RIPK3 interactions with MLKL and CaMKII mediate oligodendrocytes death in the developing brain
Published 2017 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
RIPK3 interactions with MLKL and CaMKII mediate oligodendrocytes death in the developing brain
Authors
Keywords
-
Journal
Cell Death & Disease
Volume 8, Issue 2, Pages e2629-e2629
Publisher
Springer Nature
Online
2017-02-23
DOI
10.1038/cddis.2017.54
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- MLKL inhibition attenuates hypoxia-ischemia induced neuronal damage in developing brain
- (2016) Yi Qu et al. EXPERIMENTAL NEUROLOGY
- CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress–induced myocardial necroptosis
- (2016) Ting Zhang et al. NATURE MEDICINE
- Impaired oligodendrocyte maturation in preterm infants: Potential therapeutic targets
- (2016) Erik van Tilborg et al. PROGRESS IN NEUROBIOLOGY
- Brain injury in premature neonates: A primary cerebral dysmaturation disorder?
- (2014) Stephen A. Back et al. ANNALS OF NEUROLOGY
- Distinct roles of RIP1–RIP3 hetero- and RIP3–RIP3 homo-interaction in mediating necroptosis
- (2014) X-N Wu et al. CELL DEATH AND DIFFERENTIATION
- Human oligodendrocytes in remyelination research
- (2014) Marcin Czepiel et al. GLIA
- Mixed Lineage Kinase Domain-like Protein MLKL Causes Necrotic Membrane Disruption upon Phosphorylation by RIP3
- (2014) Huayi Wang et al. MOLECULAR CELL
- Neuroprotective activities of catalpol against CaMKII-dependent apoptosis induced by LPS in PC12 cells
- (2013) Wenna Chen et al. BRITISH JOURNAL OF PHARMACOLOGY
- Plasma membrane translocation of trimerized MLKL protein is required for TNF-induced necroptosis
- (2013) Zhenyu Cai et al. NATURE CELL BIOLOGY
- TNF can activate RIPK3 and cause programmed necrosis in the absence of RIPK1
- (2013) D M Moujalled et al. Cell Death & Disease
- Mixed Lineage Kinase Domain-like Protein Mediates Necrosis Signaling Downstream of RIP3 Kinase
- (2012) Liming Sun et al. CELL
- The Mitochondrial Phosphatase PGAM5 Functions at the Convergence Point of Multiple Necrotic Death Pathways
- (2012) Zhigao Wang et al. CELL
- The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis
- (2012) Jixi Li et al. CELL
- Short term outcomes after extreme preterm birth in England: comparison of two birth cohorts in 1995 and 2006 (the EPICure studies)
- (2012) K. L. Costeloe et al. BMJ-British Medical Journal
- New components of the necroptotic pathway
- (2012) Zhenru Zhou et al. Protein & Cell
- CaMKII in the Cardiovascular System: Sensing Redox States
- (2011) Jeffrey R. Erickson et al. PHYSIOLOGICAL REVIEWS
- Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation
- (2009) YoungSik Cho et al. CELL
- 17β-estradiol protects against hypoxic/ischemic white matter damage in the neonatal rat brain
- (2009) Bettina Gerstner et al. JOURNAL OF NEUROSCIENCE RESEARCH
- RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis
- (2009) D.-W. Zhang et al. SCIENCE
- A Dynamic Pathway for Calcium-Independent Activation of CaMKII by Methionine Oxidation
- (2008) Jeffrey R. Erickson et al. CELL
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExploreBecome a Peeref-certified reviewer
The Peeref Institute provides free reviewer training that teaches the core competencies of the academic peer review process.
Get Started