{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Bhattacharya S"],"funding":["Regional Centre for Biotechnology","Baylor College of Medicine","Department of Biotechnology, Ministry of Science and Technology, India"],"pagination":["103418"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8190441"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["68"],"pubmed_abstract":["<h4>Background</h4>We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2<sup>D4E;C127S</sup>) variant that degrades the hypoxia-inducible factor (HIFα) more efficiently and protects these highlanders from hypoxia-triggered elevation in haemoglobin concentration. High altitude is known to cause acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) in a section of rapidly ascending non-acclimatised lowlanders. These morbidities are often accompanied by inflammatory response and exposure to hypobaric hypoxia is presumed to be the principal causative agent. We have investigated whether PHD2<sup>D4E;C127S</sup> variant is associated with prevention of hypoxia-mediated inflammatory milieu in Tibetan highlanders and therefore identify a potent"],"journal":["EBioMedicine"],"pubmed_title":["Gain-of-function Tibetan PHD2<sup>D4E;C127S</sup> variant suppresses monocyte function: A lesson in inflammatory response to inspired hypoxia."],"pmcid":["PMC8190441"],"funding_grant_id":["BT/PR22985"],"pubmed_authors":["Shrimali NM","Mohammad G","Guchhait P","Bhattacharya S","Koul PA","Prchal JT"],"additional_accession":[]},"is_claimable":false,"name":"Gain-of-function Tibetan PHD2<sup>D4E;C127S</sup> variant suppresses monocyte function: A lesson in inflammatory response to inspired hypoxia.","description":"<h4>Background</h4>We have previously described an evolutionarily selected Tibetan prolyl hydroxylase-2 (PHD2<sup>D4E;C127S</sup>) variant that degrades the hypoxia-inducible factor (HIFα) more efficiently and protects these highlanders from hypoxia-triggered elevation in haemoglobin concentration. High altitude is known to cause acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) in a section of rapidly ascending non-acclimatised lowlanders. These morbidities are often accompanied by inflammatory response and exposure to hypobaric hypoxia is presumed to be the principal causative agent. We have investigated whether PHD2<sup>D4E;C127S</sup> variant is associated with prevention of hypoxia-mediated inflammatory milieu in Tibetan highlanders and therefore identify a potent","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Jun","modification":"2026-05-08T23:09:09.958Z","creation":"2022-02-10T15:20:23.16Z"},"accession":"S-EPMC8190441","cross_references":{"pubmed":["34102396"],"doi":["10.1016/j.ebiom.2021.103418"]}}