What is it about?
This paper showed that a protein that transports zinc ions called transmembrane 163 (TMEM163) protein interacts with another protein called Mucolipin-1 (TRPML1; a non-selective cation channel). Both proteins are detected within the cell's recycling center called lysosomes. The loss of TRPML1 function is the cause of a neurodegenerative disease and a lysosomal storage disorder known as Mucolipidosis type IV (MLIV).
Photo by National Cancer Institute on Unsplash
Why is it important?
We previously reported that zinc accumulates in lysosomes when TRPML1 is knocked down using RNA interference in cultured cells. In the current paper, we confirmed this observation that zinc accumulates in lysosomes of MLIV patient fibroblast cells. Thus, the loss of interaction between the two proteins (TMEM163 and TRPML1) may be the reason why zinc accumulates in lysosomes of cells. More recently, our laboratory has established that TMEM163 mediates extrusion of zinc ions out of cells, suggesting that it is important in balancing the levels of zinc inside the cells. Other laboratories have also implicated TMEM163 in various human disease.
Read the Original
This page is a summary of: Cellular Zinc Levels Are Modulated by TRPML1-TMEM163 Interaction, Traffic, September 2014, Wiley, DOI: 10.1111/tra.12205.
You can read the full text:
The following have contributed to this page