Matches in SemOpenAlex for { <https://semopenalex.org/work/W2742141569> ?p ?o ?g. }
Showing items 1 to 55 of
55
with 100 items per page.
- W2742141569 abstract "To date, 31 genes associated with different forms of SCA have been identified, but the cellular and molecular bases for this pathology remain poorly defined. The autosomal dominant cerebellar ataxias (ADCA) were thought to be exclusively due to expansions of coding CAG repeats, as in the genes that underlie SCA1, SCA2, SCA3, SCA6, SCA7, SCA17, and DRPLA (dentatorubropallidoluysian atrophy)—the so-called polyglutamine expansion SCAs. About 90 % of genetically diagnosed ADCA is attributed to polyglutamine expansion SCAs [1]. However, mutations in two different kinase coding genes have been discovered in ADCA families: tau-tubulin-kinase 2 (TTBK2) in SCA11 and protein kinase c gamma (PKCγ) in SCA14. The roles of these two kinases are essential for post-translational modifications controlling neuronal degeneration or functional maintenance and, very interestingly, these kinases or their isoforms share common signaling pathways with another SCAs or neurodegenerative diseases. In this short communication, I introduce these two interesting ADAC causative kinases, their molecular signaling pathways leading to degeneration, and our published data on the topics." @default.
- W2742141569 created "2017-08-08" @default.
- W2742141569 creator A5023284749 @default.
- W2742141569 date "2013-01-01" @default.
- W2742141569 modified "2023-09-27" @default.
- W2742141569 title "Kinase Mutations in Dominant Form of Spinocerebellar Ataxia" @default.
- W2742141569 cites W2006467843 @default.
- W2742141569 cites W2118029450 @default.
- W2742141569 cites W2118994475 @default.
- W2742141569 cites W2164405838 @default.
- W2742141569 hasPublicationYear "2013" @default.
- W2742141569 type Work @default.
- W2742141569 sameAs 2742141569 @default.
- W2742141569 citedByCount "0" @default.
- W2742141569 crossrefType "journal-article" @default.
- W2742141569 hasAuthorship W2742141569A5023284749 @default.
- W2742141569 hasConcept C104317684 @default.
- W2742141569 hasConcept C184235292 @default.
- W2742141569 hasConcept C2779500118 @default.
- W2742141569 hasConcept C54355233 @default.
- W2742141569 hasConcept C86803240 @default.
- W2742141569 hasConcept C95444343 @default.
- W2742141569 hasConceptScore W2742141569C104317684 @default.
- W2742141569 hasConceptScore W2742141569C184235292 @default.
- W2742141569 hasConceptScore W2742141569C2779500118 @default.
- W2742141569 hasConceptScore W2742141569C54355233 @default.
- W2742141569 hasConceptScore W2742141569C86803240 @default.
- W2742141569 hasConceptScore W2742141569C95444343 @default.
- W2742141569 hasLocation W27421415691 @default.
- W2742141569 hasOpenAccess W2742141569 @default.
- W2742141569 hasPrimaryLocation W27421415691 @default.
- W2742141569 hasRelatedWork W1970549467 @default.
- W2742141569 hasRelatedWork W1991163497 @default.
- W2742141569 hasRelatedWork W2026025236 @default.
- W2742141569 hasRelatedWork W2053163907 @default.
- W2742141569 hasRelatedWork W2067007520 @default.
- W2742141569 hasRelatedWork W2099343116 @default.
- W2742141569 hasRelatedWork W2124622589 @default.
- W2742141569 hasRelatedWork W2128341112 @default.
- W2742141569 hasRelatedWork W2158945609 @default.
- W2742141569 hasRelatedWork W2329652948 @default.
- W2742141569 hasRelatedWork W2412002900 @default.
- W2742141569 hasRelatedWork W2501184098 @default.
- W2742141569 hasRelatedWork W2515700719 @default.
- W2742141569 hasRelatedWork W2626182344 @default.
- W2742141569 hasRelatedWork W2791710742 @default.
- W2742141569 hasRelatedWork W2890003677 @default.
- W2742141569 hasRelatedWork W2921746639 @default.
- W2742141569 hasRelatedWork W3034856796 @default.
- W2742141569 hasRelatedWork W3154919931 @default.
- W2742141569 hasRelatedWork W2009939983 @default.
- W2742141569 isParatext "false" @default.
- W2742141569 isRetracted "false" @default.
- W2742141569 magId "2742141569" @default.
- W2742141569 workType "article" @default.