Imperial College London
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Dr Woscholski

Faculty of Natural Sciences, Department of Chemistry

Reader in Chemical Biology
 
 
 
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Contact

 

+44 (0)20 7594 5305r.woscholski

 
 
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Location

 

301LMolecular Sciences Research HubWhite City Campus

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Summary

 

Publications

Citation

BibTex format

@article{Rosivatz:2011:10.1016/j.cellsig.2010.10.025,
author = {Rosivatz, E and Woscholski, R},
doi = {10.1016/j.cellsig.2010.10.025},
journal = {Cell Signal.},
pages = {478--486},
title = {Removal or masking of phosphatidylinositol(4,5)bisphosphate from the outer mitochondrial membrane causes mitochondrial fragmentation},
url = {http://dx.doi.org/10.1016/j.cellsig.2010.10.025},
volume = {23},
year = {2011}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Mitochondria are central players in programmed cell death and autophagy. While phosphoinositides are well established regulators of membrane traffic, cellular signalling and the destiny of certain organelles, their presence and role for mitochondria remain elusive. In this study we show that removal of PtdIns(4,5)P(2) by phosphatases or masking the lipid with PH domains leads to fission of mitochondria and increased autophagy. Induction of general autophagy by amino acid starvation also coincides with the loss of mitochondrial PtdIns(4,5)P(2), suggesting an important role for this lipid in the processes that govern mitophagy. Our findings reveal that PKCalpha can rescue the removal or masking of PtdIns(4,5)P(2), indicating that the inositol lipid is upstream of PKC
AU  - Rosivatz,E
AU  - Woscholski,R
DO  - 10.1016/j.cellsig.2010.10.025
EP  - 486
PY  - 2011///
SP  - 478
TI  - Removal or masking of phosphatidylinositol(4,5)bisphosphate from the outer mitochondrial membrane causes mitochondrial fragmentation
T2  - Cell Signal.
UR  - http://dx.doi.org/10.1016/j.cellsig.2010.10.025
UR  - pm:21044681
VL  - 23
ER  -
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