NDLI: CD59 signaling and membrane pores drive Syk-dependent erythrocyte necroptosis.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	LaRocca, T. J. Stivison, E. A. Mal-Sarkar, T. Hooven, T. A. Hod, E. A. Spitalnik, S. L. Ratner, A. J.
Description	Country affiliation: United States Author Affiliation: LaRocca TJ ( Department of Pediatrics, Columbia University, New York, NY, USA.); Stivison EA ( Institute of Human Nutrition, Columbia University, New York, NY, USA.); Mal-Sarkar T ( Department of Pediatrics, Columbia University, New York, NY, USA.); Hooven TA ( Department of Pediatrics, Columbia University, New York, NY, USA.); Hod EA ( Department of Pathology and Cell Biology, Columbia University, New York, NY, USA.); Spitalnik SL ( Department of Pathology and Cell Biology, Columbia University, New York, NY, USA.); Ratner AJ ( Department of Pediatrics, Columbia University, New York, NY, USA.)
Abstract	Mature erythrocytes (red blood cells (RBCs)) undergo the programmed cell death (PCD) pathway of necroptosis in response to bacterial pore-forming toxins (PFTs) that target human CD59 (hCD59) but not hCD59-independent PFTs. Here, we investigate the biochemical mechanism of RBC necroptosis with a focus on the mechanism of induction and the minimal requirements for such RBC death. Binding or crosslinking of the hCD59 receptor led to Syk-dependent induction of vesiculated morphology (echinocytes) that was associated with phosphorylation of Band 3 and was required for Fas ligand (FasL) release. FasL-dependent phosphorylation of receptor-interacting protein kinase 1 (RIP1) in combination with plasma membrane pore formation was required for execution of RBC necroptosis. RIP1 phosphorylation led to the phosphorylation of RIP3, which was also critical for RBC necroptosis. Notably, RBC necroptosis was mediated by FasL and not by other candidate inducers, including tumor necrosis factor alpha (TNF- ) and TNF-related apoptosis-inducing ligand (TRAIL). Other types of RBC damage, such as eryptotic damage, failed to induce necroptosis when combined with hCD59 crosslinking. This work sheds light on the requirements for this recently discovered PCD in RBCs and provides a clear picture of the biochemical mechanism of induction of RBC necroptosis.
File Format	HTM / HTML
e-ISSN	20414889
DOI	10.1038/cddis.2015.135
Journal	Cell Death and Disease
Volume Number	6
Language	English
Publisher	Nature Publishing Group
Publisher Date	2015-05-28
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Antigens, Cd55 Cell Membrane Phosphorylation Nuclear Pore Complex Proteins Intracellular Signaling Peptides And Proteins Signal Transduction Antigens, Cd59 Cross-linking Reagents Erythrocytes Pharmacology Metabolism Tumor Necrosis Factor-alpha Necrosis Rna-binding Proteins Fas Ligand Protein Discipline Cell Biology Pathology Immunology Protein-tyrosine Kinases Pore Forming Cytotoxic Proteins Receptor-interacting Protein Serine-threonine Kinases Tnf-related Apoptosis-inducing Ligand
Content Type	Text
Resource Type	Article

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in