Detailed Information

Cited 46 time in webofscience Cited 43 time in scopus
Metadata Downloads

Tdp-43 cryptic exons are highly variable between cell types

Full metadata record
DC Field Value Language
dc.contributor.authorJeong, Yun Ha-
dc.contributor.authorLing, Jonathan P.-
dc.contributor.authorLin, Sophie Z.-
dc.contributor.authorDonde, Aneesh N.-
dc.contributor.authorBraunstein, Kerstin E.-
dc.contributor.authorMajounie, Elisa-
dc.contributor.authorTraynor, Bryan J.-
dc.contributor.authorLaClair, Katherine D.-
dc.contributor.authorLloyd, Thomas E.-
dc.contributor.authorWong, Philip C.-
dc.date.accessioned2023-08-16T09:51:22Z-
dc.date.available2023-08-16T09:51:22Z-
dc.date.created2022-01-13-
dc.date.issued2017-02-
dc.identifier.issn1750-1326-
dc.identifier.urihttp://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/833-
dc.description.abstractBackground: TDP-43 proteinopathy is a prominent pathological feature that occurs in a number of human diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and inclusion body myositis (IBM). Our recent finding that TDP-43 represses nonconserved cryptic exons led us to ask whether cell type-specific cryptic exons could exist to impact unique molecular pathways in brain or muscle. Methods: In the present work, we investigated TDP-43's function in various mouse tissues to model disease pathogenesis. We generated mice to conditionally delete TDP-43 in excitatory neurons or skeletal myocytes and identified the cell type-specific cryptic exons associated with TDP-43 loss of function. Results: Comparative analysis of nonconserved cryptic exons in various mouse cell types revealed that only some cryptic exons were common amongst stem cells, neurons, and myocytes; the majority of these nonconserved cryptic exons were cell type-specific. Conclusions: Our results suggest that in human disease, TDP-43 loss of function may impair cell type-specific pathways.-
dc.language영어-
dc.language.isoen-
dc.publisherBMC-
dc.titleTdp-43 cryptic exons are highly variable between cell types-
dc.typeArticle-
dc.contributor.affiliatedAuthorJeong, Yun Ha-
dc.identifier.doi10.1186/s13024-016-0144-x-
dc.identifier.scopusid2-s2.0-85011304395-
dc.identifier.wosid000396291900001-
dc.identifier.bibliographicCitationMOLECULAR NEURODEGENERATION, v.12-
dc.relation.isPartOfMOLECULAR NEURODEGENERATION-
dc.citation.titleMOLECULAR NEURODEGENERATION-
dc.citation.volume12-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.subject.keywordPlusAMYOTROPHIC-LATERAL-SCLEROSIS-
dc.subject.keywordPlusFRONTOTEMPORAL LOBAR DEGENERATION-
dc.subject.keywordPlusINCLUSION-BODY MYOSITIS-
dc.subject.keywordPlusHEXANUCLEOTIDE REPEAT-
dc.subject.keywordPlusALZHEIMERS-DISEASE-
dc.subject.keywordPlusALS-FTD-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusRNA-
dc.subject.keywordPlusDEPLETION-
dc.subject.keywordPlusDEMENTIA-
dc.subject.keywordAuthorTDP-43-Nonconserved cryptic exons-
dc.subject.keywordAuthorBioinformatics-
dc.subject.keywordAuthorAmyotrophic lateral sclerosis-
dc.subject.keywordAuthorFrontotemporal dementia-
dc.subject.keywordAuthorInclusion body myositis-
Files in This Item
There are no files associated with this item.
Appears in
Collections
연구본부 > 퇴행성 뇌질환 연구그룹 > 1. Journal Articles

qrcode

Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.

Related Researcher

Researcher Jeong, Yun Ha photo

Jeong, Yun Ha
연구본부 (퇴행성뇌질환 연구그룹)
Read more

Altmetrics

Total Views & Downloads

BROWSE