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This study suggests that glutamine could protect against oxidative stress-induced injury in Alzheimer's disease (AD) mice via the Wnt3a/beta-catenin signaling pathway.
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Study shows that IKKbeta promotes adipogenesis but inhibits osteogenesis in murine and human mesenchymal stem cells (MSCs) through an NF-kappaB-independent mechanism. IKKbeta is a beta-catenin kinase that phosphorylates the degron motif of beta-catenin to prime it for beta-TrCP-mediated ubiquitination and degradation, thereby regulating MSC fate.
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These data suggest that intervertebral disc degeneration is associated with loss of Wnt signaling and that the concomitant increase in b-catenin is a regenerative response, potentially offering a therapeutic approach to degeneration.
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The authors demonstrated that FGF7 could increase the expression of Cx43 in osteocytes and promote the cell processes in the form of gap junctions between osteocytes. This modulation was due to the FGF7-induced cytoplasmic accumulation and resultant nuclear translocation of beta-catenin.
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Skeletal muscle stem cells underwent a switch from beta-catenin-Lef1 to Smad3-Lef1 interactions during the postnatal switch from proliferation to quiescence, with beta-catenin-Lef1 interactions recurring during damage-induced reactivation.
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Hepatocellular carcinomas with mutations that activate beta-catenin are characterized by increased uptake of a fluorocholine tracer, and can be detected by PET scan.
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IKKbeta negatively regulates vascular smooth muscle cell calcification through beta-catenin-Runx2 signaling.
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Conditional loss of Apc resulted in the expression of nuclear beta-catenin throughout the developing mouse liver and increased number of cells expressing glutamine synthetase.
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After ischemia-reperfusion injury in conditional knockout mice in which beta-catenin was specifically ablated in fibroblasts (Gli1-beta-cat-/-),there was less apoptosis, cytochrome C release, serum creatinine, and damage. Gene expression and phosphorylation of many proteins were affected, including HGF. Fibroblast-specific beta-catenin signaling can control tubular injury and repair in AKI by modulating HGF expression.
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Despite the induction of oxidative and metabolic stresses, Shp2 deletion in hepatocytes suppressed hepatocarcinogenesis driven by overexpression of oncoproteins MET/CAT or MET/PIK. Shp2 loss inhibited proliferative signaling from c-Met, Wnt/beta-catenin, Ras/Erk and PI3K/Akt pathways, but triggered cell senescence following exogenous expression of the oncogenes.
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Let-7c inhibits cholangiocarcinoma growth but promotes tumor cell invasion and growth at extrahepatic sites at least in part, through regulation of EZH2 protein expression and through the DVL3/beta-catenin axis.
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Stromal beta-catenin is essential for kidney development by regulating medulla formation through the differentiation of medullary stromal cells.
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when CTLA-4 and PD-1 antibodies were combined with DCR-BCAT in MMTV-Wnt1 transgenic mice, a genetic model of spontaneous Wnt-driven tumors, complete regressions were achieved in the majority of treated subjects. These data support RNAi-mediated b-catenin inhibition as an effective strategy to increase response rates to cancer immunotherapy.
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Data indicate a function of GATA binding protein 4 (GATA4) as a cardiac repressor of the transcription factor 7-like 2 protein (TCF7L2)/beta-catenin complex.
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Bioinformatic analysis of the protein networks implies potentially novel functions for beta-catenin, particularly in mRNA translation, and we confirm a direct interaction between beta-catenin and the fragile X mental retardation protein (FMRP).
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Ablation of beta-catenin resulted in STAT3 downregulation and STAT1 activation, leading to elevated macrophage inflammatory responses and increased atherosclerosis in Ldl receptor deficient mice.
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This study show that beta-catenin in excitatory neurons of the adult neocortex is essential for the optimal processing of visual information.
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nuclear organization of motor neurons is dependent on inside-out positioning, orchestrated by N-cadherin, catenin, and afadin activities, controlling cell body layering on the medio-lateral axis.
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these indicate that SLIT3/ROBO2 promotes chondrocyte maturation via the inhibition of beta-catenin signaling.
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mechanical unloading decreases MACF1 expression, and MACF1 up-regulates osteoblast proliferation through enhancing beta-catenin signaling. This study has thus provided a mechanism for mechanical unloading-induced inhibited osteoblast proliferation.