Scientists reveal what makes human cells maintain calcium equilibrium

The new found role of a membrane protein in maintaining cellular calcium levels may help probe diseases such as diabetes, Parkinson's and Alzheimer's
The mechanism and factors determining calcium movement across cell membrane has remained elusive to researchers for a long time. Credit: Ed Uthma/Flickr
The mechanism and factors determining calcium movement across cell membrane has remained elusive to researchers for a long time. Credit: Ed Uthma/Flickr

Calcium levels inside human cells play a crucial role in normal functioning of cells and even in cell death. The mechanism and factors determining calcium movement across cell membrane has remained elusive to researchers for a long time. Now a group of Indian researchers have reported that a membrane protein inside part of human cell is critical in maintaining calcium equilibrium in cells.

The membrane bound protein is named LRRC8B and is found inside a cell’s subunit, called endoplasmic reticulum (ER).

“ER serves as a reservoir of calcium ions dictating multiple cellular functions. We have found that the protein LRRC8B acts as a calcium leak channel in the ER, thereby causing perturbations in calcium flux across the cell,” explained Amal Kanti Bera, a senior researcher involved in the study. The work has been published in the Journal of Cell Science.

The researchers have built upon the recent discovery of ER-targeted calcium sensitive fluorescent protein constructs reported in 2014. This enabled them to record calcium changes in ER more effectively, explained Arijita Ghosh, a researcher who was part of the study. The study was conducted on cultured human cells under laboratory conditions.

Alteration in calcium movement across the cell membrane has been shown to be liked with several diseases such as diabetes, Parkinson’s and Alzheimer’s. Bera hopes the new found role of LRRC8B in maintaining cellular calcium levels would open up avenues to probe these diseases which are linked with calcium level dysfunction.

The research team included Arijita Ghosh, Nitin Khandelwal, Arvind Kumar and Amal Kanti Bera from the Indian Institute of Technology, Madras and CSIR-Centre for Cellular and Molecular Biology, Hyderabad. The research was supported by the Board of Research in Nuclear Science.

(This story is by India Science Wire).

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