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APC truncation mutants are not K63 polyubiquitinated
Stable Identifier
R-HSA-5246696
Type
Reaction [transition]
Species
Homo sapiens
Compartment
cytosol
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)
APC truncation mutants are not K63 polyubiquitinated (Homo sapiens)
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APC is K63 polyubiquitinated in the absence of WNT signal and this modification correlates with AXIN binding. Depletion of AXIN or beta-catenin by RNAi abrogates APC polyubiquitination, as does inhibition of GSK3 kinase activity, suggesting that polyubiquitination depends on the assembly of a functional destruction complex. WNT3A pathway activation promotes a loss of APC-AXIN interaction concurrent with loss of APC polyubiquitination (Tran and Polakis, 2012).
Polyubiquitination of APC is lost in a number of human cancer cell lines that express truncated forms of APC and which show hyperactivation of the WNT signaling pathway (Tran and Polakis, 2012). The loss of APC polyubiquitination in these lines may reflect the fact that the APC mutants are compromised in their ability to interact with AXIN due to truncation/loss of the AXIN-binding SAMP repeats (Spink et al, 2000); alternately, the truncations may remove as-yet unidentified polyubiquitination sites. APC polyubiquitination is also lost in cancer lines carrying mutations in AXIN that disrupt interaction with GSK3 as well as in cell lines with phosphodegron mutations of beta-catenin (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
Input
APC polyubiquitination mutants [cytosol]
(Homo sapiens)
Participates
as an event of
APC truncation mutants are not K63 polyubiquitinated (Homo sapiens)
Normal reaction
APC is K63-polyubiquitinated
(Homo sapiens)
Functional status
Loss of function of APC polyubiquitination mutants [cytosol]
Normal Entity
APC [cytosol]
(Homo sapiens)
Disease Entity
APC [cytosol]
(Homo sapiens)
Status
loss of function
via
stop gained
Disease
Name
Identifier
Synonyms
colorectal cancer
DOID:9256
Authored
Rothfels, K (2014-01-17)
Reviewed
Salahshor, S (2014-05-12)
Woodgett, J (2014-05-22)
Created
Rothfels, K (2014-01-23)
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