samples (n = 4,003).
Maturity onset diabetes of the young: identification and diagnosis.
Ellard et al., Exeter, United Kingdom. In Ann Clin Biochem, Sep 2013
Maturity-onset diabetes of the young (MODY) is a monogenic disorder that results in a familial, young-onset non-insulin dependent form of diabetes, typically presenting in lean young adults before 25 years.
Transcription factor EBF1 is essential for the maintenance of B cell identity and prevention of alternative fates in committed cells.
Grosschedl et al., Freiburg, Germany. In Nat Immunol, Aug 2013
In particular, genes encoding the transcription factors Id2 and TCF-1 were bound and repressed by EBF1.
Collagen VI in cancer and its biological mechanisms.
Bonaldo et al., Padova, Italy. In Trends Mol Med, Jul 2013
A growing number of studies indicate that collagen VI directly affects malignant cells by acting on the Akt-GSK-3β-β-catenin-TCF/LEF axis, enhancing the production of protumorigenic factors and inducing epithelial-mesenchymal transition.
T cell factor 1 is required for group 2 innate lymphoid cell generation.
Bhandoola et al., Philadelphia, United States. In Immunity, May 2013
Here we report that ILC2 development required T cell factor 1 (TCF-1, the product of the Tcf7 gene), a transcription factor also implicated in T cell lineage specification.
TERT promoter mutations in familial and sporadic melanoma.
Kumar et al., Heidelberg, Germany. In Science, Mar 2013
The majority of those mutations occurred at two positions in the TERT promoter and also generated binding motifs for Ets/TCF transcription factors.
Recent progresses in identifying nuclear receptors and their families.
Chou et al., Jingdezhen, China. In Curr Top Med Chem, 2012
According to their different action mechanisms or functions, NR superfamily has been classified into seven families: NR1 (thyroid hormone like), NR2 (HNF4-like), NR3 (estrogen like), NR4 (nerve growth factor IB-like), NR5 (fushi tarazu-F1 like), NR6 (germ cell nuclear factor like), and NR0 (knirps or DAX like).
The TCF-1 and LEF-1 transcription factors have cooperative and opposing roles in T cell development and malignancy.
Xue et al., Iowa City, United States. In Immunity, 2012
We further demonstrated that TCF-1 directly repressed LEF-1 expression in early thymocytes and that conditional inactivation of Lef1 greatly delayed or prevented T cell malignancy in Tcf7(-/-) mice.
Mucroporin-M1 inhibits hepatitis B virus replication by activating the mitogen-activated protein kinase (MAPK) pathway and down-regulating HNF4α in vitro and in vivo.
Cao et al., Wuhan, China. In J Biol Chem, 2012
Mucroporin-M1 peptide can activate the MAPK pathway and then reduce the expression of HNF4alpha, resulting in the inhibition of HBV replication in vitro and in vivo.
Identification of a binding motif specific to HNF4 by comparative analysis of multiple nuclear receptors.
Sladek et al., Riverside, United States. In Nucleic Acids Res, 2012
HNF4-specific DNA recognition and transactivation are mediated by residues Asp69 and Arg76 in the DNA-binding domain.
The transcription factor HNF-4α: a key factor of the intestinal uptake of fatty acids in mouse.
Lacorte et al., Paris, France. In Am J Physiol Gastrointest Liver Physiol, 2012
We conclude that the transcription factor HNF-4alpha is a key factor of the intestinal absorption of dietary lipids, which controls this process as early as in the initial step of fatty acid uptake by enterocytes.
Systematic assessment of etiology in adults with a clinical diagnosis of young-onset type 2 diabetes is a successful strategy for identifying maturity-onset diabetes of the young.
Owen et al., Oxford, United Kingdom. In Diabetes Care, 2012
In the type 1 diabetic group, two HNF1A mutations were found (0.8% prevalence). In type 2 diabetic subjects, 10 HNF1A, two HNF4A, and one GCK mutation were identified
Modulation of mouse coagulation gene transcription following acute in vivo delivery of synthetic small interfering RNAs targeting HNF4α and C/EBPα.
van Vlijmen et al., Leiden, Netherlands. In Plos One, 2011
In the mouse, HNF4alpha has a direct and essential regulatory role for multiple hepatic coagulation genes, while a role for C/EBPalpha is more restricted.
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