Zobrazeno 1 - 4
of 4
pro vyhledávání: '"Anthony S. Valente"'
Autor:
David A. Guertin, Judit Villén, Robert T. Lawrence, Anthony S. Valente, Camila Martinez Calejman, Samuel W. Entwisle, Chien-Min Hung
Publikováno v:
Mol Cell Proteomics
Stimulating brown adipose tissue (BAT) activity represents a promising therapy for overcoming metabolic diseases. mTORC2 is important for regulating BAT metabolism, but its downstream targets have not been fully characterized. In this study, we apply
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5b3fe186068dc471352cabb1d3b3eafc
https://pubmed.ncbi.nlm.nih.gov/32234964
https://pubmed.ncbi.nlm.nih.gov/32234964
Publikováno v:
Plant Gene. 15:37-43
In Arabidopsis thaliana, chromosomal rearrangements are commonly associated with compound T-DNA insertions due to endogenous double-stranded break and repair mechanisms. During the production of a double homozygous mutant for the CCCH zinc finger pro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8874911b34e96c50eeb55ce07eafcb55
https://doi.org/10.1016/j.plgene.2018.06.001
https://doi.org/10.1016/j.plgene.2018.06.001
Autor:
Anthony S. Valente, Takashi K. Ito, Matt Kaeberlein, Heather Z. Huang, Anthony S. Grillo, Judit Villén, Dayae Kim, Jeehae Han, Samuel W. Entwisle, Masanao Yajima, Miguel Martin-Perez
Publikováno v:
Nature metabolism
Leigh syndrome is a fatal neurometabolic disorder caused by defects in mitochondrial function. mTOR inhibition with rapamycin attenuates disease progression in a mouse model of Leigh syndrome (Ndufs4 KO mouse); however, the mechanism of rescue is unk
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9b9d40edb6acbc1a601d99c9adc06288
https://pubmed.ncbi.nlm.nih.gov/33324011
https://pubmed.ncbi.nlm.nih.gov/33324011
Autor:
Jeehae Han, Dayae Kim, Samuel W. Entwisle, Heather Z. Huang, Anthony S. Grillo, Anthony S. Valente, Judit Villén, Matt Kaeberlein, Takashi K. Ito, Masanao Yajima, Miguel Martin-Perez
Leigh syndrome is a fatal neurometabolic disorder caused by defects in mitochondrial function. mTOR inhibition with rapamycin attenuates disease progression in a mouse model of Leigh syndrome (Ndufs4 KO mouse); however, the mechanism of rescue is unk
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::84280ca903e8c9f24c5ba5124e71a3a4
https://doi.org/10.1101/562207
https://doi.org/10.1101/562207
