THE HUMAN PROTEIN ATLAS BLOG

Image of the week - FDXR by solartech0

2016-06-10
Citizen Science Image of the week Mitochondria Project Discovery Subcell Atlas


Figure 1. Staining of FDXR (green) with DNA (blue) and microtubules (red) in A549 cells.

Welcome to HPA image of the week! This week's image was brought to us by citizen scientists in Project Discovery, and specifically by solartech0 who found this image while playing Project Discovery in EVE online.

The protein stained in Fig 1. is an image of ferredoxin reductase (FDXR) found in the mitochondria of the cell. This sample shows a staining of FDXR in A549 adenocarcinomic alveolar basal epithelial cells.

FDXR is a protein involved in cellular metabolism. This process is what provides energy for our cells and is carried out in the mitochondria of the cell. FDXR is also involved in "steroidogenesis", the natural production of steroids in your body and can lead to stem cell differentiation, the process by which cells become specialized (Imamichi Y. et al. 2012). For this reason, FDXR is highly expressed in steroidgenic tissues such as the reproductive tissues which is observed in the HPA Tissue atlas page for FDXR.

FDXR is also involved in the regulation of cellular death and viability through a process known as apoptosis (Elmore S. 2007). Importantly, FDXR also directly interacts with the most infamous protein in cancer biology, TP53. Because of its role in cancers, TP53 is a common target of chemotheraputic drugs such as 5-fluorouracil (5-FU). Recently, it has been shown that FDXR plays a major role in the mechanism of 5-FU where disruption of FDXR inhibits the ability of 5-FU to cause apoptosis in colorectal cancer cells suggesting a feed-forward mechanism between TP53, FDXR and the apoptotic pathway (Hwang P. M. et al. 2014).

This protein has not previously been characterized in the Subcellular HPA, and solartech0 brought this image to our attention as having significant cell-to-cell variation. The interaction of FDXR with TP53 and the role of FDXR in metabolism strongly suggest that these differential expressions are significant. These differences may be due to cell cycle position as TP53 is a well known regulator of of the cell cycle (Shaw P.H. 1996), and the role of cellular metabolism in cell growth is well documented (Mason E.F. 2011).

A special thanks to solartech0 for suggesting this image and pointing out the cell-to-cell variant characteristics. This data will be available in HPA16 at the end of this year. As always, a big thanks to the all the citizen scientists participating in Project Discovery and particularly to solartech0 for their contribution to science!


Devin Sullivan



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