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APC truncation mutants are not K63 polyubiquitinated
Stable Identifier
R-HSA-5467333
Type
Pathway
Species
Homo sapiens
ReviewStatus
5/5
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Disease (Homo sapiens)
Diseases of signal transduction by growth factor receptors and second messengers (Homo sapiens)
Signaling by WNT in cancer (Homo sapiens)
Signaling by APC mutants (Homo sapiens)
APC truncation mutants are not K63 polyubiquitinated (Homo sapiens)
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APC has been shown to be reversibly modified with K63-linked polyubiquitin chains. This modification is required for the assembly of the destruction complex and subsequent degradation of beta-catenin in the absence of WNT ligand. K63-polyubiquitination of APC is lacking in a number of colorectal cancer cell lines expressing truncated forms of APC, and these lines have aberrantly high beta-catenin levels and WNT pathway activation (Tran and Polakis, 2012).
Literature References
PubMed ID
Title
Journal
Year
22761442
Reversible modification of adenomatous polyposis coli (APC) with K63-linked polyubiquitin regulates the assembly and activity of the ?-catenin destruction complex
Polakis, P
,
Tran, H
J. Biol. Chem.
2012
Participants
Events
APC truncation mutants are not K63 polyubiquitinated
(Homo sapiens)
Participates
as an event of
Signaling by APC mutants (Homo sapiens)
Disease
Name
Identifier
Synonyms
cancer
DOID:162
malignant tumor, malignant neoplasm, primary cancer
Cross References
BioModels Database
BIOMD0000000656
,
BIOMD0000000655
,
BIOMD0000000648
,
BIOMD0000000657
,
BIOMD0000000652
,
BIOMD0000000654
,
BIOMD0000000653
Authored
Rothfels, K (2014-01-17)
Reviewed
Salahshor, S (2014-05-12)
Woodgett, J (2014-05-22)
Created
Rothfels, K (2014-05-16)
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