Carolina Gogerty
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Carolina Gogerty has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Bertram L. Jacobs
Arizona State University
1 shared publication - Brian P. Johnson
Biodesign Center for Immunotherapy, Vaccines and Virotherapy, Arizona State University, Tempe, AZ 85281, USA
1 shared publication - Francesco Acciai
College of Health Solutions, Arizona State University, Phoenix, AZ 85004, USA
1 shared publication - Jacqueline Williams
Biodesign Center for Immunotherapy, Vaccines and Virotherapy, Arizona State University, Tempe, AZ 85281, USA
1 shared publication Karen V. Kibler
Biodesign Center for Immunotherapy, Vaccines and Virotherapy, Arizona State University, Tempe, AZ 85281, USA
1 shared publication- Mateusz Szczerba
Biodesign Center for Immunotherapy, Vaccines and Virotherapy, Arizona State University, Tempe, AZ 85281, USA
1 shared publication
Latest Publications
- 14 March 2023
- Published by American Association for the Advancement of Science (AAAS) in Science Signaling
- Vol. 16 (776) , eabq0837
Canonical cellular stress granules are required for arsenite-induced necroptosis mediated by Z-DNA–binding protein 1
Cellular stress granules arise in cells subjected to stress and promote cell survival. A cellular protein that localizes to stress granules is Z-DNA–binding protein 1 (ZBP1), which plays a major role in necroptosis, a programmed cell death pathway mediated by the kinase RIPK3. Here, we showed that the stress granule inducer arsenite activated RIPK3-dependent necroptosis. This pathway required ZBP1, which localized to arsenite-induced stress granules. RIPK3 localized to stress granules in the presence of ZBP1, leading to the formation of ZBP1-RIPK3 necrosomes, phosphorylation of the RIPK3 effector MLKL, and execution of necroptosis. Cells that did not form stress granules did not induce necroptosis in response to arsenite. Together, these results show that arsenite induces ZBP1-mediated necroptosis in a manner dependent on stress granule formation.
- 14 March 2023
- Published by American Association for the Advancement of Science (AAAS) in Science Signaling
- Vol. 16 (776) , eabq0837
Canonical cellular stress granules are required for arsenite-induced necroptosis mediated by Z-DNA–binding protein 1
Cellular stress granules arise in cells subjected to stress and promote cell survival. A cellular protein that localizes to stress granules is Z-DNA–binding protein 1 (ZBP1), which plays a major role in necroptosis, a programmed cell death pathway mediated by the kinase RIPK3. Here, we showed that the stress granule inducer arsenite activated RIPK3-dependent necroptosis. This pathway required ZBP1, which localized to arsenite-induced stress granules. RIPK3 localized to stress granules in the presence of ZBP1, leading to the formation of ZBP1-RIPK3 necrosomes, phosphorylation of the RIPK3 effector MLKL, and execution of necroptosis. Cells that did not form stress granules did not induce necroptosis in response to arsenite. Together, these results show that arsenite induces ZBP1-mediated necroptosis in a manner dependent on stress granule formation.