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William J. Kaiser

Researcher at University of Texas Health Science Center at San Antonio

Publications -  227
Citations -  25963

William J. Kaiser is an academic researcher from University of Texas Health Science Center at San Antonio. The author has contributed to research in topics: Wireless sensor network & Necroptosis. The author has an hindex of 67, co-authored 224 publications receiving 21404 citations. Previous affiliations of William J. Kaiser include University of Georgia & University of California, Los Angeles.

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Wireless integrated network sensors

TL;DR: The WINS network represents a new monitoring and control capability for applications in such industries as transportation, manufacturing, health care, environmental oversight, and safety and security, and opportunities depend on development of a scalable, low-cost, sensor-network architecture.
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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
Journal Article

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Lorenzo Galluzzi, +168 more
- 01 Jan 2018 - 
TL;DR: An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
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RIP3 mediates the embryonic lethality of caspase-8-deficient mice

TL;DR: It is found that RIP3 is responsible for the mid-gestational death of Casp8-deficient embryos and together completely dispensable for mammalian development.
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Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL

TL;DR: Two small molecule RIP3 kinase inhibitors are described and employ them to demonstrate the common requirement for RIP3 Kinase in programmed necrosis induced by RIP1-RIP3, DAI- RIP3, and TRIF-RIP 3 complexes.