Renal expression of JAK2 is high in polycystic kidney disease and its inhibition reduces cystogenesis.
Animals
Cell Line
Cell Proliferation
Curcumin
/ pharmacology
Disease Models, Animal
Epithelial Cells
/ cytology
Humans
Janus Kinase 2
/ metabolism
Kidney
/ metabolism
Mice
Phosphorylation
/ drug effects
Piperidines
/ pharmacology
Polycystic Kidney, Autosomal Dominant
/ genetics
Pyrimidines
/ pharmacology
Pyrroles
/ pharmacology
TRPP Cation Channels
/ genetics
Up-Regulation
/ drug effects
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
14 03 2019
14 03 2019
Historique:
received:
05
09
2018
accepted:
28
02
2019
entrez:
16
3
2019
pubmed:
16
3
2019
medline:
6
10
2020
Statut:
epublish
Résumé
Autosomal dominant polycystic kidney disease (ADPKD) is the most common renal genetic disorder, however it still lacks a cure. The discovery of new therapies heavily depends on understanding key signalling pathways that lead to ADPKD. The JAnus Kinase and Signal Transducers and Activators of Transcription (JAK/STAT) pathway is aberrantly activated and contributes to ADPKD pathogenesis via enhancing epithelial proliferation. Yet the mechanisms underlying the upregulation of JAK/STAT activity in this disease context is completely unknown. Here, we investigate the role of JAK2 in ADPKD using a murine model of ADPKD (Pkd1
Identifiants
pubmed: 30872773
doi: 10.1038/s41598-019-41106-3
pii: 10.1038/s41598-019-41106-3
pmc: PMC6418191
doi:
Substances chimiques
Piperidines
0
Pyrimidines
0
Pyrroles
0
TRPP Cation Channels
0
polycystic kidney disease 1 protein
0
tofacitinib
87LA6FU830
JAK2 protein, human
EC 2.7.10.2
Janus Kinase 2
EC 2.7.10.2
Curcumin
IT942ZTH98
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
4491Références
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