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Connexins : substrates and regulators of autophagy

(2016) BMC CELL BIOLOGY. 17(suppl. 1).
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Abstract
Connexins mediate intercellular communication by assembling into hexameric channel complexes that act as hemichannels and gap junction channels. Most connexins are characterized by a very rapid turn-over in a variety of cell systems. The regulation of connexin turn-over by phosphorylation and ubiquitination events has been well documented. Moreover, different pathways have been implicated in connexin degradation, including proteasomal and lysosomal-based pathways. Only recently, autophagy emerged as an important connexin-degradation pathway for different connexin isoforms. As such, conditions well known to induce autophagy have an immediate impact on the connexin-expression levels. This is not only limited to experimental conditions but also several pathophysiological conditions associated with autophagy (dys) function affect connexin levels and their presence at the cell surface as gap junctions. Finally, connexins are not only substrates of autophagy but also emerge as regulators of the autophagy process. In particular, several connexin isoforms appear to recruit pre-autophagosomal autophagy-related proteins, including Atg16 and PI3K-complex components, to the plasma membrane, thereby limiting their availability and capacity for regulating autophagy.
Keywords
Autophagy, Connexins, Degradation, Regulation, JUNCTION PROTEIN CONNEXIN43, INOSITOL TRISPHOSPHATE RECEPTOR, ISCHEMIA-REPERFUSION INJURY, TRAUMATIC BRAIN-INJURY, GAP-JUNCTIONS, CELL-DEATH, ENDOPLASMIC-RETICULUM, DOWN-REGULATION, CONNEXIN43-INTERACTING PROTEIN, INTERCELLULAR COMMUNICATION

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Chicago
Iyyathurai, Jegan, Jean-Paul Decuypere, Luc Leybaert, Catheleyne D’hondt, and Geert Bultynck. 2016. “Connexins : Substrates and Regulators of Autophagy.” Bmc Cell Biology 17 (suppl. 1).
APA
Iyyathurai, J., Decuypere, J.-P., Leybaert, L., D’hondt, C., & Bultynck, G. (2016). Connexins : substrates and regulators of autophagy. BMC CELL BIOLOGY, 17(suppl. 1). Presented at the International Gap Junction Conference 2015.
Vancouver
1.
Iyyathurai J, Decuypere J-P, Leybaert L, D’hondt C, Bultynck G. Connexins : substrates and regulators of autophagy. BMC CELL BIOLOGY. 2016;17(suppl. 1).
MLA
Iyyathurai, Jegan et al. “Connexins : Substrates and Regulators of Autophagy.” BMC CELL BIOLOGY 17.suppl. 1 (2016): n. pag. Print.
@article{8119855,
  abstract     = {Connexins mediate intercellular communication by assembling into hexameric channel complexes that act as hemichannels and gap junction channels. Most connexins are characterized by a very rapid turn-over in a variety of cell systems. The regulation of connexin turn-over by phosphorylation and ubiquitination events has been well documented. Moreover, different pathways have been implicated in connexin degradation, including proteasomal and lysosomal-based pathways. Only recently, autophagy emerged as an important connexin-degradation pathway for different connexin isoforms. As such, conditions well known to induce autophagy have an immediate impact on the connexin-expression levels. This is not only limited to experimental conditions but also several pathophysiological conditions associated with autophagy (dys) function affect connexin levels and their presence at the cell surface as gap junctions. Finally, connexins are not only substrates of autophagy but also emerge as regulators of the autophagy process. In particular, several connexin isoforms appear to recruit pre-autophagosomal autophagy-related proteins, including Atg16 and PI3K-complex components, to the plasma membrane, thereby limiting their availability and capacity for regulating autophagy.},
  articleno    = {20},
  author       = {Iyyathurai, Jegan and Decuypere, Jean-Paul and Leybaert, Luc and D'hondt, Catheleyne and Bultynck, Geert},
  issn         = {1471-2121},
  journal      = {BMC CELL BIOLOGY},
  keywords     = {Autophagy,Connexins,Degradation,Regulation,JUNCTION PROTEIN CONNEXIN43,INOSITOL TRISPHOSPHATE RECEPTOR,ISCHEMIA-REPERFUSION INJURY,TRAUMATIC BRAIN-INJURY,GAP-JUNCTIONS,CELL-DEATH,ENDOPLASMIC-RETICULUM,DOWN-REGULATION,CONNEXIN43-INTERACTING PROTEIN,INTERCELLULAR COMMUNICATION},
  language     = {eng},
  location     = {Valparaiso, Chile},
  number       = {suppl. 1},
  pages        = {16},
  title        = {Connexins : substrates and regulators of autophagy},
  url          = {http://dx.doi.org/10.1186/s12860-016-0093-9},
  volume       = {17},
  year         = {2016},
}

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