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The critical role of JNK in the ER‐mitochondrial crosstalk during apoptotic cell death
Author(s) -
Verma Gaurav,
Datta Malabika
Publication year - 2012
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22903
Subject(s) - microbiology and biotechnology , crosstalk , apoptosis , endoplasmic reticulum , programmed cell death , mitochondrion , kinase , unfolded protein response , p38 mitogen activated protein kinases , biology , signal transduction , caspase , mapk/erk pathway , biochemistry , physics , optics
Apoptosis or programmed cell death is an extremely coordinated phenomenon that involves the participation of a complex interacting crosstalk between the endoplasmic reticulum and mitochondria. This involves a series of signaling molecules like stress kinases, caspases, Bcl‐2 family of proteins, etc. that coordinately induce apoptosis by releasing apoptotic proteins from the mitochondria and mediate DNA damage of the cell. Among the stress kinases, JNK, a member of the MAPK family has been believed to be critically mediating these apoptotic phenomena. The involvement of JNK has been clouded by controversies because of its role both as a pro‐apoptotic and an anti‐apoptotic mediator. A very significant initiator of JNK activation is the pro‐inflammatory cytokine, IL‐1β, levels of which are significantly elevated in varied diseases especially diabetes where it is believed to significantly contribute to pancreatic β‐cell death. During apoptotic cell death, the endoplasmic reticulum and the mitochondrion participate in a relay of cellular events that determine the onset of the classical apoptotic pathways. Here we discuss the details of this ER‐mitochondrial crosstalk and the role of JNK herein that ultimately culminates into apoptotic cell death that is evident in various pathophysiological conditions. J. Cell. Physiol. 227: 1791–1795, 2012. © 2011 Wiley Periodicals, Inc.