Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2015 Sep 15;29(18):1903–1914. doi: 10.1101/gad.268482.115

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2015 Boynton and Shimkets; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

PMC Copyright notice

Figure 6. — Proposed functions of CsgA and HSD10 in Myxococcus and humans. (A) M. xanthus lipid bodies are synthesized from existing membrane phospholipids. This reaction is proposed to occur directly from the breakdown of PG and CL into DAGs by CsgA. An as yet uncharacterized acyltransferase could then convert the DAGs into TAGs. (B) In the presence of ROS created from oxidative stress, HSD10 is recruited to the inner mitochondrial membrane where CytC simultaneously converts CL to CL_ox. HSD10 removes CL_ox before it is exported to the outer membrane, and CytC is released, inhibiting apoptosis. In Parkinson's disease, HSD10 levels within the mitochondria are greatly diminished. In Alzheimer's disease, HSD10 is inactivated within the matrix by the binding of the Aβ peptide. In both instances, oxidative damage occurs, leading to apoptosis.