Zobrazeno 1 - 10
of 32
pro vyhledávání: '"Samuel Sidi"'
Autor:
Peter H. Liu, Samuel Sidi
Publikováno v:
Frontiers in Oncology, Vol 9 (2019)
Antitumor immunity has emerged as a favorable byproduct of radiation therapy (RT), whereby tumor-associated antigens released from irradiated cells unleash innate and adaptive attacks on tumors located both within and outside the radiation field. RT-
Externí odkaz:
https://doaj.org/article/9fa2a59629304891a3673ee844c0aeb8
Autor:
Samuel Sidi, Lisa Bouchier-Hayes
Publikováno v:
Molecular & Cellular Oncology, Vol 4, Iss 5 (2017)
Despite being frequently mutated or deregulated in acute myeloid leukemia (AML) and many other cancers, the mechanisms by which nucleophosmin (NPM1) regulates oncogenesis remain elusive. We found that NPM1 plays a direct and conserved role in DNA dam
Externí odkaz:
https://doaj.org/article/99997e69800f4c1dacd7fa9ad5a9df3b
Publikováno v:
Cells, Vol 8, Iss 9, p 1049 (2019)
Mitosis is controlled by a complex series of signaling pathways but mitotic control following DNA damage remains poorly understood. Effective DNA damage sensing and repair is integral to survival but is largely thought to occur primarily in interphas
Externí odkaz:
https://doaj.org/article/4875816e175547419b81d9b2ac32b648
Autor:
Yuanyuan Li, Richa B. Shah, Samanta Sarti, Alicia L. Belcher, Brian J. Lee, Andrej Gorbatenko, Francesca Nemati, Ian Yu, Zoe Stanley, Zhengping Shao, Jose M. Silva, Shan Zha, Samuel Sidi
Publikováno v:
bioRxiv
Interleukin-1 receptor (IL-1R)-associated kinases (IRAKs) are core effectors of Toll-like receptor (TLR) and IL-1R signaling, with no reported roles outside of innate immunity. We find that vertebrate cells exposed to ionizing radiation (IR) sequenti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::145271a44514f51d38e0476c189df026
https://doi.org/10.1101/2023.02.08.527716
https://doi.org/10.1101/2023.02.08.527716
Autor:
Samuel Sidi, Andrei M. Bussenault, Settara C. Chandrasekharappa, Ramanagouda Ramanagoudr-Bhojappa, Richa B. Shah, Alan D. D'Andrea, Tony T. Huang, Alicia L. Belcher, Anya van Hoogstraten, Aneel K. Aggarwal, Yuanyuan Li, Ivy Mininger, Renuka Raman, Kiyohiro Ando, Jennifer L. Kernan, Ruth Thompson
Publikováno v:
Dev Cell
Cells counter DNA damage through repair or apoptosis, yet a direct mechanism for this choice has remained elusive. When facing interstrand crosslinks (ICLs), the ICL-repair protein FANCI heterodimerizes with FANCD2 to initiate ICL excision. We found
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5c775bac3a9ef9fb1266cbae56b6b96c
https://europepmc.org/articles/PMC8378530/
https://europepmc.org/articles/PMC8378530/
Autor:
Xiao Zhen Zhou, Richard M. White, Ruth Thompson, Peter Man-Un Ung, Samuel Sidi, Peter H. Liu, John V. Heymach, Richa B. Shah, Julio A. Aguirre-Ghiso, Arshi Arora, Shingo Kozono, Yuanyuan Li, Heath D. Skinner, Robert G. Maki, John M. Barbaro, Vincent Brechin, Avner Schlessinger, Kun Ping Lu, Elisa de Stanchina, Andrej Gorbatenko, Jose M. Silva, Katherine S. Panageas, Renuka Raman
Publikováno v:
Nature cell biology
Drug-based strategies to overcome tumour resistance to radiotherapy (R-RT) remain limited by the single-agent toxicity of traditional radiosensitizers (for example, platinums) and a lack of targeted alternatives. In a screen for compounds that restor
Autor:
Evon Poon, Anli Yang, Xiao Zhou, Efrat Resnick, Daniel Zaidman, Roni Oren, Yann Jamin, Shingo Kozono, Colin J. Daniel, Ellen M. Langer, Shijie He, Behnam Nabet, Yu-Hong Chen, Christopher M. Browne, Hyuk-Soo Seo, Louis Chesler, Kun Ping Lu, Benika J. Pinch, Rosalie C. Sears, Shin Kibe, Liat Stoler-Barak, Ziv Shulman, Nir London, Samuel Sidi, Christian Dubiella, Thomas Look, Nicholas E. Vangos, Kazuhiro Koikawa, Xiaolan Lian, Chunhui Wang, Nathaniel Gray, Trevor Manz, Jarrod A. Marto, Richa B. Shah, Ezekiel A. Geffken, Sirano Dhe-Paganon, Scott B. Ficarro
The peptidyl-prolyl cis-trans isomerase, Pin1, acts as a unified signaling hub that is exploited in cancer to activate oncogenes and inactivate tumor suppressors, in particular through up-regulation of c-Myc target genes. However, despite considerabl
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2e3ceb5d0f3a7e590d161df59af1ffd9
https://doi.org/10.1101/2020.03.20.998443
https://doi.org/10.1101/2020.03.20.998443
Autor:
Sirano Dhe-Paganon, Benika J. Pinch, Mark W. Zimmerman, Richa B. Shah, Kun Ping Lu, Jarrod A. Marto, Shuning He, Eriko Koide, Daniel Zaidman, Christopher M. Browne, Ziv Shulman, Barbara Martins da Costa, Christian Dubiella, Evon Poon, Guillaume Adelmant, Nir London, Xiao Zhen Zhou, Chu Wang, Ellen M. Langer, Kazuhiro Koikawa, Theresa D. Manz, Thomas Look, Xiaolan Lian, Hyuk-Soo Seo, Annan Yang, Louis Chesler, Ezekiel A. Geffken, Liat Stoler-Barak, Shin Kibe, Efrat Resnick, Nicholas E. Vangos, Shabnam Sharifzadeh, Shingo Kozono, Colin J. Daniel, Scott B. Ficarro, Roni Oren, Ying Chen, Nathanael S. Gray, Rosalie C. Sears, Samuel Sidi, Adi Rogel, Zainab M. Doctor, Behnam Nabet, Yann Jamin
Publikováno v:
Nat Chem Biol
The peptidyl-prolyl isomerase, Pin1, is exploited in cancer to activate oncogenes and inactivate tumor suppressors. However, despite considerable efforts, Pin1 has remained an elusive drug target. Here, we screened an electrophilic fragment library t
Autor:
Kiyohiro Ando, Sara R. Fassio, Ruth Thompson, Sheré L. Paris, Andrew Oberst, Brittany A. Rohrman, Peter H. Liu, Richa B. Shah, Chloé I. Charendoff, Lisa Bouchier-Hayes, Melissa J. Parsons, Samuel Sidi
Publikováno v:
Journal of Cell Biology. 216:1795-1810
The PIDDosome (PIDD–RAIDD–caspase-2 complex) is considered to be the primary signaling platform for caspase-2 activation in response to genotoxic stress. Yet studies of PIDD-deficient mice show that caspase-2 activation can proceed in the absence
Autor:
Ruth Thompson, Yogesh K. Gupta, Samuel Sidi, Aneel K. Aggarwal, Peter H. Liu, Kiyohiro Ando, Richa B. Shah
Publikováno v:
Molecular Cell. 58(5):767-779
SUMMARY The PIDDosome—PIDD-RAIDD-caspase-2 complex—is a proapoptotic caspase-activation platform of elusive significance. DNA damage can initiate complex assembly via ATM phosphorylation of the PIDD death domain (DD), which enables RAIDD recruitm