BCL-2 family protein BOK is a positive regulator of uridine metabolism in mammals.
Animals
Apoptosis
/ drug effects
Biomarkers, Tumor
/ metabolism
Cell Proliferation
/ drug effects
DNA Damage
Drug Resistance, Neoplasm
/ drug effects
Fluorouracil
/ pharmacology
Mammals
Mice
Multienzyme Complexes
/ metabolism
Orotate Phosphoribosyltransferase
/ metabolism
Orotidine-5'-Phosphate Decarboxylase
/ metabolism
Protein Binding
/ drug effects
Protein Domains
Proto-Oncogene Proteins c-bcl-2
/ chemistry
Tumor Suppressor Protein p53
/ metabolism
Uridine
/ metabolism
Bok
UMPS
apoptosis
chemoresistance
metabolism
Journal
Proceedings of the National Academy of Sciences of the United States of America
ISSN: 1091-6490
Titre abrégé: Proc Natl Acad Sci U S A
Pays: United States
ID NLM: 7505876
Informations de publication
Date de publication:
30 07 2019
30 07 2019
Historique:
pubmed:
18
7
2019
medline:
31
3
2020
entrez:
18
7
2019
Statut:
ppublish
Résumé
BCL-2 family proteins regulate the mitochondrial apoptotic pathway. BOK, a multidomain BCL-2 family protein, is generally believed to be an adaptor protein similar to BAK and BAX, regulating the mitochondrial permeability transition during apoptosis. Here we report that BOK is a positive regulator of a key enzyme involved in uridine biosynthesis; namely, uridine monophosphate synthetase (UMPS). Our data suggest that BOK expression enhances UMPS activity, cell proliferation, and chemosensitivity. Genetic deletion of
Identifiants
pubmed: 31311867
pii: 1904523116
doi: 10.1073/pnas.1904523116
pmc: PMC6681708
doi:
Substances chimiques
Biomarkers, Tumor
0
Bok protein, mouse
0
Multienzyme Complexes
0
Proto-Oncogene Proteins c-bcl-2
0
Tumor Suppressor Protein p53
0
uridine 5'-monophosphate synthase
74870-74-9
Orotate Phosphoribosyltransferase
EC 2.4.2.10
Orotidine-5'-Phosphate Decarboxylase
EC 4.1.1.23
Fluorouracil
U3P01618RT
Uridine
WHI7HQ7H85
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
15469-15474Informations de copyright
Copyright © 2019 the Author(s). Published by PNAS.
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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