Transcriptional repressor REST drives lineage stage-specific chromatin compaction at
Adult
Animals
Cell Line, Tumor
Cerebellar Neoplasms
/ genetics
Child
Chromatin
/ genetics
Disease Models, Animal
Female
Gene Expression Regulation, Neoplastic
Hedgehog Proteins
/ genetics
Humans
Infant
Male
Medulloblastoma
/ genetics
Mice, Inbred C57BL
Mice, Inbred NOD
Mice, Knockout
Mice, SCID
Mice, Transgenic
Neoplasm Staging
Patched-1 Receptor
/ genetics
Proto-Oncogene Proteins c-akt
/ genetics
Repressor Proteins
/ genetics
Signal Transduction
/ genetics
Transplantation, Heterologous
Journal
Science signaling
ISSN: 1937-9145
Titre abrégé: Sci Signal
Pays: United States
ID NLM: 101465400
Informations de publication
Date de publication:
22 01 2019
22 01 2019
Historique:
entrez:
24
1
2019
pubmed:
24
1
2019
medline:
17
3
2020
Statut:
epublish
Résumé
In medulloblastomas (MBs), the expression and activity of RE1-silencing transcription factor (REST) is increased in tumors driven by the sonic hedgehog (SHH) pathway, specifically the SHH-α (children 3 to 16 years) and SHH-β (infants) subgroups. Neuronal maturation is greater in SHH-β than SHH-α tumors, but both correlate with poor overall patient survival. We studied the contribution of REST to MB using a transgenic mouse model (
Identifiants
pubmed: 30670636
pii: 12/565/eaan8680
doi: 10.1126/scisignal.aan8680
pmc: PMC8939892
mid: NIHMS1025141
pii:
doi:
Substances chimiques
Chromatin
0
Hedgehog Proteins
0
Patched-1 Receptor
0
RE1-silencing transcription factor
0
Repressor Proteins
0
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
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
Subventions
Organisme : NCI NIH HHS
ID : R01 CA185402
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS079715
Pays : United States
Organisme : NINDS NIH HHS
ID : R03 NS077021
Pays : United States
Informations de copyright
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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