About: Beta-Catenin Accumulation Pathway

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About: Beta-Catenin Accumulation Pathway Goto Sponge NotDistinct Permalink

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Attributes	Values
rdf:type	Class
rdfs:label	Beta-Catenin Accumulation Pathway
rdfs:subClassOf	Signaling Pathway
Semantic_Type	Functional Concept
Preferred_Name	Beta-Catenin Accumulation Pathway
UMLS_CUI	C1511110
BioCarta_ID	h_gsk3Pathway
ALT_DEFINITION	Lipopolysaccharide (LPS) from XX bacteria induces a wide range of inflammatory responses, including the response of alveolar macrophages to bacteria in the lungs. CD14 and the Toll-like receptor TLR4 are activated by LPS, initiating a signaling cascade that activates PI3 kinase and increases synthesis of the inositol phosphate PIP3. PIP3 activates the inositol phosphate dependent protein kinase PDK1, which activates AKT (protein kinase B). One of the key actions of AKT is to block apoptosis. AKT phosphorylation of NF-kB promotes the survival and activation of macrophages responding to LPS. Another substrate of AKT is the protein kinase Gsk3-beta. AKT phosphorylates and deactivates Gsk3-beta. Non-phosphorylated Gsk3-beta is active and phosphorylates beta-catenin, leading to its degradation in the ubiquitin dependent proteasome pathway. Stimulation by LPS causes the accumulation of beta-catenin in the nucleus and the activation of genes in concert with the transcription factor LEF1. This pathway is probably not restricted to alveolar pathway, but leads to the activation of beta-catenin dependent genes by LPS in other cells as well. Other pathways regulate this pathway also, such as the modulation of PI3 kinase activity by ceramide and the inhibition of Gsk3-beta activity by the Wnt/frizzled/disheveled (DSH) pathway.BIOCARTA
Legacy_Concept_Name	Beta-Catenin_Accumulation_Pathway
FULL_SYN	Beta-Catenin Accumulation PathwayPTNCI Inactivation of Gsk3 by AKT causes accumulation of b-catenin in Alveolar MacrophagesPTBIOCARTA
code	C39098
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