Reactome: A Curated Pathway Database
Results 1 to 10 of 140
Pathways (44) Reactions (47) Proteins (2) Others (47)
Protein: UniProt:P35222 CTNNB1 (Homo sapiens)
Last changed: 2014-11-26 10:20:21

Pathway: Developmental Biology (Homo sapiens)
As a first step towards capturing the array of processes by which a fertilized egg gives rise to the diverse tissues of the body, examples of three kinds of processes have been annotated. These are aspects of the roles of cell adhesion molecules in axonal guidance and myogenesis, of transcriptional regulation in hematopoiesis (specifically, B lymphopoiesis), pancreatic beta cell and whit
Last changed: 2014-11-21 19:49:01

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: 2014-11-21 19:49:01

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: 2014-11-21 19:49:01

Pathway: Programmed Cell Death (Homo sapiens)
Cell death is a fundamental cellular response that has a crucial role in shaping our bodies during development and in regulating tissue homeostasis by eliminating unwanted cells. There are a number of different forms of cell death, each with a corresponding number of complex subprocesses. The first form of regulated or programmed cell death to be characterized was apoptosis. Evidence has emerged for a
Last changed: 2014-11-21 19:49:01

Pathway: Immune System (Homo sapiens)
Humans are exposed to millions of potential pathogens daily, through contact, ingestion, and inhalation. Our ability to avoid infection depends on the adaptive immune system and during the first critical hours and days of exposure to a new pathogen, our innate immune system
Last changed: 2014-11-21 19:49:01

Pathway: RNF mutants show enhanced WNT signaling and proliferation (Homo sapiens)
RNF43 and related protein ZNRF3 are E3 ubiquitin ligases that negatively regulate WNT signaling by downregulating FZD receptors at the cell surface (Mukai et al, 2010; Hao et al, 2012). Frameshift loss-of-function mutations in RNF43 that enhance WNT signaling have been identified in pancreatic and colorectal cancers; the proliferation of these cells is dependent on the presence of secreted WNT, as the
Last changed: 2014-11-21 14:40:22

Pathway: S33 mutants of beta-catenin aren't phosphorylated (Homo sapiens)
S33 mutations of beta-catenin interfere with GSK3 phosphorylation and result in stabilization and nuclear localization of the protein and enhanced WNT signaling (Groen et al, 2008; Nhieu et al, 1999; Clements et al, 2002; reviewed in Polakis, 2000). S33 mutations have been identified in cancers of the central nervous system, liver, endometrium and stomach, among others (reviewed in Polakis, 2000)
Last changed: 2014-11-21 14:40:22

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: 2014-11-21 14:40:22

Pathway: XAV939 inhibits tankyrase, stabilizing AXIN (Homo sapiens)
XAV939 binds to the catalytic sites of tankyrase 1 and 2 and inhibits the ADP-ribosylation of AXIN1 and 2. Treatment of cells with XAV939 significantly increases the protein, but not the mRNA levels of AXIN1 and 2 and supports a strong increase in the level of GSK3beta-AXIN complexes. These cells also show increased phosphorylation of beta-catenin, decreased beta-catenin protein levels and a correspon
Last changed: 2014-11-21 14:40:22

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