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


beta Catenin, CTNNB1
The protein encoded by this gene is part of a complex of proteins that constitute adherens junctions (AJs). AJs are necessary for the creation and maintenance of epithelial cell layers by regulating cell growth and adhesion between cells. The encoded protein also anchors the actin cytoskeleton and may be responsible for transmitting the contact inhibition signal that causes cells to stop dividing once the epithelial sheet is complete. Finally, this protein binds to the product of the APC gene, which is mutated in adenomatous polyposis of the colon. Mutations in this gene are a cause of colorectal cancer (CRC), pilomatrixoma (PTR), medulloblastoma (MDB), and ovarian cancer. Three transcript variants encoding the same protein have been found for this gene.[provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: p53, APC, HAD, CAN, BRAF
Papers on beta Catenin
Concise Review: Paracrine Role of Stem Cells in Pituitary Tumors: A Focus on Adamantinomatous Craniopharyngioma.
Andoniadou et al., London, United Kingdom. In Stem Cells, Feb 2016
In addition, they play a critical role in tumor formation, specifically in the etiology of human adamantinomatous craniopharyngioma, a clinically relevant tumor that is associated with mutations in CTNNB1 (gene encoding β-catenin).
MicroRNA-340 inhibits the migration, invasion, and metastasis of breast cancer cells by targeting Wnt pathway.
Soleimani et al., Tehrān, Iran. In Tumour Biol, Feb 2016
Over-expression of key genes such as c-MYC and CTNNB1 (encoding β-catenin) in Wnt/β-catenin-dependent and ROCK1 in Wnt/β-catenin-independent signaling pathways (Rho/Rho-associated kinase (ROCK) signaling pathway) has already been identified as the hallmarks of many tumors, and their role in breast cancer has also been investigated and confirmed.
Polymorphisms in Wnt signaling pathway genes are associated with peak bone mineral density, lean mass, and fat mass in Chinese male nuclear families.
Zhang et al., Shanghai, China. In Osteoporos Int, Feb 2016
Our study identified that WNT5B and CTNNBL1 for both BMD and body composition, and WNT4 and CTNNB1 gene polymorphisms contribute to the variation in BMD and body composition in young Chinese men, respectively.
Clinical, pathologic, and genetic features of Wilms tumors with WTX gene mutation.
Vargas et al., Boston, United States. In Pediatr Dev Pathol, Feb 2016
All cases had been previously analyzed for WTX, WT1, and CTNNB1 aberrations via array comparative genomic hybridization; OncoMap 4 high throughput genotyping was performed on 18 cases.
CTNNB1 (β-Catenin)-altered Neoplasia: A Review Focusing on Soft Tissue Neoplasms and Parenchymal Lesions of Uncertain Histogenesis.
Haller et al., Erlangen, Germany. In Adv Anat Pathol, Jan 2016
β-catenin (CTNNB1) is a key regulatory molecule of the Wnt signaling pathway, which is important for tissue homeostasis and regulation of cell proliferation, differentiation, and function.
Second generation sequencing of microRNA in Human Bone Cells treated with Parathyroid Hormone or Dexamethasone.
Kindmark et al., Uppsala, Sweden. In Bone, Jan 2016
miR-30c2, miR-203 and miR-205 targeting RUNX2, and miR-320 targeting β-catenin (CTNNB1) mRNA expression.
Pregnancy, Primary Aldosteronism, and Adrenal CTNNB1 Mutations.
Brown et al., Cambridge, United Kingdom. In N Engl J Med, Nov 2015
Their aldosterone-producing adenomas harbored activating mutations of CTNNB1, encoding β-catenin in the Wnt cell-differentiation pathway, and expressed LHCGR and GNRHR, encoding gonadal receptors, at levels that were more than 100 times as high as the levels in other aldosterone-producing adenomas.
Targeting the Wnt signaling pathway in colorectal cancer.
Yamada et al., Kōbe, Japan. In Expert Opin Ther Targets, Nov 2015
The great majority of colorectal cancers have mutations in one of two genes involved in the Wnt signaling pathway: the adenomatous polyposis coli (APC) and β-catenin (CTNNB1) genes.
TERT promoter mutations in primary liver tumors.
Zucman-Rossi et al., Paris, France. In Clin Res Hepatol Gastroenterol, Oct 2015
UNASSIGNED: Next-generation sequencing has drawn the genetic landscape of hepatocellular carcinoma and several signaling pathways are altered at the DNA level in tumors: Wnt/β-catenin, cell cycle regulator, epigenetic modifier, histone methyltransferase, oxidative stress, ras/raf/map kinase and akt/mtor pathways.
Gene mutations in gastric cancer: a review of recent next-generation sequencing studies.
Li et al., Shanghai, China. In Tumour Biol, Sep 2015
Mutations in genes relating to genome integrity (TP53, BRCA2), chromatin remodeling (ARID1A), cell adhesion (CDH1, FAT4, CTNNA1), cytoskeleton and cell motility (RHOA), Wnt pathway (CTNNB1, APC, RNF43), and RTK pathway (RTKs, RAS family, MAPK pathway, PIK pathway) are discussed.
Exome sequencing of hepatocellular carcinomas identifies new mutational signatures and potential therapeutic targets.
Zucman-Rossi et al., Paris, France. In Nat Genet, May 2015
Associations of mutations defined 3 groups of genes related to risk factors and centered on CTNNB1 (alcohol), TP53 (hepatitis B virus, HBV) and AXIN1.
Phase II study of everolimus and letrozole in patients with recurrent endometrial carcinoma.
Coleman et al., Houston, United States. In J Clin Oncol, Apr 2015
Patients with endometrioid histology and CTNNB1 mutations responded well to everolimus and letrozole.
Analysis of differentially expressed genes based on microarray data of glioma.
Zhou et al., Nanjing, China. In Int J Clin Exp Med, 2014
In addition, the transcription factor analysis showed these DEGs were regulated by the binding sites of transcription factors GLI2, SP1, SMAD7, SMAD3, RELA, STAT5B, CTNNB1, STAT5A, TFAP2A and SP3.
Integrated genomic characterization of adrenocortical carcinoma.
Bertherat et al., Paris, France. In Nat Genet, 2014
We performed exome sequencing and SNP array analysis of 45 ACCs and identified recurrent alterations in known driver genes (CTNNB1, TP53, CDKN2A, RB1 and MEN1) and in genes not previously reported in ACC (ZNRF3, DAXX, TERT and MED12), which we validated in an independent cohort of 77 ACCs.
Recurrent activating mutation in PRKACA in cortisol-producing adrenal tumors.
Lifton et al., New Haven, United States. In Nat Genet, 2014
Six of these had known gain-of-function mutations in CTNNB1 (β-catenin) or GNAS (Gαs).
Immune suppression and resistance mediated by constitutive activation of Wnt/β-catenin signaling in human melanoma cells.
Kawakami et al., Tokyo, Japan. In J Immunol, 2012
Mice implanted with human mutant beta-catenin-overexpressed melanoma cells have less ability to activate T cells than do dendritic cells from mice with control melanoma cells.
Progression to adrenocortical tumorigenesis in mice and humans through insulin-like growth factor 2 and β-catenin.
Hammer et al., Ann Arbor, United States. In Am J Pathol, 2012
With the combination of stabilized beta-catenin and elevated Igf2 expression, adrenal glands were larger, displayed earlier onset of hyperplasia, and developed more frequent macroscopic adenomas.
GSK3β/axin-1/β-catenin complex is involved in semaphorin3A signaling.
Goshima et al., Yokohama, Japan. In J Neurosci, 2012
Colocalization of glycogen synthase kinase-3beta, axin-1, and beta-catenin is enhanced in response to semaphorin3A in cultured mouse dorsal root ganglion neurons.
Endothelial Wnt/β-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression.
Liebner et al., Frankfurt am Main, Germany. In J Exp Med, 2012
beta-catenin transcriptional activity directly regulated endothelial expression of platelet-derived growth factor B, leading to mural cell recruitment thereby contributing to vascular quiescence
S-Nitrosation of β-catenin and p120 catenin: a novel regulatory mechanism in endothelial hyperpermeability.
Sánchez et al., Valdivia, Chile. In Circ Res, 2012
S-nitrosation correlated with diminished abundance of beta-catenin and p120 at the adherens junction and with hyperpermeability.
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