Reactome: A Curated Pathway Database
Results 1 to 10 of 15
Pathways (8) Reactions (3) Proteins (1) Others (3)
Protein: UniProt:O75197 LRP5 (Homo sapiens)
Last changed: 2015-03-10 08:59:22

Pathway: Disease (Homo sapiens)
Biological processes are captured in Reactome by identifying the molecules (DNA, RNA, protein, small molecules) involved in them and describing the details of their interactions. From this molecular viewpoint, human disease pathways have three mechanistic causes: the inclusion of microbially-expressed proteins, altered functions of human proteins, or changed expression levels of otherwise functionally
Last changed: 2015-03-06 23:15:47

Pathway: Signal Transduction (Homo sapiens)
Signal transduction is a process in which extracellular signals elicit changes in cell state and activity. Transmembrane receptors sense changes in the cellular environment by binding ligands, such as hormones and growth factors, or reacting to other types of stimuli, such as light. Stimulation of transmembrane receptors leads to their conformational change which propagates the signal to the intracellu
Last changed: 2015-03-06 23:15:47

Pathway: Signaling by Wnt (Homo sapiens)
WNT signaling pathways control a wide range of developmental and adult process in metozoans including cell proliferation, cell fate decisions, cell polarity and stem cell maintenance (reviewed in Saito-Diaz et al, 2013; MacDonald et al, 2009). The pathway is named for the WNT ligands, a large family of secreted cysteine-rich glycoproteins. At least 19 WNT members have been identified in humans and mic
Last changed: 2015-03-06 18:40:03

Pathway: Diseases of signal transduction (Homo sapiens)
Signaling processes are central to human physiology (e.g., Pires-da Silva & Sommer 2003), and their disruption by either germ-line and somatic mutation can lead to serious disease. Here, the molecular consequences of mutations affecting visual signal transduction and signaling by diverse growth factors are annotated
Last changed: 2015-01-15 22:40:17

Pathway: Signaling by WNT in cancer (Homo sapiens)
The WNT signaling pathway has been linked with cancer ever since the identification of the first WNT as a gene activated by integration of mouse mammary tumor virus proviral DNA in virally-induced breast tumors (Nusse et al, 1984). The most well known example of aberrant WNT signaling in cancer is in colorectal cancer, where an activating mutation in a WNT pathway component is seen in 90% of sporadic
Last changed: 2014-05-28 18:17:31

Pathway: misspliced LRP5 mutants have enhanced beta-catenin-dependent signaling (Homo sapiens)
LRP5 is subject to an in-frame missplicing event in breast and parathyroid cancers that renders the protein insensitive to inhibition by the WNT antagonist DKK1. Expression of the mutant protein results in elevated levels of active, unphosphorylated beta-catenin and enhanced TCF-dependent WNT-signaling, promoting cellular proliferation (Bjorklund et al 2007a, b; Bjorklund et al, 2009)
Last changed: 2015-02-09 16:16:33

Pathway: TCF dependent signaling in response to WNT (Homo sapiens)
19 WNT ligands and 10 FZD receptors have been identified in human cells; interactions amongst these ligands and receptors vary in a developmental and tissue-specific manner and lead to activation of so-called 'canonical' and 'non-canonical' WNT signaling. In the canonical WNT signaling pathway, binding of a WNT ligand to the Frizzled (FZD) and lipoprotein receptor-related protein (LRP) receptors resul
Last changed: 2015-03-06 18:40:03

Pathway: disassembly of the destruction complex and recruitment of AXIN to the membrane (Homo sapiens)
Upon stimulation with WNT ligand, AXIN and GSK3beta are recruited to the plasma membrane through interaction with DVL (Tamai et al, 2004; Mao et al, 2001; reviewed in He et al, 2004). Polymerization of membrane-associated DVL and GSK3beta- and CSNK1-mediated phosphorylation of LRP5/6 establish a feed-forward mechanism for enhanced membrane recruitment of AXIN upon WNT signaling (Tamai et al, 2004; Con
Last changed: 2015-03-06 18:40:03

FailedReaction: misspliced mutants of LRP5 support enhanced beta-catenin-dependent signaling (Homo sapiens)
Frequent expression of an internally deleted LRP5 has been identified in parathyroid and breast cancers. Expression of the internally deleted LRP5 protein results in elevated levels of the active, unphosphorylated beta-catenin, enhanced expression of the both WNT-dependent reporter genes and the endogenous WNT-target gene MYC, and is required for cellular proliferation (Bjorklund et al, 2007a, b; Bjor
Last changed: 2014-05-22 18:19:05

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