PMID- 24642372
OWN - NLM
STAT- MEDLINE
DCOM- 20140615
LR  - 20211021
IS  - 1873-3468 (Electronic)
IS  - 0014-5793 (Print)
IS  - 0014-5793 (Linking)
VI  - 588
IP  - 8
DP  - 2014 Apr 17
TI  - The role of pannexin1 in the induction and resolution of inflammation.
PG  - 1416-22
LID - S0014-5793(14)00203-8 [pii]
LID - 10.1016/j.febslet.2014.03.009 [doi]
AB  - Extracellular ATP is an important signaling molecule throughout the inflammatory 
      cascade, serving as a danger signal that causes activation of the inflammasome, 
      enhancement of immune cell infiltration, and fine-tuning of several signaling 
      cascades including those important for the resolution of inflammation. Recent 
      studies demonstrated that ATP can be released from cells in a controlled manner 
      through pannexin (Panx) channels. Panx1-mediated ATP release is involved in 
      inflammasome activation and neutrophil/macrophage chemotaxis, activation of T 
      cells, and a role for Panx1 in inducing and propagating inflammation has been 
      demonstrated in various organs, including lung and the central and peripheral 
      nervous system. The recognition and clearance of dying cells and debris from 
      focal points of inflammation is critical in the resolution of inflammation, and 
      Panx1-mediated ATP release from dying cells has been shown to recruit phagocytes. 
      Moreover, extracellular ATP can be broken down by ectonucleotidases into ADP, 
      AMP, and adenosine, which is critical in the resolution of inflammation. 
      Together, Panx1, ATP, purinergic receptors, and ectonucleotidases contribute to 
      important feedback loops during the inflammatory response, and thus represent 
      promising candidates for new therapies.
CI  - Copyright (c) 2013 Federation of European Biochemical Societies. Published by 
      Elsevier B.V. All rights reserved.
FAU - Adamson, Samantha E
AU  - Adamson SE
AD  - Department of Pharmacology, University of Virginia, United States.
FAU - Leitinger, Norbert
AU  - Leitinger N
AD  - Department of Pharmacology, University of Virginia, United States. Electronic 
      address: nl2q@virginia.edu.
LA  - eng
GR  - P01 HL120840/HL/NHLBI NIH HHS/United States
GR  - R01 DK096076/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20140315
PL  - England
TA  - FEBS Lett
JT  - FEBS letters
JID - 0155157
RN  - 0 (Connexins)
RN  - 0 (Inflammasomes)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (PANX1 protein, human)
RN  - 0 (Panx1 protein, mouse)
SB  - IM
MH  - *Adaptive Immunity
MH  - Animals
MH  - Connexins/genetics/immunology/*metabolism
MH  - Humans
MH  - *Immunity, Innate
MH  - Inflammasomes/immunology/metabolism
MH  - Inflammation/metabolism
MH  - Nerve Tissue Proteins/genetics/immunology/*metabolism
PMC - PMC4060616
MID - NIHMS580883
OTO - NOTNLM
OT  - Extracellular ATP
OT  - Inflammation
OT  - Pannexin 1
OT  - Resolution
EDAT- 2014/03/20 06:00
MHDA- 2014/06/16 06:00
PMCR- 2015/04/17
CRDT- 2014/03/20 06:00
PHST- 2014/02/06 00:00 [received]
PHST- 2014/03/03 00:00 [revised]
PHST- 2014/03/03 00:00 [accepted]
PHST- 2014/03/20 06:00 [entrez]
PHST- 2014/03/20 06:00 [pubmed]
PHST- 2014/06/16 06:00 [medline]
PHST- 2015/04/17 00:00 [pmc-release]
AID - S0014-5793(14)00203-8 [pii]
AID - 10.1016/j.febslet.2014.03.009 [doi]
PST - ppublish
SO  - FEBS Lett. 2014 Apr 17;588(8):1416-22. doi: 10.1016/j.febslet.2014.03.009. Epub 
      2014 Mar 15.