Low-density lipoprotein receptor-related protein-5 binds to Axin and regulates the canonical Wnt signaling pathway.
By J. Mao, Ji-yong Wang, Bo Liu, Weijun Pan, G. Farr, C. Flynn, Huidong Yuan, S. Takada, D. Kimelman, Lin Li and 1 more. Molecules and Cells, 2001
872 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/9fd8cb55ca9a4ca8f7d7717085c69c617fe87c6c
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Citations in the corpus
- A mutation in the LDL receptor-related protein 5 gene results in the autosomal dominant high-bone-mass trait. (2002, background): “Recently, the LRP5 and LRP6 proteins have been shown to play a role in Wnt signaling (Pinson et al. 2000; Tamai et al. 2000; Wehrli et al. 2000; Mao et al. 2001), which is a key pathway involved in various developmental processes, including skeletal differentiation (Yamaguchi et al.”
- Cbfa1-independent decrease in osteoblast proliferation, osteopenia, and persistent embryonic eye vascularization in mice deficient in Lrp5, a Wnt coreceptor (2002, background): “Wnt proteins and postnatal bone formation Cell culture analyses have shown that LRP5 acts as a coreceptor for Wnt proteins (Mao et al., 2001).”
- Reaching a genetic and molecular understanding of skeletal development. (2002, background): “Here, we willceptor for Wnt proteins (Mao et al., 2001), and Lrp5 can directly bind Wnt proteins in vitro (Kato et al., 2001), only briefly describe the origin of the osteoclast and will The individual molecules presumably acting at different stages during precursor cell proliferation and…”
- Osteoblasts in prostate cancer metastasis to bone (2005, background): “This complex activates the canonical WNT signalling pathwa”
- Canonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytes. (2005, background): “…osteoblasto- l sgenesis came from the finding that loss-of-function mutations in the Lrp5 gene, encoding a coreceptor of d ocanonical Wnt signaling (Mao et al., 2001), result in a decrease in bone density associated with defects in os- n wteoblast differentiation and proliferation (Gong et al.,…”
- The Wnt signaling pathway in development and disease. (2004, background): “Because LRP can interact with the cytosolic protein Axin (Mao et al. 2001b, Tolwinski et al. 2003) (Figures 2 and 3), Wnts are thought to induce the phosphorylation of LRP on a PPP(S/T)P motif, thus allowing the docking of Axin to the LRP cytoplasmic tail.”
- β-Catenin destruction complex: insights and questions from a structural perspective (2006, background): “For example, as discussed above, under certain conditions LRP5/6 can function in a Frizzled and Dishevelled-independent manner whereas normally all of these components function synergistically (Li et al., 2002; Schweizer and Varmus, 2003; Cong et al., 2004b).”
- YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response. (2014, background): “Wnt ligands are known to induce clustering of LRP6, in turn triggering functional inactivation of the destruction complex via association of LRP6 to Axin (Mao et al., 2001).”
- Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer. (2004, background): “4C and 4D), which, in Axin1, mediates oligomerization and interactions with protein phosphatase 2A, disheveled, and LRP5/6 (Seidensticker and Behrens 2000; Mao et al. 2001).”