Over-expression by degradation rescue of RTKs via cancer-secreted autocrine growth factors:
RTK
UPS
UbE3L
degron
gf
pDegron
paDegron
piDegron
Journal
Frontiers in oncology
ISSN: 2234-943X
Titre abrégé: Front Oncol
Pays: Switzerland
ID NLM: 101568867
Informations de publication
Date de publication:
2023
2023
Historique:
received:
16
08
2023
accepted:
06
09
2023
medline:
12
10
2023
pubmed:
12
10
2023
entrez:
12
10
2023
Statut:
epublish
Résumé
Recently published work provide the first known evidence of a malignancy-associated regulatory mechanism, functionally connecting a phospho-regulated degron domain embedded in a receptor tyrosine kinase (RTK), with its ectopic expression in cancer, conditional to a specific autocrine growth factor signal. Mechanistically, the growth factor-triggered phosphorylation inhibits the degron domain present in the regulated RTK, blocking access to a specific degradation complex. This ultimately rescues the RTK from rapid ubiquitin-proteasome-system-mediated degradation and, most importantly, causes its cellular overexpression. This mechanism, which has been here assigned the new functional name "
Identifiants
pubmed: 37823054
doi: 10.3389/fonc.2023.1278402
pmc: PMC10562641
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1278402Informations de copyright
Copyright © 2023 Scalia and Williams.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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