Matches in SemOpenAlex for { <https://semopenalex.org/work/W4200392045> ?p ?o ?g. }
Showing items 1 to 80 of
80
with 100 items per page.
- W4200392045 endingPage "222" @default.
- W4200392045 startingPage "211" @default.
- W4200392045 abstract "Background: Neural stem cells (NSC) in divide asymmetrically to generate one cell that retains stem cell identity and another that is routed to differentiation. Prolonged mitotic activity of the NSCs gives rise to the plethora of neurons and glial cells that wire the brain and nerve cord. Genetic insults, such as excess of Notch signaling, perturb the normal NSC proliferation programs and trigger the formation of NSC hyperplasias, which can subsequently progress to malignancies. Hes proteins are crucial mediators of Notch signaling, and in the NSC context they act by repressing a cohort of early pro-differentiation transcription factors. Downregulation of these pro-differentiation factors makes NSC progeny cells susceptible to adopting an aberrant stem cell program. We have recently shown that Hes overexpression in Drosophila leads to NSC hyperplasias that progress to malignant tumours after allografting to adult hosts. Methods: We have combined genetic analysis, tissue allografting and transcriptomic approaches to address the role of Hes genes in NSC malignant transformation. Results: We show that the E (spl) genes are important mediators in the progression of Notch hyperplasias to malignancy, since allografts lacking the E (spl) genes grow much more slowly. We further present RNA profiling of Hes -induced tumours at two different stages after allografting. We find that the same cohort of differentiation-promoting transcription factors that are repressed in the primary hyperplasias continue to be downregulated after transplantation. This is accompanied by an upregulation of stress-response genes and metabolic reprogramming. Conclusions: The combination of dedifferentiation and cell physiology changes most likely drive tumour growth." @default.
- W4200392045 created "2021-12-31" @default.
- W4200392045 creator A5002809671 @default.
- W4200392045 creator A5004685717 @default.
- W4200392045 creator A5008486837 @default.
- W4200392045 creator A5008518267 @default.
- W4200392045 creator A5016553741 @default.
- W4200392045 creator A5048913894 @default.
- W4200392045 creator A5081175102 @default.
- W4200392045 creator A5089552392 @default.
- W4200392045 creator A5090192137 @default.
- W4200392045 date "2022-01-01" @default.
- W4200392045 modified "2023-10-01" @default.
- W4200392045 title "Repression of differentiation genes by Hes transcription factors fuels neural tumour growth in Drosophila" @default.
- W4200392045 doi "https://doi.org/10.1387/ijdb.210187cd" @default.
- W4200392045 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34881794" @default.
- W4200392045 hasPublicationYear "2022" @default.
- W4200392045 type Work @default.
- W4200392045 citedByCount "2" @default.
- W4200392045 countsByYear W42003920452023 @default.
- W4200392045 crossrefType "journal-article" @default.
- W4200392045 hasAuthorship W4200392045A5002809671 @default.
- W4200392045 hasAuthorship W4200392045A5004685717 @default.
- W4200392045 hasAuthorship W4200392045A5008486837 @default.
- W4200392045 hasAuthorship W4200392045A5008518267 @default.
- W4200392045 hasAuthorship W4200392045A5016553741 @default.
- W4200392045 hasAuthorship W4200392045A5048913894 @default.
- W4200392045 hasAuthorship W4200392045A5081175102 @default.
- W4200392045 hasAuthorship W4200392045A5089552392 @default.
- W4200392045 hasAuthorship W4200392045A5090192137 @default.
- W4200392045 hasBestOaLocation W42003920451 @default.
- W4200392045 hasConcept C104317684 @default.
- W4200392045 hasConcept C127561419 @default.
- W4200392045 hasConcept C136834591 @default.
- W4200392045 hasConcept C150194340 @default.
- W4200392045 hasConcept C161879069 @default.
- W4200392045 hasConcept C162317418 @default.
- W4200392045 hasConcept C28328180 @default.
- W4200392045 hasConcept C502942594 @default.
- W4200392045 hasConcept C54355233 @default.
- W4200392045 hasConcept C62478195 @default.
- W4200392045 hasConcept C77255625 @default.
- W4200392045 hasConcept C86339819 @default.
- W4200392045 hasConcept C86803240 @default.
- W4200392045 hasConcept C95444343 @default.
- W4200392045 hasConceptScore W4200392045C104317684 @default.
- W4200392045 hasConceptScore W4200392045C127561419 @default.
- W4200392045 hasConceptScore W4200392045C136834591 @default.
- W4200392045 hasConceptScore W4200392045C150194340 @default.
- W4200392045 hasConceptScore W4200392045C161879069 @default.
- W4200392045 hasConceptScore W4200392045C162317418 @default.
- W4200392045 hasConceptScore W4200392045C28328180 @default.
- W4200392045 hasConceptScore W4200392045C502942594 @default.
- W4200392045 hasConceptScore W4200392045C54355233 @default.
- W4200392045 hasConceptScore W4200392045C62478195 @default.
- W4200392045 hasConceptScore W4200392045C77255625 @default.
- W4200392045 hasConceptScore W4200392045C86339819 @default.
- W4200392045 hasConceptScore W4200392045C86803240 @default.
- W4200392045 hasConceptScore W4200392045C95444343 @default.
- W4200392045 hasIssue "1-2-3" @default.
- W4200392045 hasLocation W42003920451 @default.
- W4200392045 hasLocation W42003920452 @default.
- W4200392045 hasOpenAccess W4200392045 @default.
- W4200392045 hasPrimaryLocation W42003920451 @default.
- W4200392045 hasRelatedWork W1980073120 @default.
- W4200392045 hasRelatedWork W2029071485 @default.
- W4200392045 hasRelatedWork W2098313605 @default.
- W4200392045 hasRelatedWork W2121878535 @default.
- W4200392045 hasRelatedWork W2618432580 @default.
- W4200392045 hasRelatedWork W3105474311 @default.
- W4200392045 hasRelatedWork W3182986720 @default.
- W4200392045 hasRelatedWork W4211264400 @default.
- W4200392045 hasRelatedWork W4294669864 @default.
- W4200392045 hasRelatedWork W4386049819 @default.
- W4200392045 hasVolume "66" @default.
- W4200392045 isParatext "false" @default.
- W4200392045 isRetracted "false" @default.
- W4200392045 workType "article" @default.