IndraLab

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CTNNB1 dephosphorylates CTNNB1. 50 / 50
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"Wnt and beta-catenin signaling pathway leads to dephosphorylation, stabilization, and nuclear translocation of beta-catenin."
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"In the absence of a mitotic signal from outside the cell, beta-catenin is sequestered in a complex with the adenomatous polyposis coli (APC) gene product, a serine threonine glycogen synthetase kinase (GSK-3beta) and an adapter protein axin (or a homologue conductin), enabling phosphorylation and degradation of free beta-catenin by the ubiquitin-proteasome system [XREF_BIBR]."
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"In the absence of Wnt, the association of beta-catenin with glycogen synthase kinase 3beta (GSK3beta), Axin, and the adenomatous polyposis coli (APC) protein leads to GSK3beta mediated phosphorylation[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Beta-catenin functions as a significant component in the Wnt signaling pathway, and interactions with frizzled and LRP5/6 receptors result in the dephosphorylation of beta-catenin (non phosphorylated active beta-catenin)."
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"Mutations in the N-terminal region of beta-catenin abrogate the phosphorylation of beta-catenin and, subsequently, its degradation."
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"Mutations in CTNNB1 result in attenuated β-catenin phosphorylation with the ultimate consequence of reduced β-catenin degradation and the subsequent unregulated activation of the WNT pathway."
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"In normal cells the degradation of beta-catenin is regulated by Wnt signaling : beta-catenin is constitutively phosphorylated by the beta-catenin destruction complex, which marks beta-catenin for ubiquitination followed by rapid proteasomal degradation; Wnt signaling inactivates the beta-catenin destruction complex, thereby inhibiting phosphorylation of beta-catenin and consequently ubiquitination and degradation of the protein."
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"Degradation of phosphorylated β-catenin limits β-catenin nuclear translocation to inactivate LEF1 translation, resulting in an inhibited Wnt/β-catenin signaling activation."
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"Dephosphorylation and stabilization of β-catenin is promoted by signal transduction from the fizzled receptor and subsequent localization of β-catenin to the nucleus leading to increased expression of target genes."
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"Western blotting results revealed that Wnt2 overexpression suppressed inhibitory phosphorylation of β-catenin and increased total β-catenin level (Figure 7F)."
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"This β-catenin isoform increases the stability of full-length β-catenin by antagonizing GSK3β-induced β-catenin phosphorylation and degradation and eventually results in the activation of the Wnt pathway (113)."
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"In the absence of Wnt signals, this multi protein complex promotes degradation of free beta-catenin via GSK3beta mediated phosphorylation of specific beta-catenin residues; phosphorylated beta-catenin is subsequently ubiquitinated and degraded by the proteasome."
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"Most beta-catenin pathway activating mutations were missense mutations in exon 3 of CTNNB1 that disrupt phosphorylation of beta-catenin and its ubiquitin mediated degradation, leading to increased beta-catenin levels XREF_BIBR - XREF_BIBR."
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"In addition, this miRNA downstream target NCAPH can compete with Akt1 to form a complex with β-catenin, which prevents β-catenin phosphorylation and ubiquitin interceded protein destruction, resulting in triggered Wnt signaling and a more favorable niche for cancer stem cells in NSCLC [84]."
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"TRIB2 overexpression induced GSK3beta inactivation by augmenting AKT-dependent phosphorylation of GSK3beta at Ser9, followed by increasing beta-catenin level via reducing the GSK3beta-mediated phosphorylation of beta-catenin."
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"SBSN-2 in ESCC cell lines increased the activity of WNT and beta-catenin signalling pathway, which resulted in TCF/LEF transcriptional activity, nuclear translocation and reduced phosphorylation of WNT and beta-catenin, and increased transcript levels of WNT / beta-catenin signalling regulated genes such as AXIN2, MYC, CCND1, FRA1, MMP7 and JUN.."
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"The β-catenin destruction complex is then inactivated, leading to the aggregation of unphosphorylated β-catenin in the cytoplasm and nucleus [105]."
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"We found that, in addition to the previously implicated Galpha o [XREF_BIBR, XREF_BIBR] and Galpha q [XREF_BIBR, XREF_BIBR], Galpha i2 also inhibited exogenous beta-catenin degradation and phosphorylation of endogenous beta-catenin by GSK3."
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"Pgam5 dependent stabilization of beta-catenin after hypoxia is in line with CCCP induced beta-catenin dephosphorylation by Pgam5."
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"Together, we could show that PGAM5 released from damaged mitochondria activates Wnt and beta-catenin signaling cell intrinsically via direct dephosphorylation of beta-catenin."
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"We also show that the core component of the beta-catenin destruction complex, axin, promotes beta-catenin dephosphorylation by Pgam5."
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"We observed that compared to control cultures, DKK3-overexpressing organoids showed higher level of phosphorylated (inactive) β-catenin and reduced levels of non-phosphorylated (active) β-catenin."
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"In cancer cells, β-catenin act as oncoprotein which causes cell proliferation; GSK-3 inhibits β-catenin by phosphorylating β-catenin molecule resulting in degradation of β-catenin (46,47)."
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"We use nuclease-free base editing to install a S33F mutation in beta-catenin that blocks beta-catenin phosphorylation, impedes beta-catenin degradation, and upregulates Wnt signaling."
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"Canagliflozin promotes the degradation of beta-catenin via inhibiting PP2A-mediated dephosphorylation of beta-catenin."
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"Canonical Wnt signaling is transduced intracellularly by the interaction of the Dvl DIX protein domain with the β-catenin destruction complex, which prevents β-catenin phosphorylation and degradation (Fiedler et al., 2011; Kimelman and Xu, 2006; Kishida et al., 1999; Wallingford and Habas, 2005)."
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"It has been documented that in some CRCs, hyperactive Wnt signaling might result from mutations affecting additional pathway negative regulators AXIN1 [12] and AXIN2 [13], or upon missense mutations in the CTNNB1 gene that impair β-catenin protein N-terminal phosphorylation [14]."
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"Thus, the multiprotein β-catenin “destruction complex” is inactivated to prevent β-catenin phosphorylation and its proteasomal degradation."
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"It acts as a scaffold structure for the destruction complex that promotes phosphorylation and subsequent ubiquitin-dependent degradation of CTNNB1(Catenin beta-1), a key WNT pathway activator.21,22 APC enhances the effectiveness of this destruction machinery by encouraging axin multimerization and stabilising the axin complex."
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"28,29 We used western blotting to measure expression levels of β-catenin and Akt in HUVECs exposed to C069 (0, 0.2, or 0.5 μM) for 24 h. HUVECs were western blotting revealed no obviously diversificat[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In the absence of Wnt ligands stimulation, adenomatous polyposis coli (APC), Axin, casein kinase 1α (CK1α), and GSK3 form the β-catenin destruction complex, which induces the phosphorylation and subse[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Furthermore, the effect of GSK-3β inhibition, as assessed by TCF3-mediated transactivation, was substantially more pronounced than that of activated cytosolic β-catenin ( Fig. 6 A), indicating that GS[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Since phosphorylated Axin binds beta-catenin better than unphosphorylated Axin [27], beta-catenin will no longer be recruited to the Axin and GSK-3beta complex, thus preventing beta-catenin phosphoryl[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Both phosphorylation of beta-catenin and betaTrCP binding are required for beta-catenin degradation.Abrogation of NH2-terminal phosphorylation of beta-catenin as a result either of oncogenic mutations[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"13 Upon activation of the Wnt/β-catenin pathway, β-catenin enters the nucleus and interacts with transcription factors T-cell and lymphoid enhancer factors (Tcf/Lef1) to activate transcription of Axin[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In the cytoplasm, the DUF1669 structural domain of FAM83A mediated the interaction between FAM83A and AXIN1, GSK3β, and β-catenin, which in turn inhibited the phosphorylation and degradation of β-catenin protein [96]."
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"The following primary antibodies were employed: VE-cadherin (1 : 1000, ab33168, Abcam, USA), β-catenin (1 : 1000, 610154, BD Transduction Laboratories, USA), dephosphorylated active β-catenin (05-665, Millipore, Germany), Sirt3 (1 : 500, ab189860, Abcam, USA), matrix metallopeptidase-7 (MMP-7, 1 : 400, ab5706; Abcam, USA), and cyclooxygenase-2 (COX-2, 1 : 1000, ab62331, Abcam, USA)."
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"The results of the present study revealed that the knockdown of FUT2 increased the phosphorylation levels of β-catenin and GSK3β expression, which mediated the phosphorylation of β-catenin."
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"MUC1 increases cytoplasmic and nuclear beta-catenin levels by inhibiting GSK3beta mediated phosphorylation and degradation of beta-catenin."
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"The B55a subunit directly binds to the beta-catenin destruction complex, where PP2A dephosphorylates beta-catenin and induces its degradation [XREF_BIBR]."
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"Another study demonstrated that total β-catenin and nuclear β-catenin expression were significantly decreased and phosphorylated β-catenin expression was increased after Uba2, an important component of the E1 activating enzyme, was knocked out (71)."
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"In the context of canonical Wnt signaling, non-active conditions enable the continuous phosphorylation of β-catenin mediated by the inhibitory complex of β-catenin, which includes AXIN, GSK3β, APC, and CK1."
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"When the pathway is activated, Wnt inhibits β-catenin phosphorylation, which in turn will increase the levels of unphosphorylated β-catenin in the cytoplasm."
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"We examined changes in the expression of beta-catenin target genes and DP signature genes by real-time PCR using hDPCs treated with MPA and/or IFN-gamma for 24 h. Expression of Axin-2 was used as an indicator of beta-catenin signaling pathway activity, which promotes the phosphorylation and degradation of beta-catenin [XREF_BIBR]."
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"We found that RNF125 overexpression significantly reduced GSK3β phosphorylation and total β-catenin levels, as well as enhanced β-catenin phosphorylation, while showed no effects on total GSK3β levels[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The activation of WNT and beta-catenin inhibits the phosphorylation of beta-catenin and releases it from the destruction complex, which prevents TAZ degradation, resulting in the concomitant beta-catenin and TAZ accumulation."
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"The data revealed that derivative #5 overcame LANA-mediated β-catenin stabilization via the enhancement of β-catenin phosphorylation, which leads to β-catenin polyubiquitination and degradation.The phosphorylation of β-catenin is essential for polyubiquitination mediated by the E3 ubiquitin ligase, SCF ."
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"Blocking the Wnt /β-catenin might cause down regulations of those transcriptions, lead to defect of the upper jaw structures.LiCl is shown to activate the Wnt /β-catenin pathway through inhibition of [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"The ubiquitin ligase activity of HUWE1 is required to enhance WNT signaling (Fig 5), suggesting that a substrate of HUWE1 mediates its function.One of the mechanisms whereby HUWE1 enhances WNT/CTNNB1 signaling is by antagonizing phosphorylation of the CTNNB1 phosphodegron by the DC complex, thereby increasing CTNNB1 abundance, but surprisingly this happens in the absence of CSNK1A1."
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"The Wnt and beta-catenin signaling pathway leads to de-phosphorylation, stabilization, and nuclear translocation of beta-catenin."
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