Phenotypic drug screen uncovers the metabolic GCH1/BH4 pathway as key regulator of EGFR/KRAS-mediated neuropathic pain and lung cancer.
Journal
Science translational medicine
ISSN: 1946-6242
Titre abrégé: Sci Transl Med
Pays: United States
ID NLM: 101505086
Informations de publication
Date de publication:
31 08 2022
31 08 2022
Historique:
entrez:
31
8
2022
pubmed:
1
9
2022
medline:
9
9
2022
Statut:
ppublish
Résumé
Increased tetrahydrobiopterin (BH4) generated in injured sensory neurons contributes to increased pain sensitivity and its persistence. GTP cyclohydrolase 1 (GCH1) is the rate-limiting enzyme in the de novo BH4 synthetic pathway, and human single-nucleotide polymorphism studies, together with mouse genetic modeling, have demonstrated that decreased GCH1 leads to both reduced BH4 and pain. However, little is known about the regulation of
Identifiants
pubmed: 36044597
doi: 10.1126/scitranslmed.abj1531
pmc: PMC9985140
mid: NIHMS1878035
doi:
Substances chimiques
Analgesics
0
KRAS protein, human
0
Biopterins
0
EGFR protein, human
EC 2.7.10.1
ErbB Receptors
EC 2.7.10.1
GTP Cyclohydrolase
EC 3.5.4.16
Gch1 protein, mouse
EC 3.5.4.16
Proto-Oncogene Proteins p21(ras)
EC 3.6.5.2
sapropterin
EGX657432I
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
eabj1531Subventions
Organisme : British Heart Foundation
ID : CH/16/1/32013
Pays : United Kingdom
Organisme : NINDS NIH HHS
ID : R01 NS112266
Pays : United States
Organisme : NINDS NIH HHS
ID : R35 NS105076
Pays : United States
Organisme : Austrian Science Fund FWF
ID : Z 271
Pays : Austria
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