Asset Details
Do you wish to reserve the book?
Phosphorylation-mediated activation of mouse Xkr8 scramblase for phosphatidylserine exposure
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Phosphorylation-mediated activation of mouse Xkr8 scramblase for phosphatidylserine exposure
Do you wish to request the book?
Phosphorylation-mediated activation of mouse Xkr8 scramblase for phosphatidylserine exposure
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Phosphorylation-mediated activation of mouse Xkr8 scramblase for phosphatidylserine exposure
2019
Overview
The exposure of phosphatidylserine (PtdSer) to the cell surface is regulated by the down-regulation of flippases and the activation of scramblases. Xkr8 has been identified as a scramblase that is activated during apoptosis, but its exogenous expression in the mouse Ba/F3 pro B cell line induces constitutive PtdSer exposure. Here we found that this Xkr8-mediated PtdSer exposure occurred at 4 °C, but not at 20 °C, although its scramblase activity was observed at 20 °C. The Xkr8-mediated PtdSer exposure was inhibited by a kinase inhibitor and enhanced by phosphatase inhibitors. Phosphorylated Xkr8 was detected by Phos-tag PAGE, and a mass spectrometric and mutational analysis identified three phosphorylation sites. Their phosphomimic mutation rendered Xkr8 resistant to the kinase inhibitor for PtdSer exposure at 4 °C, but unlike phosphatase inhibitors, it did not induce constitutive PtdSer exposure at 20 °C. On the other hand, when the flippase genes were deleted, the Xkr8 induced constitutive PtdSer exposure at high temperature, indicating that the flippase activity normally counteracted Xkr8’s ability to expose PtdSer. These results indicate that PtdSer exposure can be increased by the phosphorylation-mediated activation of Xkr8 scramblase and flippase down-regulation.
Publisher
National Academy of Sciences
Subject
/ Animals
/ Apoptosis Regulatory Proteins - chemistry
/ Apoptosis Regulatory Proteins - genetics
/ Cell Membrane - drug effects
/ Exposure
/ Gene Expression Regulation - genetics
/ Humans
/ Kinases
/ Membrane Proteins - chemistry
/ Membrane Proteins - genetics
/ Mice
/ Mutation
/ Phosphatidylserines - chemistry
/ Phosphatidylserines - pharmacology
/ Phospholipid Transfer Proteins - chemistry
/ Phosphoric Monoester Hydrolases - antagonists & inhibitors
/ Phosphoric Monoester Hydrolases - chemistry
/ Phosphorylation - drug effects
/ Protein Kinase Inhibitors - chemistry
