Cell Communication and Signaling

Cell Communication and Signaling (CCS) is an open access journal that encompasses all basic and translational aspects of cellular communications and signaling pathways in normal and pathological conditions.

Beginning in January of 2019, CCS is pleased to announce their affiliation with the International Cell Death Society. 

The journal encourages submissions in all aspects of cell death, that include apoptotic and non-apoptotic mechanisms of cell death, cell death in model systems, autophagy, clearance of dying cells, as well as the immunological and pathological consequences of dying cells in the tissue microenvironment. 

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Kinases, adaptor proteins, and actin cytoskeleton rearrangements in EMT and cancer
Edited by Dr. Leszek Kotula and Dr. Patrycja Dubielecka-Sczerba

The roles of intrinsically disordered proteins and regions (IDPs and IDRs) in cell communication and cell signaling
Edited by Dr. Sarah Bondos, Dr. A. Keith Dunker and Dr. Vladimir Uversky

Biology of phosphatidylserine (PS): basic physiology and implications in immunology, infectious disease, and cancer
Edited by Dr. Raymond Birge and Dr. David Calianese

At Cell Communication and Signaling, we are passionate about the dissemination of research.

We are pleased to announce that as of the 12th August 2019, all authors whose papers are accepted will receive a Video Byte.

Created by our partners, Research Square, a Video Byte is a 1-2 minute video summary of a paper that will be incorporated into the abstract of the paper and published on the journal website. Authors will also receive a shareable version of their Video Byte.

25th Anniversary of the International Cell Death Society Collection

Curated by Editor-in-Chief Raymond Birge, we're celebrating the 25th anniversary of the ICDS with a collection highlighting the most important Cell Death papers published in Cell Communication and Signaling in the last decade.

Cell death induced by the ER stressor thapsigargin involves death receptor 5, a non-autophagic function of MAP1LC3B, and distinct contributions from unfolded protein response components

In this recent paper, Lindner et al. examined how the ER stressor thapsigargin and therapy-relevant analogs induce cell death in human cancer cells. They revealed crucial roles for DR5 and MAP1LC3B upstream of caspase-8. Upregulation of DR5 and MAP1LC3B required independent contributions from ATF4 and CHOP, while PERK elicited pro-death signals via other mechanisms. IRE1 and XBP1 promoted death in a cell type-specific manner, via a novel identified XBP1-dependent activation of JNK.