Zobrazeno 1 - 10
of 22
pro vyhledávání: '"Jonathan M Goodwin"'
Autor:
Marek J Kobylarz, Jonathan M Goodwin, Zhao B Kang, John W Annand, Sarah Hevi, Ellen O'Mahony, Gregory McAllister, John Reece-Hoyes, Qiong Wang, John Alford, Carsten Russ, Alicia Lindeman, Martin Beibel, Guglielmo Roma, Walter Carbone, Judith Knehr, Joseph Loureiro, Christophe Antczak, Dmitri Wiederschain, Leon O Murphy, Suchithra Menon, Beat Nyfeler
Publikováno v:
PLoS ONE, Vol 15, Iss 8, p e0235551 (2020)
VPS34 is a key regulator of endomembrane dynamics and cargo trafficking, and is essential in cultured cell lines and in mice. To better characterize the role of VPS34 in cell growth, we performed unbiased cell line profiling studies with the selectiv
Externí odkaz:
https://doaj.org/article/405ec165a99f440886a38bc379ff0399
Autor:
Kirsty M. Hooper, Elise Jacquin, Taoyingnan Li, Jonathan M. Goodwin, John H. Brumell, Joanne Durgan, Oliver Florey
Publikováno v:
Journal of Cell Biology. 221
Non-canonical autophagy is a key cellular pathway in immunity, cancer, and neurodegeneration, characterized by conjugation of ATG8 to endolysosomal single membranes (CASM). CASM is activated by engulfment (endocytosis, phagocytosis), agonists (STING,
Autor:
Jennifer Cable, Eilika Weber‐Ban, Tim Clausen, Kylie J. Walters, Michal Sharon, Daniel J. Finley, Yangnan Gu, John Hanna, Yue Feng, Sascha Martens, Anne Simonsen, Malene Hansen, Hong Zhang, Jonathan M. Goodwin, Alessio Reggio, Chunmei Chang, Liang Ge, Brenda A. Schulman, Raymond J. Deshaies, Ivan Dikic, J. Wade Harper, Ingrid E. Wertz, Nicolas H. Thomä, Mikołaj Słabicki, Judith Frydman, Ursula Jakob, Della C. David, Eric J. Bennett, Carolyn R. Bertozzi, Richa Sardana, Vinay V. Eapen, Serena Carra
Publikováno v:
Annals of the New York Academy of Sciences 1510(1), 79-99 (2022). doi:10.1111/nyas.14745
Targeted protein degradation is critical for proper cellular function and development. Protein degradation pathways, such as the ubiquitin proteasomes system, autophagy, and endosome-lysosome pathway, must be tightly regulated to ensure proper elimin
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::88110e83b56645cb723743deb2706a33
Autor:
Daniel Baird, John H. Brumell, Kirsty Hooper, Leon Murphy, Jonathan M. Goodwin, Jeff Saunders, Sreekanth R. Rouduri, Sravya Kommineni, Archana Jha, Aylwin Ng, Oliver Florey, Menghao Wei, Taoyingnan Li, Mark R. Chance, Ward G. Walkup, Timothy Lehmberg, Sagar R. Budhe, Qing Tang, Jorge Garcia-Fortanet, Yaya Fan, Asmita Agrawal, Katherine Fletcher, Brent A. Appleton, Andrea Ballabio, Chieko Kishi-Itakura, Janna Kiselar
Publikováno v:
Science Advances. 7
Adaptive changes in lysosomal capacity are driven by the transcription factors TFEB and TFE3 in response to increased autophagic flux and endolysosomal stress, yet the molecular details of their activation are unclear. LC3 and GABARAP members of the
Autor:
Oliver Florey, Jonathan M. Goodwin, Elise Jacquin, John H. Brumell, Taoyingnan Li, Joanne Durgan, Kirsty Hooper
Non-canonical autophagy is a key cellular pathway in immunity, cancer and neurodegeneration, characterised by Conjugation of ATG8 to endolysosomal Single-Membranes (CASM). CASM is activated by engulfment (endocytosis, phagocytosis), agonists (STING,
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::8a4ff1d215b4b2102cc66c2f2c5a0d95
https://doi.org/10.1101/2021.05.20.444917
https://doi.org/10.1101/2021.05.20.444917
Autor:
Sagar R. Budhe, Qing Tang, Timothy Lehmberg, Andrea Ballabio, Katherine Fletcher, Menghao Wei, Asmita Agrawal, Daniel Baird, Sreekanth R. Rouduri, Ward G. Walkup, Oliver Florey, Archana Jha, John H. Brumell, Jorge Garcia-Fortanet, Leon Murphy, Sravya Kommineni, Kirsty Hooper, Jonathan M. Goodwin, Chieko Kishi-Itakura, Brent A. Appleton, Yaya Fan, Aylwin Ng, Janna Kiselar, Jeffrey J. Saunders, Mark R. Chance, Taoyingnan Li
Adaptive changes in lysosomal capacity are driven by the transcription factors TFEB and TFE3 in response to increased autophagic flux and endolysosomal stress, yet the molecular details of their activation are unclear. LC3 and GABARAP members of the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::539ee4ceb1fc409289003ea1203b8149
https://doi.org/10.1101/2021.02.22.432209
https://doi.org/10.1101/2021.02.22.432209
Autor:
Marek J. Kobylarz, Leon Murphy, William E. Dowdle, Rowena DeJesus, Jonathan M. Goodwin, Alicia Lindeman, Beat Nyfeler, Gregory McAllister, Zuncai Wang, Gregory R. Hoffman, Ramnik J. Xavier, Philip Bergman
Publikováno v:
Cell Reports, Vol 20, Iss 10, Pp 2341-2356 (2017)
Iron is vital for many homeostatic processes and its liberation from ferritin nanocages occurs in the lysosome. Studies indicate that ferritin and its binding partner nuclear receptor coactivator-4 (NCOA4) are targeted to lysosomes by a form of selec
Autor:
Leon Murphy, Zhao Kang, Zinger Yang, Debora Bonenfant, Isabelle Claerr, Rowena DeJesus, Carsten Russ, Matthias Mueller, Damien Begue, John S. Reece-Hoyes, Christophe Antczak, Alexandra Graff, Christel Genoud, Beat Nyfeler, Jonathan M. Goodwin, Phil Bergman, Gregory R. Hoffman, Stacie Dodgson, Ramnik J. Xavier, David Marcellin, Francesca Moretti
Publikováno v:
EMBO reports. 19(9)
Autophagy maintains cellular homeostasis by targeting damaged organelles, pathogens, or misfolded protein aggregates for lysosomal degradation. The autophagic process is initiated by the formation of autophagosomes, which can selectively enclose carg
Autor:
Robert U. Svensson, Monte M. Winslow, Jonathan M. Goodwin, Reuben J. Shaw, Hua Jane Lou, Benjamin E. Turk
Publikováno v:
Molecular Cell. 55:436-450
The serine/threonine kinase LKB1 is a tumor suppressor whose loss is associated with increased metastatic potential. In an effort to define biochemical signatures of metastasis associated with LKB1 loss, we discovered that the epithelial-to-mesenchym
Autor:
Jonathan M. Goodwin, Leon Murphy
Publikováno v:
Nature Chemical Biology. 11:758-760
A new small-molecule inhibitor of the autophagy-initiating kinase ULK1 serves to block a critical survival mechanism activated upon inhibition of mTORC1, potentially enhancing treatment efficacy for mTOR inhibitors currently in clinical trials for ca