<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Byts, Nadiya</style></author><author><style face="normal" font="default" size="100%">Sharma, Subodh</style></author><author><style face="normal" font="default" size="100%">Laurila, Jenny</style></author><author><style face="normal" font="default" size="100%">Paudel, Prodeep</style></author><author><style face="normal" font="default" size="100%">Miinalainen, Ilkka</style></author><author><style face="normal" font="default" size="100%">Ronkainen, Veli-Pekka</style></author><author><style face="normal" font="default" size="100%">Hinttala, Reetta</style></author><author><style face="normal" font="default" size="100%">Törnquist, Kid</style></author><author><style face="normal" font="default" size="100%">Koivunen, Peppi</style></author><author><style face="normal" font="default" size="100%">Myllyharju, Johanna</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Transmembrane Prolyl 4-Hydroxylase is a Novel Regulator of Calcium Signaling in Astrocytes</style></title><secondary-title><style face="normal" font="default" size="100%">eneuro</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2021</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2021-01-01 00:00:00</style></date></pub-dates></dates><elocation-id><style  face="normal" font="default" size="100%">ENEURO.0253-20.2020</style></elocation-id><doi><style  face="normal" font="default" size="100%">10.1523/ENEURO.0253-20.2020</style></doi><volume><style face="normal" font="default" size="100%">8</style></volume><issue><style face="normal" font="default" size="100%">1</style></issue><abstract><style  face="normal" font="default" size="100%">Prolyl 4-hydroxylases (P4Hs) have vital roles in regulating collagen synthesis and hypoxia response. A transmembrane P4H (P4H-TM) is a recently identified member of the family. Biallelic loss of function P4H-TM mutations cause a severe autosomal recessive intellectual disability syndrome in humans, but functions of P4H-TM are essentially unknown at cellular level. Our microarray data on P4h-tm−/− mouse cortexes where P4H-TM is abundantly expressed indicated expression changes in genes involved in calcium signaling and expression of several calcium sequestering ATPases was upregulated in P4h-tm−/− primary mouse astrocytes. Cytosolic and intraorganellar calcium imaging of P4h-tm−/− cells revealed that receptor-operated calcium entry (ROCE) and store-operated calcium entry (SOCE) and calcium re-uptake by mitochondria were compromised. HIF1, but not HIF2, was found to be a key mediator of the P4H-TM effect on calcium signaling. Furthermore, total internal reflection fluorescence (TIRF) imaging showed that calcium agonist-induced gliotransmission was attenuated in P4h-tm−/− astrocytes. This phenotype was accompanied by redistribution of mitochondria from distal processes to central parts of the cell body and decreased intracellular ATP content. Our data show that P4H-TM is a novel regulator of calcium dynamics and gliotransmission.</style></abstract></record></records></xml>