PMID- 28174541
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 8
DP  - 2017
TI  - Regulation of Connexin-Based Channels by Fatty Acids.
PG  - 11
LID - 10.3389/fphys.2017.00011 [doi]
LID - 11
AB  - In this mini-review, we briefly summarize the current knowledge about the effects 
      of fatty acids (FAs) on connexin-based channels, as well as discuss the limited 
      information about the impact FAs may have on pannexins (Panxs). FAs regulate 
      diverse cellular functions, some of which are explained by changes in the 
      activity of channels constituted by connexins (Cxs) or Panxs, which are known to 
      play critical roles in maintaining the functional integrity of diverse organs and 
      tissues. Cxs are transmembrane proteins that oligomerize into hexamers to form 
      hemichannels (HCs), which in turn can assemble into dodecamers to form gap 
      junction channels (GJCs). While GJCs communicate the cytoplasm of contacting 
      cells, HCs serve as pathways for the exchange of ions and small molecules between 
      the intra and extracellular milieu. Panxs, as well as Cx HCs, form channels at 
      the plasma membrane that enable the interchange of molecules between the intra 
      and extracellular spaces. Both Cx- and Panx-based channels are controlled by 
      several post-translational modifications. However, the mechanism of action of FAs 
      on these channels has not been described in detail. It has been shown however 
      that FAs frequently decrease GJC-mediated cell-cell communication. The opposite 
      effect also has been described for HC or Panx-dependent intercellular 
      communication, where, the acute FA effect can be reversed upon washout. 
      Additionally, changes in GJCs mediated by FAs have been associated with 
      post-translational modifications (e.g., phosphorylation), and seem to be directly 
      related to chemical properties of FAs (e.g., length of carbon chain and/or degree 
      of saturation), but this possible link remains poorly understood.
FAU - Puebla, Carlos
AU  - Puebla C
AD  - Instituto de Ciencias Biomedicas, Facultad de Ciencias de la Salud, Universidad 
      Autonoma de ChileSantiago, Chile; Centro de Fisiologia Celular e Integrativa, 
      Facultad de Medicina, Clinica Alemana Universidad del DesarrolloSantiago, Chile.
FAU - Retamal, Mauricio A
AU  - Retamal MA
AD  - Centro de Fisiologia Celular e Integrativa, Facultad de Medicina, Clinica Alemana 
      Universidad del Desarrollo Santiago, Chile.
FAU - Acuna, Rodrigo
AU  - Acuna R
AD  - Centro de Fisiologia Celular e Integrativa, Facultad de Medicina, Clinica Alemana 
      Universidad del Desarrollo Santiago, Chile.
FAU - Saez, Juan C
AU  - Saez JC
AD  - Departamento de Fisiologia, Facultad de Ciencias Biologicas, Pontificia 
      Universidad Catolica de ChileSantiago, Chile; Centro Interdisciplinario de 
      Neurociencias de Valparaiso, Intituto Milenio, Universidad de 
      ValparaisoValparaiso, Chile.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170124
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC5258758
OTO - NOTNLM
OT  - G-protein coupled receptor
OT  - connexon
OT  - gap junction channel
OT  - hemichannel
OT  - pannexon
EDAT- 2017/02/09 06:00
MHDA- 2017/02/09 06:01
PMCR- 2017/01/24
CRDT- 2017/02/09 06:00
PHST- 2016/11/25 00:00 [received]
PHST- 2017/01/06 00:00 [accepted]
PHST- 2017/02/09 06:00 [entrez]
PHST- 2017/02/09 06:00 [pubmed]
PHST- 2017/02/09 06:01 [medline]
PHST- 2017/01/24 00:00 [pmc-release]
AID - 10.3389/fphys.2017.00011 [doi]
PST - epublish
SO  - Front Physiol. 2017 Jan 24;8:11. doi: 10.3389/fphys.2017.00011. eCollection 2017.