Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Lucas D Serdar"'
Publikováno v:
eLife, Vol 9 (2020)
Recognition and rapid degradation of mRNA harboring premature translation termination codons (PTCs) serves to protect cells from accumulating non-functional and potentially toxic truncated polypeptides. Targeting of PTC-containing transcripts is medi
Externí odkaz:
https://doaj.org/article/fd066d60f8264efaa942bf24035b446d
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-8 (2016)
Nonsense-mediated mRNA decay (NMD) is a quality control pathway that recognizes and degrades transcripts harbouring nonsense mutations. Here the authors show that the ATPase activity of UPF1 mediates functional interactions between the NMD machinery
Externí odkaz:
https://doaj.org/article/6c4b427687ad4141ab4421be6022f015
Publikováno v:
Neuroscience in the 21st Century ISBN: 9781461464341
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71f9920814d9deeae0ac24d657e1a344
https://doi.org/10.1007/978-3-030-88832-9_184
https://doi.org/10.1007/978-3-030-88832-9_184
Publikováno v:
eLife, Vol 9 (2020)
eLife
eLife
Recognition and rapid degradation of mRNA harboring premature translation termination codons (PTCs) serves to protect cells from accumulating non-functional and potentially toxic truncated polypeptides. Targeting of PTC-containing transcripts is medi
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-8 (2016)
Nature Communications
Nature Communications
Nonsense-mediated mRNA decay (NMD) represents a eukaryotic quality control pathway that recognizes and rapidly degrades transcripts harbouring nonsense mutations to limit accumulation of non-functional and potentially toxic truncated polypeptides. A
Publikováno v:
Development
Embryonic interneuron development underlies cortical function and its disruption contributes to neurological disease. Yet the mechanisms by which viable interneurons are produced from progenitors remain poorly understood. Here, we demonstrate dosage-
Publikováno v:
Development.
Embryonic interneuron development underlies cortical function and its disruption contributes to neurological disease. Yet the mechanisms by which viable interneurons are produced from progenitors remain poorly understood. Here, we demonstrate dosage-