Axin Signaling Complex
Adenomatous Polyposis Coli
Tumor Markers, Biological
Cell Adhesion Molecules
Receptors, Adrenergic, beta
Transforming Growth Factor beta
Armadillo Domain Proteins
Glycogen Synthase Kinase 3
Integrin beta Chains
beta 2-Glycoprotein I
Receptors, Adrenergic, beta-2
rhoA GTP-Binding Protein
rac1 GTP-Binding Protein
Molecular Sequence Data
Receptors, Adrenergic, beta-1
Fluorescent Antibody Technique
rho GTP-Binding Proteins
Recombinant Fusion Proteins
Alzheimer's disease: clues from flies and worms. (1/5919)Presenilin mutations give rise to familial Alzheimer's disease and result in elevated production of amyloid beta peptide. Recent evidence that presenilins act in developmental signalling pathways may be the key to understanding how senile plaques, neurofibrillary tangles and apoptosis are all biochemically linked. (+info)
The human F box protein beta-Trcp associates with the Cul1/Skp1 complex and regulates the stability of beta-catenin. (2/5919)Ubiquitin-conjugation targets numerous cellular regulators for proteasome-mediated degradation. Thus, the identification of ubiquitin ligases and their physiological substrates is crucially important, especially for those cases in which aberrant levels of regulatory proteins (e.g., beta-catenin, p27) result from a deregulated ubiquitination pathway. In yeast, the proteolysis of several G1 regulators is controlled by ubiquitin ligases (or SCFs) formed by three subunits: Skp1, Cul A (Cdc53), and one of many F-box proteins. Specific F-box proteins (Fbps) recruit different substrates to the SCF. Although many Fbps have been identified in mammals, their specific substrates and the existence of multiple SCFs have not yet been reported. We have found that one human Fbp, beta-Trcp (beta-Transducin repeat containing protein), does indeed form a novel SCF with human Skp1 and Cul1. Consistent with recent reports indicating that Xenopus and Drosophila beta-Trcp homologs act as negative regulators of the Wnt/beta-catenin signaling pathway, we report here that human beta-Trcp interacts with beta-catenin in vivo. Furthermore, beta-catenin is specifically stabilized in vivo by the expression of a dominant negative beta-Trcp. These results indicate that the Cul1/Skp1/beta-Trcp complex forms a ubiquitin ligase that mediates the degradation of beta-catenin. (+info)
Axin prevents Wnt-3a-induced accumulation of beta-catenin. (3/5919)When Axin, a negative regulator of the Wnt signaling pathway, was expressed in COS cells, it coeluted with glycogen synthase kinase-3beta (GSK-3beta), beta-catenin, and adenomatous polyposis coli protein (APC) in a high molecular weight fraction on gel filtration column chromatography. In this fraction, GSK-3beta, beta-catenin, and APC were co-precipitated with Axin. Although beta-catenin was detected in the high molecular weight fraction in L cells on gel filtration column chromatography, addition of conditioned medium expressing Wnt-3a to the cells increased beta-catenin in the low molecular weight fraction. However, Wnt-3a-dependent accumulation of beta-catenin was greatly inhibited in L cells stably expressing Axin. Axin also suppressed Wnt-3a-dependent activation of Tcf-4 which binds to beta-catenin and acts as a transcription factor. These results suggest that Axin forms a complex with GSK-3beta, beta-catenin, and APC, resulting in the stimulation of the degradation of beta-catenin and that Wnt-3a induces the dissociation of beta-catenin from the Axin complex and accumulates beta-catenin. (+info)
Glucocorticoid down-regulation of fascin protein expression is required for the steroid-induced formation of tight junctions and cell-cell interactions in rat mammary epithelial tumor cells. (4/5919)Glucocorticoid hormones, which are physiological regulators of mammary epithelium development, induce the formation of tight junctions in rat Con8 mammary epithelial tumor cells. We have discovered that, as part of this process, the synthetic glucocorticoid dexamethasone strongly and reversibly down-regulated the expression of fascin, an actin-bundling protein that also interacts with the adherens junction component beta-catenin. Ectopic constitutive expression of full-length mouse fascin containing a Myc epitope tag (Myc-fascin) in Con8 cells inhibited the dexamethasone stimulation of transepithelial electrical resistance, disrupted the induced localization of the tight junction protein occludin and the adherens junction protein beta-catenin to the cell periphery, and prevented the rearrangement of the actin cytoskeleton. Ectopic expression of either the carboxyl-terminal 213 amino acids of fascin, which includes the actin and beta-catenin-binding sites, or the amino-terminal 313 amino acids of fascin failed to disrupt the glucocorticoid induction of tight junction formation. Mammary tumor cells expressing the full-length Myc-fascin remained generally glucocorticoid responsive and displayed no changes in the levels or protein-protein interactions of junctional proteins or the amount of cytoskeletal associated actin filaments. However, a cell aggregation assay demonstrated that the expression of Myc-fascin abrogated the dexamethasone induction of cell-cell adhesion. Our results implicate the down-regulation of fascin as a key intermediate step that directly links glucocorticoid receptor signaling to the coordinate control of junctional complex formation and cell-cell interactions in mammary tumor epithelial cells. (+info)
Frequent nuclear/cytoplasmic localization of beta-catenin without exon 3 mutations in malignant melanoma. (5/5919)Beta-Catenin has a critical role in E-cadherin-mediated cell-cell adhesion, and it also functions as a downstream signaling molecule in the wnt pathway. Mutations in the putative glycogen synthase kinase 3beta phosphorylation sites near the beta-catenin amino terminus have been found in some cancers and cancer cell lines. The mutations render beta-catenin resistant to regulation by a complex containing the glycogen synthase kinase 3beta, adenomatous polyposis coli, and axin proteins. As a result, beta-catenin accumulates in the cytosol and nucleus and activates T-cell factor/ lymphoid enhancing factor transcription factors. Previously, 6 of 27 melanoma cell lines were found to have beta-catenin exon 3 mutations affecting the N-terminal phosphorylation sites (Rubinfeld B, Robbins P, Elgamil M, Albert I, Porfiri E, Polakis P: Stabilization of beta-catenin by genetic defects in melanoma cell lines. Science 1997, 275:1790-1792). To assess the role of beta-catenin defects in primary melanomas, we undertook immunohistochemical and DNA sequencing studies in 65 melanoma specimens. Nuclear and/or cytoplasmic localization of beta-catenin, a potential indicator of wnt pathway activation, was seen focally within roughly one third of the tumors, though a clonal somatic mutation in beta-catenin was found in only one case (codon 45 Ser-->Pro). Our findings demonstrate that beta-catenin mutations are rare in primary melanoma, in contrast to the situation in melanoma cell lines. Nonetheless, activation of beta-catenin, as indicated by its nuclear and/or cytoplasmic localization, appears to be frequent in melanoma, and in some cases, it may reflect focal and transient activation of the wnt pathway within the tumor. (+info)
Expression of CD44 in Apc and Tcf mutant mice implies regulation by the WNT pathway. (6/5919)Overexpression of cell surface glycoproteins of the CD44 family is an early event in the colorectal adenoma-carcinoma sequence. This suggests a link with disruption of APC tumor suppressor protein-mediated regulation of beta-catenin/Tcf-4 signaling, which is crucial in initiating tumorigenesis. To explore this hypothesis, we analyzed CD44 expression in the intestinal mucosa of mice and humans with genetic defects in either APC or Tcf-4, leading to constitutive activation or blockade of the beta-catenin/Tcf-4 pathway, respectively. We show that CD44 expression in the non-neoplastic intestinal mucosa of Apc mutant mice is confined to the crypt epithelium but that CD44 is strongly overexpressed in adenomas as well as in invasive carcinomas. This overexpression includes the standard part of the CD44 (CD44s) as well as variant exons (CD44v). Interestingly, deregulated CD44 expression is already present in aberrant crypt foci with dysplasia (ACFs), the earliest detectable lesions of colorectal neoplasia. Like ACFs of Apc-mutant mice, ACFs of familial adenomatous polyposis (FAP) patients also overexpress CD44. In sharp contrast, Tcf-4 mutant mice show a complete absence of CD44 in the epithelium of the small intestine. This loss of CD44 concurs with loss of stem cell characteristics, shared with adenoma cells. Our results indicate that CD44 expression is part of a genetic program controlled by the beta-catenin/Tcf-4 signaling pathway and suggest a role for CD44 in the generation and turnover of epithelial cells. (+info)
Cadherin-11 is expressed in invasive breast cancer cell lines. (7/5919)In several cancers, including breast cancer, loss of E-cadherin expression is correlated with a loss of the epithelial phenotype and with a gain of invasiveness. Cells that have lost E-cadherin expression are either poorly invasive with a rounded phenotype, or highly invasive, with a mesenchymal phenotype. Most cells lacking E-cadherin still retain weak calcium-dependent adhesion, indicating the presence of another cadherin family member. We have now examined the expression of the mesenchymal cadherin, cadherin-11, in breast cancer cell lines. Cadherin-11 mRNA and protein, as well as a variant form, are expressed in the most invasive cell lines but not in any of the noninvasive cell lines. Cadherin-11 is localized to a detergent-soluble pool and is associated with both alpha- and beta-catenin. Immunocytochemistry shows that cadherin-11 is localized to the cell membrane at sites of cell-cell contact as well as at lamellipodia-like projections, which do not interact with other cells. These results suggest that cadherin-11 expression may be well correlated with the invasive phenotype in cancer cells and may serve as a molecular marker for the more aggressive, invasive subset of tumors. Cadherin-11 may mediate the interaction between malignant tumor cells and other cell types that normally express cadherin-11, such as stromal cells or osteoblasts or perhaps even with the surrounding extracellular matrix, thus facilitating tumor cell invasion and metastasis. (+info)
Coupling assembly of the E-cadherin/beta-catenin complex to efficient endoplasmic reticulum exit and basal-lateral membrane targeting of E-cadherin in polarized MDCK cells. (8/5919)The E-cadherin/catenin complex regulates Ca++-dependent cell-cell adhesion and is localized to the basal-lateral membrane of polarized epithelial cells. Little is known about mechanisms of complex assembly or intracellular trafficking, or how these processes might ultimately regulate adhesion functions of the complex at the cell surface. The cytoplasmic domain of E-cadherin contains two putative basal-lateral sorting motifs, which are homologous to sorting signals in the low density lipoprotein receptor, but an alanine scan across tyrosine residues in these motifs did not affect the fidelity of newly synthesized E-cadherin delivery to the basal-lateral membrane of MDCK cells. Nevertheless, sorting signals are located in the cytoplasmic domain since a chimeric protein (GP2CAD1), comprising the extracellular domain of GP2 (an apical membrane protein) and the transmembrane and cytoplasmic domains of E-cadherin, was efficiently and specifically delivered to the basal-lateral membrane. Systematic deletion and recombination of specific regions of the cytoplasmic domain of GP2CAD1 resulted in delivery of <10% of these newly synthesized proteins to both apical and basal-lateral membrane domains. Significantly, >90% of each mutant protein was retained in the ER. None of these mutants formed a strong interaction with beta-catenin, which normally occurs shortly after E-cadherin synthesis. In addition, a simple deletion mutation of E-cadherin that lacks beta-catenin binding is also localized intracellularly. Thus, beta-catenin binding to the whole cytoplasmic domain of E-cadherin correlates with efficient and targeted delivery of E-cadherin to the lateral plasma membrane. In this capacity, we suggest that beta-catenin acts as a chauffeur, to facilitate transport of E-cadherin out of the ER and the plasma membrane. (+info)
There are several types of intestinal polyps, including:
1. Adenomatous polyps: These are the most common type of polyp and have the potential to become malignant (cancerous) over time if left untreated.
2. Hyperplastic polyps: These polyps are benign and do not have the potential to become cancerous.
3. Inflammatory polyps: These polyps are caused by inflammation in the intestines and are typically seen in conditions such as ulcerative colitis or Crohn's disease.
4. Villous adenomas: These polyps are benign growths that occur on the villi (small projections) of the intestinal lining. They have the potential to become malignant over time if left untreated.
Intestinal polyps can cause a variety of symptoms, including abdominal pain, rectal bleeding, and changes in bowel movements. However, many people with intestinal polyps do not experience any symptoms at all. Intestinal polyps are typically detected during a colonoscopy or other imaging tests.
If you have been diagnosed with an intestinal polyp, your doctor may recommend one of the following treatments:
1. Watchful waiting: If your polyp is small and not causing any symptoms, your doctor may recommend monitoring it closely with regular colonoscopies to see if it grows or changes over time.
2. Removal: Polyps can be removed during a colonoscopy using a technique called endoscopic mucosal resection (EMR) or by surgery.
3. Chemoprevention: In some cases, your doctor may recommend medications such as aspirin or sulindac to help reduce the risk of polyps growing back.
It's important to note that while intestinal polyps are generally not cancerous, they can sometimes become malignant over time if left untreated. Therefore, it is important to follow your doctor's recommendations for monitoring and treatment closely.
The main features of PJS include:
* Multiple hamartomas in the gastrointestinal tract, which can lead to abdominal pain, nausea, vomiting, and rectal bleeding.
* Hamartomas in the lungs, which can cause coughing, wheezing, and shortness of breath.
* Hamartomas in the sex organs, which can lead to infertility, irregular menstrual cycles, and breast tumors.
* An increased risk of developing various types of cancer, including colon, lung, pancreatic, and breast cancer.
* A characteristic "speckled" appearance of the skin, caused by the accumulation of pigmented cells.
PJS is usually diagnosed in children or young adults, and it affects approximately 1 in 250,000 to 1 in 500,000 individuals worldwide. There is no cure for PJS, but regular monitoring and surveillance can help detect and treat hamartomas and cancerous lesions early on. Treatment options may include surgery, chemotherapy, and radiation therapy, depending on the location and severity of the tumors.
Wilms tumor accounts for about 5% of all childhood kidney cancers and usually affects only one kidney. The cancerous cells in the kidney are called blastema cells, which are immature cells that have not yet developed into normal kidney tissue.
The symptoms of Wilms tumor can vary depending on the size and location of the tumor, but they may include:
* Abdominal pain or swelling
* Blood in the urine
* Weight loss
* Loss of appetite
Wilms tumor is diagnosed through a combination of imaging tests such as ultrasound, CT scans, and MRI scans, and a biopsy to confirm the presence of cancer cells.
Treatment for Wilms tumor typically involves a combination of surgery, chemotherapy, and radiation therapy. The specific treatment plan will depend on the stage and location of the tumor, as well as the age and overall health of the child. In some cases, the affected kidney may need to be removed if the cancer is not completely removable by surgery or if it has spread to other parts of the body.
The prognosis for Wilms tumor has improved significantly over the past few decades due to advances in treatment and early detection. According to the American Cancer Society, the 5-year survival rate for children with Wilms tumor is about 90% if the cancer is diagnosed before it has spread to other parts of the body. However, the cancer can recur in some cases, especially if it has spread to other parts of the body at the time of initial diagnosis.
Overall, while Wilms tumor is a serious and potentially life-threatening condition, with prompt and appropriate treatment, many children with this disease can achieve long-term survival and a good quality of life.
The APC gene is a tumor suppressor gene that helps regulate cell growth and prevent the formation of tumors. Mutations in the APC gene can cause the development of adenomas, which are precancerous growths that can eventually become colon cancer if left untreated.
APC mutations can be inherited from one's parents or can occur spontaneously. The risk of developing colorectal cancer is increased in people with an APC mutation, and regular screening and monitoring is recommended to detect and remove any precancerous growths before they become cancerous.
Symptoms of APC may include abdominal pain, diarrhea, rectal bleeding, and weight loss. Treatment for APC typically involves removal of the affected portion of the colon and rectum, followed by ongoing monitoring and screening to detect any recurrences.
In summary, adenomatous polyposis coli (APC) is a genetic condition that increases the risk of developing colorectal cancer and other cancers. It is caused by mutations in the APC gene and can be inherited or acquired spontaneously. Symptoms may include abdominal pain, diarrhea, rectal bleeding, and weight loss, and treatment typically involves removal of the affected portion of the colon and rectum, followed by ongoing monitoring and screening.
The causes of colorectal neoplasms are not fully understood, but factors such as age, genetics, diet, and lifestyle have been implicated. Symptoms of colorectal cancer can include changes in bowel habits, blood in the stool, abdominal pain, and weight loss. Screening for colorectal cancer is recommended for adults over the age of 50, as it can help detect early-stage tumors and improve survival rates.
There are several subtypes of colorectal neoplasms, including adenomas (which are precancerous polyps), carcinomas (which are malignant tumors), and lymphomas (which are cancers of the immune system). Treatment options for colorectal cancer depend on the stage and location of the tumor, but may include surgery, chemotherapy, radiation therapy, or a combination of these.
Research into the causes and treatment of colorectal neoplasms is ongoing, and there has been significant progress in recent years. Advances in screening and treatment have improved survival rates for patients with colorectal cancer, and there is hope that continued research will lead to even more effective treatments in the future.
Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:
1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)
The symptoms of adenocarcinoma depend on the location of the cancer and can include:
1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
8. Coughing up blood (in the case of lung adenocarcinoma)
The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.
Treatment options for adenocarcinoma depend on the location of the cancer and can include:
1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.
The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.
Dishevelled binding antagonist of beta catenin 2
Dishevelled binding antagonist of beta catenin 1
Signaling Gateway (website)
Protein chibby homolog 1
Primary effusion lymphoma
Nuclear receptor 4A1
Mir-344 microRNA precursor family
Developmentally Programmed Tankyrase Activity Upregulates Beta-catenin and Licenses Progression of Embryonic Genome Activation
beta-Catenin Polyclonal Antibody (51067-2-AP)
CTNNB1 catenin beta 1 [Homo sapiens (human)] - Gene - NCBI
Convergence of Wnt, beta-catenin, and cadherin pathways - PubMed
Chemoprevention of colon carcinogenesis by polyethylene glycol: suppression of epithelial proliferation via modulation of SNAIL...
Retraction Note: Combination Cancer Immunotherapy with Dendritic Cell Vaccine and Nanoparticles Loaded with Interleukin-15 and...
Epigenetic Mechanisms in Autism Spectrum Disorders | IntechOpen
Mapping Wnt/beta-catenin signaling during mouse development and in colorectal tumors. - Oxford Neuroscience
beta-Catenin signaling contributes to stemness and regulates early differentiation in murine embryonic stem cells
Mechanism and function of signal transduction by the Wnt/beta-catenin and Wnt/Ca2+ pathways
AbMiner - Antibody Detail | Genomics and Pharmacology Facility
Frontiers | Phosphofructokinase 1 Platelet Isoform Promotes β-Catenin Transactivation for Tumor Development
CTNNB1 Syndrome - Symptoms, Causes, Treatment | NORD
Cancers | Free Full-Text | Nucleolin Targeting by N6L Inhibits Wnt/β-Catenin Pathway Activation in Pancreatic Ductal...
LGR5 promotes cancer stem cell traits and chemoresistance in cervical cancer | Cell Death & Disease
Staff Listing - The University of Nottingham
Childhood Cancer Epidemiology: Overview, Tools of Study, Cancer Incidence
Pilomatrixoma: Background, Pathophysiology, Etiology
Xuyu Yang Curriculum Vitae - Y. Peng Loh Lab | NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human...
SFARI | Impact of PTEN mutations: Brain growth trajectory and scaling of cell types
ADAM10-Mediated Ectodomain Shedding Is an Essential Driver o... : Journal of the American Society of Nephrology
JCI - Sustained activation of SMAD3/SMAD4 by FOXM1 promotes TGF-β-dependent cancer metastasis
PA-06-282: Stem Cells and Cancer (R21)
- Because beta-catenin is the major regulator of cyclin D1 in colorectal cancer, we used the T-cell factor (Tcf)-TOPFLASH reporter assay to show that PEG markedly inhibited beta-catenin transcriptional activity. (nih.gov)
- Moreover, BAT-gal expression identifies novel sites of Wnt signaling, like notochord, endothelia, and areas of the adult brain, revealing an unsuspected dynamic pattern of beta-catenin transcriptional activity. (ox.ac.uk)
- Analyses of BAT-gal expression in the adenomatous polyposis coli (multiple intestinal neoplasia+) background revealed betacatenin transcriptional activity in intestinal adenomas but surprisingly not in normal crypt cells. (ox.ac.uk)
- Increased transcriptional activity of β-catenin, which is essential for cell proliferation, migration, invasion, and survival ( 1 , 2 ), has been detected in many types of human cancer ( 3 - 6 ). (frontiersin.org)
- 15. Negative regulation of the Wnt-beta-catenin pathway by the transcriptional repressor HBP1. (nih.gov)
Mutants of beta-catenin2
- Extracellular Vesicles Released from Cancer Cells Promote Tumorigenesis by Inducing Epithelial to Mesenchymal Transition via β-Catenin Signaling. (nih.gov)
- Chemoprevention of colon carcinogenesis by polyethylene glycol: suppression of epithelial proliferation via modulation of SNAIL/beta-catenin signaling. (nih.gov)
- 13. WNT-1 and HGF regulate GSK3 beta activity and beta-catenin signaling in mammary epithelial cells. (nih.gov)
- Activation of the Wnt/β-catenin pathway has effects on prostate cell proliferation, differentiation and the epithelial-mesenchymal transition, which is thought to regulate the invasive behaviour of tumour cells. (cicbiogune.es)
- 36. Järvinen E, Salazar-Ciudad I, Birchmeier W, Taketo MM, Jernvall J, Thesleff I. Continuous tooth generation in mouse is induced by activated epithelial Wnt/beta-catenin signaling. (bvsalud.org)
- Characterization of the Subcellular Distribution of Phospho-β-catenin in Colorectal Cancer. (nih.gov)
- In this study, we assessed the ability of PEG to target cyclin D1-beta-catenin-mediated hyperproliferation in the azoxymethane-treated rat model and the human colorectal cancer cell line, HT-29. (nih.gov)
- The discovery of genes responsible for inherited colorectal cancer syndromes has been important in identifying important etiologic pathways such as the beta-catenin/ APC and TGF beta/SMAD pathways. (cdc.gov)
- The relationship between long non-coding RNAs and Wnt/β-catenin signaling pathway in the pathogenesis of Alzheimer's disease. (nih.gov)
- Overloaded axial stress activates the Wnt/β-Catenin pathway in nucleus pulposus cells of adult degenerative scoliosis combined with intervertebral disc degeneration. (nih.gov)
- Of the many growth factors involved in these events, Wnts are particularly interesting regulators, because a key component of their signaling pathway, beta-catenin, also functions as a component of the cadherin complex, which controls cell-cell adhesion and influences cell migration. (nih.gov)
- Wnt signaling, proceeding through Frizzled and Arrow-LRP-5/6, activates Dishevelled (Dsh), which results in uncoupling β-catenin from the degradation pathway and its entry into the nucleus, where it interacts with TCF/LEF to control transcription. (nih.gov)
- Our previous study showed that LGR5 functions as a tumor promoter in cervical cancer by activating the Wnt/ β -catenin pathway. (nature.com)
- Finally, we found that the increased tumorsphere-forming efficiency induced by LGR5 could be regulated through the inhibition or activation of the Wnt/ β -catenin pathway in cervical cancer cells. (nature.com)
- 5. Constitutive activation of Wnt/beta-catenin signaling pathway in migration-active melanoma cells: role of LEF-1 in melanoma with increased metastatic potential. (nih.gov)
- Page and his colleagues predict that PTEN and Wnt-beta-catenin signaling act in a common pathway to control brain growth trajectory via cell number, and that this network may be a point of vulnerability in a subset of individuals with autism and abnormal brain growth. (sfari.org)
- Beta-catenin participates in signal transduction and developmental patterning in Xenopus and Drosophila embryos as a component of the Wnt signaling pathway. (embl.de)
- 9. Chromatin-specific regulation of LEF-1-beta-catenin transcription activation and inhibition in vitro. (nih.gov)
- PEG did not alter total beta-catenin expression but rather its nuclear localization, leading us to assess E-cadherin expression (a major determinant of beta-catenin subcellular localization), which was increased by 73% and 71% in the azoxymethane-rat and HT-29 cells, respectively. (nih.gov)
- To define which cells respond to activated beta-catenin during mammalian development, we generated the beta-catenin-activated transgene driving expression of nuclear beta-galactosidase reporter (BAT-gal) transgenic mice, expressing the lacZ gene under the control of beta-cateninT cell factor responsive elements. (ox.ac.uk)
- Here, we demonstrate that phosphofructokinase 1 platelet isoform (PFKP), which catalyzes a rate-limiting reaction in glycolysis, promotes EGFR activation-induced nuclear translocation and activation of β-catenin, thereby enhancing the expression of its downstream genes CCND1 and MYC in human glioblastoma cells. (frontiersin.org)
- EGFR activation-induced and CK2α-mediated α-catenin phosphorylation releases β-catenin from the β-catenin/α-catenin protein complex whereas nuclear pyruvate kinase M2 (PKM2) associates with β-catenin and induces gene expression by direct phosphorylation of histone H3 ( 12 - 17 ). (frontiersin.org)
- In addition, AKT directly phosphorylates β-catenin at Ser552 (S552), which promotes nuclear translocation and transactivation of β-catenin ( 18 ). (frontiersin.org)
- Catenina multifuncional que participa en la ADHESIÓN CELULAR y en la señalización nuclear. (bvsalud.org)
- A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. (bvsalud.org)
- It is now clear that Armadillo and beta-catenin bind directly to members of the T-cell factor/lymphoid enhancer factor subfamily of HMG box DNA-binding proteins, forming bipartite transcription factors that regulate Wingless/Wnt responsive genes in both Drosophila and vertebrates. (embl.de)
- Molecular studies showed that the spectrum of beta-catenin mutations was markedly different in chlorophyllin-promoted colon tumors--many of the mutations led to direct substitutions of critical Ser/Thr residues within the glycogen synthase kinase-3beta (GSK-3beta) region, whereas in all other groups, including DMH and IQ controls, the mutations typically affected amino acids adjacent to Ser(33). (nih.gov)
- The adenomatous polyposis coli tumor suppressor protein is also implicated in beta-catenin signaling. (embl.de)
- 2. Lef/Tcf-dependent Wnt/beta-catenin signaling during Xenopus axis specification. (nih.gov)
- β-catenin can be activated not only by Wnt ligands but also by receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR), whose mutation or overexpression of EGFR gene occurs in many types of human cancer, including more than 50% of glioblastoma (GBM) ( 10 , 11 ). (frontiersin.org)
- Tandem repeats form superhelix of helices that is proposed to mediate interaction of beta-catenin with its ligands. (embl.de)
- Mapping Wnt/beta-catenin signaling during mouse development and in colorectal tumors. (ox.ac.uk)
- The carcinogens 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and 1,2-dimethylhydrazine (DMH) induce colon tumors in the rat that contain mutations in beta-catenin, but the mutation pattern can be influenced by exposure to dietary phytochemicals, such as the water-soluble derivative of chlorophyll called chlorophyllin. (nih.gov)
- Importance of P-cadherin, beta-catenin, and Wnt5a/frizzled for progression of melanocytic tumors and prognosis in cutaneous melanoma. (uib.no)
- Importantly, we showed that EGFR-phosphorylated PFKP Y64 has a critical role in AKT activation and AKT-mediated β-catenin S552 phosphorylation and subsequent β-catenin transactivation and promotion of tumor cell glycolysis, migration, invasion, proliferation, and brain tumor growth. (frontiersin.org)
- 19. A GSK3beta phosphorylation site in axin modulates interaction with beta-catenin and Tcf-mediated gene expression. (nih.gov)
- 11. Visualization and exploration of Tcf/Lef function using a highly responsive Wnt/β-catenin signaling-reporter transgenic zebrafish. (nih.gov)
- Promotion versus suppression of rat colon carcinogenesis by chlorophyllin and chlorophyll: modulation of apoptosis, cell proliferation, and beta-catenin/Tcf signaling. (nih.gov)
- These findings highlight a novel mechanism underlying a glycolytic enzyme-mediated β-catenin transactivation and underscore the integrated and reciprocal regulation of metabolism and gene expression, which are two fundamental biological processes in tumor development. (frontiersin.org)
- In lipoprotein receptor-related protein 6-null homozygous mice, which lack a Wnt coreceptor, BAT-gal staining is absent in mutant tissues, indicating that BAT-gal mice are bona fide in vivo indicators of Wntbeta-catenin signaling. (ox.ac.uk)
- Identification of ESE1 as a β-Catenin Binding Protein. (nih.gov)
- The protein cleaves cell-adhesion molecules at the slit diaphragm, leading to Wnt/ β -catenin signaling and podocyte loss. (lww.com)
- 10. Fluorescence-based functional assay for Wnt/beta-catenin signaling activity. (nih.gov)
- In summary, BAT-gal mice unveil the entire complexity of Wntbeta-catenin signaling in mammals and have broad application potentials for the identification of Wnt-responsive cell populations in development and disease. (ox.ac.uk)
- β-catenin promotes resistance to trastuzumab in breast cancer cells through enhancing interaction between HER2 and SRC. (nih.gov)
- The cylindrical structure features a positively charged grove, which presumably interacts with the acidic surfaces of the known interaction partners of beta-catenin. (embl.de)
- Retraction Note: Combination Cancer Immunotherapy with Dendritic Cell Vaccine and Nanoparticles Loaded with Interleukin-15 and Anti-beta-catenin siRNA Significantly Inhibits Cancer Growth and Induces Anti-Tumor Immune Response. (bvsalud.org)
- Testing this hypothesis will involve mapping beta-catenin activity in the developing PTEN haploinsufficient mouse brain and modulating beta-catenin activity in a PTEN haploinsufficient background. (sfari.org)
- Wntbeta-catenin signaling plays key roles in several developmental and pathological processes. (ox.ac.uk)
- Detaching necrotic cells also often lost beta-catenin and e-cadherin expression. (cdc.gov)
- Here, we assemble evidence of possible interrelations between Wnt and other growth factor signaling, beta-catenin functions, and cadherin-mediated adhesion. (nih.gov)
- They hypothesize that PTEN haploinsufficiency alters brain growth trajectory and scaling of neuronal and glial populations through elevated beta-catenin signaling. (sfari.org)
- Beta-catenin is essential for cadherin-based cell adhesion and Wnt/Wingless growth factor signaling. (embl.de)
- these data directly implicate beta-catenin/LEF misregulation as the major cause of hair matrix cell tumorigenesis in humans. (medscape.com)
- In some necrotic foci in the mainstem bronchus epithelium, the normal thin linear staining of beta-catenin at intercellular junctions was replaced by more focal globular expression. (cdc.gov)
- β-catenin transactivation leads to enhanced T-cell factor (TCF)/lymphoid enhancer factor (LEF)-driven transcription of genes, such as CCND1 (encoding cyclin D1) and MYC (encoding c-Myc) ( 7 - 9 ). (frontiersin.org)
- A core region of beta-catenin, composed of 12 copies of a 42 amino acid sequence motif known as an armadillo repeat, mediates these interactions. (embl.de)
- Signal transduction of beta-catenin. (embl.de)
- In human skin , DCXR localizes to the cytoplasm near the adhesion molecules, e-cadherin and beta-catenin. (cdc.gov)
- Wnt/β-catenin signalling can be controlled by secreted Wnt antagonists, many of which are downregulated in cancer. (cicbiogune.es)