Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Selina Kindelay"'
Autor:
Elliot Imler, Jin Sang Pyon, Selina Kindelay, Meaghan Torvund, Yong-quan Zhang, Sreeganga S Chandra, Konrad E Zinsmaier
Publikováno v:
eLife, Vol 8 (2019)
The autosomal dominant neuronal ceroid lipofuscinoses (NCL) CLN4 is caused by mutations in the synaptic vesicle (SV) protein CSPα. We developed animal models of CLN4 by expressing CLN4 mutant human CSPα (hCSPα) in Drosophila neurons. Similar to pa
Externí odkaz:
https://doaj.org/article/f2b8e28170ce43eca67cf76ac007b248
Autor:
Konrad E. Zinsmaier, Meaghan Torvund, Sreeganga S. Chandra, Selina Kindelay, Jin Sang Pyon, Elliot Imler, Yong-quan Zhang
Publikováno v:
eLife, Vol 8 (2019)
The autosomal dominant neuronal ceroid lipofuscinoses (NCL) CLN4 is caused by mutations in the synaptic vesicle (SV) protein CSPα. We developed animal models of CLN4 by expressing CLN4 mutant human CSPα (hCSPα) in Drosophila neurons. Similar to pa
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::40e6e19e4978c015fd662eecca67baa3
https://doi.org/10.7554/elife.46607
https://doi.org/10.7554/elife.46607
Autor:
Jin Sang Pyon, Sreeganga S. Chandra, Yong-quan Zhang, Konrad E. Zinsmaier, Elliot Imler, Selina Kindelay
The autosomal dominant neuronal ceroid lipofuscinoses (NCL)CLN4is caused by mutations in the synaptic vesicle (SV) protein CSPα, which is a critical co-chaperone of Hsc70 protecting synapses from activity-dependent degeneration. We developed the fir
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ce4026d8c10cb1f777b8f9aaeb36d7dd
Autor:
Elliot, Imler, Jin Sang, Pyon, Selina, Kindelay, Meaghan, Torvund, Yong-Quan, Zhang, Sreeganga S, Chandra, Konrad E, Zinsmaier
Publikováno v:
eLife
Experiments on flies suggest that a gain-of-function mechanism in a protein called CSPɑ contributes to the progressive brain disease CLN4.
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::0a839f8ffc0f24cfa79c22f14f43747f
https://pubmed.ncbi.nlm.nih.gov/31808420
https://pubmed.ncbi.nlm.nih.gov/31808420