Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Conversely, S246→L and S246→M missense mutations, which reduce the ICPB in Xaa246-P247 in human β-catenin, can enhance interactions between β-catenin and APC and between β-catenin and E-cadherin, leading to decreased nuclear migration of β-catenin.
|
30807699 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, the activity of key molecules of the adenomatous polyposis coli (APC)/β‑catenin complex was altered following treatment with BITC, which suggested a potential role for the APC/β‑catenin complex in the BITC‑mediated induction of apoptosis and inhibition of metastasis in murine mammary carcinoma.
|
31257529 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Aberrant activation of this signaling pathway is a key early event in the development of colorectal neoplasms, and is mainly caused by loss of function mutations in Adenomatous Polyposis Coli (APC), and less frequently by β-catenin stabilization mutations via missense or interstitial genomic deletions in CTNNB1.
|
30177831 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Colorectal cancer (CRC) is categorized by alteration of vital pathways such as β-catenin (CTNNB1) mutations, WNT signaling activation, tumor protein 53 (TP53) inactivation, BRAF, Adenomatous polyposis coli (APC) inactivation, KRAS, dysregulation of epithelial to mesenchymal transition (EMT) genes, MYC amplification, etc.
|
31699039 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we provide direct evidence for a strict requirement for constant β-catenin degradation through the APC destruction complex in order to maintain pluripotency, highlighting a fundamental role for APC in self-renewal of hESCs.Stem Cells 2019;37:1505-1515.
|
31461190 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The most common recurrent somatic mutations were in TP53 (36%), androgen receptor (AR) (22%), adenomatous polyposis coli (APC) (10%), neurofibromin 1 (NF1) (9%), epidermal growth factor receptor (EGFR), catenin beta-1 (CTNNB1), and AT-rich interactive domain-containing protein 1A (ARID1A) (6% each); and BRCA1, BRCA2, and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) (5% each) The most common genes with increased copy numbers were AR (30%), MYC (20%), and BRAF (18%).
|
30620391 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Surprisingly, patients with C-L syndrome-like phenotype caused by APC truncating mutations have no polyposis despite the increased levels of β catenin.
|
30569497 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
The underlying mechanism was explored by quantitative real-time polymerase chain reaction of miRNA (miR-155-5p and miR-26b-5p), luciferase reporter assay, western blotting of Wnt signaling pathway-related proteins (β-catenin, adenomatous polyposis coli (APC), glycogen synthase kinase 3β (GSK3β), ZEB1, and E-cadherin), mitogen-activated protein kinase (MAPK) signaling pathway-related proteins (extracellular signal-regulated kinase [ERK]1/2, p-ERK1/2, c-Jun N-terminal kinase (JNK), p-JNK, P38, and p-P38), and immunofluorescence staining of β-catenin.
|
30945380 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Routine CTNNB1 sequencing may also rule out FAP and allow for deferral of colonoscopy.
|
30610557 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Transfection of APC small interfering RNA re‑activated β‑catenin and stimulated the expression of cyclin D1 and c‑Myc.
|
31364752 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This study aims to determine the contribution of polymorphisms in the genes of the β-catenin destruction complex to develop CRC, specifically adenomatous polyposis coli (APC) (rs11954856 G>T and rs459552 A>T), axis inhibition protein 1 (AXIN1) (rs9921222 C>T and rs1805105 C>T), AXIN2 (rs7224837 A>G), and dishevelled 2 (DVL2) (2074222 G>A and rs222836 C>T).
|
31723073 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Identification of Endogenous Adenomatous Polyposis Coli Interaction Partners and β-Catenin-Independent Targets by Proteomics.
|
31160382 |
2019 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Two miRs that target the canonical wingless (Wnt)/β-catenin pathway, at different levels, were found to be differentially regulated when comparing the miR-cargo of naive TEC-derived EVs (EVs) and anti-IL-3R-EVs. miR-214-3p, which directly targets β-catenin, was found to be upregulated, whereas miR-24-3p, which targets adenomatous polyposis coli (APC) and glycogen synthase kinase-3β (GSK3β), was found to be downregulated.
|
29238040 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We revealed that the effect of C2C12 exosomes depended on its miR-27a-3p component, they can increase miR-27a-3p level in the recipient cells, and decrease its direct target adenomatous polyposis coli (APC) expression, thus activating β-catenin pathway.
|
29476741 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The levels of β-catenin, EGFR, and RAS, especially mutant KRAS, are increased in CRC patient tissues due to mutations of adenomatous polyposis coli (APC), which occur in 90% of human CRCs.
|
30459318 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We also show that inducible loss of APC is rapidly followed by Wnt receptor activation and increased β-catenin levels.
|
29533772 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mechanistic analysis demonstrated that miR-106a-3p specifically targeted the adenomatous polyposis coli (APC) gene, and LINC01133/miR-106a-3p suppressed the EMT and metastasis by inactivating the Wnt/β-catenin pathway in an APC-dependent manner.
|
30134915 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The corresponding hot spot mutations are located in exon 3 of the CTNNB1 gene or alternatively, in the APC tumor suppressor gene, most often as a germline mutation.
|
29705714 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
Unlike its role in PPP in which RPIA functions within the cytosol, RPIA enters the nucleus to form a complex with the adenomatous polyposis coli (APC) and β-catenin.
|
29337987 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Moreover, 6G significantly inhibited nuclear factor kappa B (P65), p38, cyclooxygenase-2, and β-catenin whereas it enhanced IL-10 and adenomatous polyposis coli expression in DSS-treated mice.
|
29350052 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In the classical model for Wnt signaling, the primary role of APC is to act, together with the concentration-limiting scaffold protein Axin, in a "destruction complex" that directs the phosphorylation and consequent proteasomal degradation of the transcriptional activator β-catenin, thereby preventing signaling in the Wnt-off state.
|
29408853 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
It has been suggested that inactivation of APC plays an important role in activation of the Wnt/β-catenin pathway and in the progression of colorectal tumorigenesis.
|
29304823 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
The N-terminal and central domains of APC that regulate the microtubule cytoskeleton and stability of β-catenin in the Wnt pathway, were co-expressed with GFP in individual optic axons, and their terminal arbors were then imaged in tectal midbrains of intact tadpoles.
|
29856981 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
Biomarker
|
disease |
BEFREE |
There are at least five mechanisms by which APC can regulate the formation of the β-catenin/TCF complex: This paper presents a computational model for the Wnt pathway that explicitly includes the above five roles of APC in regulating β-catenin/TCF formation.
|
30110600 |
2018 |
Adenomatous Polyposis Coli
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, we establish and validate a tissue-based β-catenin gene and immunohistochemical analysis, which complements germline mutation screening to exclude the diagnosis of FAP among HB patients.
|
29446530 |
2018 |