S
Samuel W. Entwisle
Researcher at University of Washington
Publications - 9
Citations - 632
Samuel W. Entwisle is an academic researcher from University of Washington. The author has contributed to research in topics: PI3K/AKT/mTOR pathway & Phosphorylation. The author has an hindex of 5, co-authored 9 publications receiving 440 citations. Previous affiliations of Samuel W. Entwisle include Harvard University.
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Journal ArticleDOI
A comparison of non-integrating reprogramming methods.
Thorsten M. Schlaeger,Laurence Daheron,Thomas Brickler,Samuel W. Entwisle,Karrie Chan,Amelia Cianci,Alex Devine,Andrew Ettenger,Kelly Fitzgerald,Michelle Godfrey,Dipti Gupta,Jade McPherson,Prerana Malwadkar,Manav Gupta,Blair Bell,Akiko Doi,Namyoung Jung,Xin Li,Maureen M. Lynes,Emily Brookes,Anne Cherry,Didem Demirbas,Alexander M. Tsankov,Leonard I. Zon,Lee L. Rubin,Andrew P. Feinberg,Alexander Meissner,Chad A. Cowan,George Q. Daley +28 more
TL;DR: Comparing Sendai-viral (SeV), episomal (Epi) and mRNA transfection mRNA methods for generating integration-free hiPSCs provides a valuable resource to inform the use of specific reprogramming methods for different laboratories and different applications, including clinical translation.
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mTORC2-AKT signaling to ATP-citrate lyase drives brown adipogenesis and de novo lipogenesis.
C. Martinez Calejman,Sophie Trefely,Sophie Trefely,Samuel W. Entwisle,Amelia K. Luciano,Su Myung Jung,Wen-Yu Hsiao,AnnMarie Torres,Chien-Min Hung,Huawei Li,Nathaniel W. Snyder,Judit Villén,Kathryn E. Wellen,David A. Guertin +13 more
TL;DR: It is reported that a mTORC2-Akt axis specifically activates ACLY to promote lipid synthesis and histone acetylation during brown adipocyte differentiation.
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Decoding Post-Translational Modification Crosstalk With Proteomics.
TL;DR: In this paper, the authors provide an overview of the basic modes of PTM crosstalk, the proteomic methods to elucidate PTM co-stalk and approaches that can inform about the functional consequences.
Journal ArticleDOI
PKC downregulation upon rapamycin treatment attenuates mitochondrial disease
Miguel Martin-Perez,Anthony S. Grillo,Takashi K. Ito,Anthony S. Valente,Jeehae Han,Samuel W. Entwisle,Samuel W. Entwisle,Heather Z. Huang,Dayae Kim,Masanao Yajima,Matt Kaeberlein,Judit Villén +11 more
TL;DR: It is found that rapamycin restores mitochondrial protein levels, inhibits signaling through both mTOR complexes, and reduces the abundance and activity of multiple protein kinase C (PKC) isoforms, and PKC may be a viable therapeutic target for treating severe mitochondrial disease.
Journal ArticleDOI
The phosphatidic acid-binding, polybasic domain is responsible for the differences in the phosphoregulation of lipins 1 and 3.
Salome Boroda,Sankeerth Takkellapati,Robert T. Lawrence,Samuel W. Entwisle,Jennifer M. Pearson,Mitchell E. Granade,Garrett R. Mullins,James M. Eaton,Judit Villén,Thurl E. Harris +9 more
TL;DR: It is shown that phosphorylation does not affect the catalytic activity of lipin 3 or its ability to associate with PA in vitro or a mechanism for the observed differences in lipin phosphoregulation in vitro is indicated.