K
Kathleen M. Sakamoto
Researcher at Stanford University
Publications - 172
Citations - 8851
Kathleen M. Sakamoto is an academic researcher from Stanford University. The author has contributed to research in topics: CREB & Myeloid leukemia. The author has an hindex of 43, co-authored 172 publications receiving 7489 citations. Previous affiliations of Kathleen M. Sakamoto include University of California, Los Angeles & Boston Children's Hospital.
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Journal ArticleDOI
Protacs: chimeric molecules that target proteins to the Skp1-Cullin-F box complex for ubiquitination and degradation.
Kathleen M. Sakamoto,Kyung Bo Kim,Akiko Kumagai,Frank Mercurio,Craig M. Crews,Raymond J. Deshaies +5 more
TL;DR: It is shown that MetAP-2 can be tethered to SCFβ-TRCP, ubiquitinated, and degraded in a Protac-1-dependent manner, which may be useful for conditional inactivation of proteins, and for targeting disease-causing proteins for destruction.
Journal ArticleDOI
The role of the transcription factor CREB in immune function.
TL;DR: Current advances involving CREB in immune function are summarized and phosphorylated CREB has been proposed to directly inhibit NF-κB activation by blocking the binding of CREB binding protein to the NF-σκB complex, thereby limiting proinflammatory responses.
Journal ArticleDOI
Chemical genetic control of protein levels: selective in vivo targeted degradation.
John S. Schneekloth,Fabiana N. Fonseca,Michael A. Koldobskiy,Amit K. Mandal,Raymond J. Deshaies,Kathleen M. Sakamoto,Craig M. Crews +6 more
TL;DR: These are the first in vivo examples of direct small molecule-induced recruitment of target proteins to the proteasome for degradation upon addition to cultured cells and PROTAC-mediated protein degradation offers a general strategy to create "chemical knockouts," thus opening new possibilities for the control of protein function.
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The Role of HDAC6 in Cancer
TL;DR: The role of HDAC6 in the pathogenesis and treatment of cancer is discussed since its upregulation increases cell motility in breast cancer MCF-7 cells and its interaction with cortactin regulates motility.
Journal ArticleDOI
Development of Protacs to Target Cancer-promoting Proteins for Ubiquitination and Degradation
Kathleen M. Sakamoto,Kathleen M. Sakamoto,Kyung Bo Kim,Rati Verma,Andy Ransick,Bernd Stein,Craig M. Crews,Raymond J. Deshaies +7 more
TL;DR: It is shown that an estradiol- based Protac can enforce the ubiquitination and degradation of the α isoform of ER in vitro, and a dihydroxytestosterone-based Protac introduced into cells promotes the rapid disappearance of AR in a proteasome-dependent manner.