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Sökning: onr:"swepub:oai:gup.ub.gu.se/306845" > Integrative genetic...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003540naa a2200457 4500
001oai:gup.ub.gu.se/306845
003SwePub
008240528s2021 | |||||||||||000 ||eng|
024a https://gup.ub.gu.se/publication/3068452 URI
024a https://doi.org/10.1038/s41598-021-96374-92 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Huusko, Johanna M4 aut
2451 0a Integrative genetic, genomic and transcriptomic analysis of heat shock protein and nuclear hormone receptor gene associations with spontaneous preterm birth.
264 c 2021-08-24
264 1b Springer Science and Business Media LLC,c 2021
520 a Heat shock proteins are involved in the response to stress including activation of the immune response. Elevated circulating heat shock proteins are associated with spontaneous preterm birth (SPTB). Intracellular heat shock proteins act as multifunctional molecular chaperones that regulate activity of nuclear hormone receptors. Since SPTB has a significant genetic predisposition, our objective was to identify genetic and transcriptomic evidence of heat shock proteins and nuclear hormone receptors that may affect risk for SPTB. We investigated all 97 genes encoding members of the heat shock protein families and all 49 genes encoding nuclear hormone receptors for their potential role in SPTB susceptibility. We used multiple genetic and genomic datasets including genome-wide association studies (GWASs), whole-exome sequencing (WES), and placental transcriptomics to identify SPTB predisposing factors from the mother, infant, and placenta. There were multiple associations of heat shock protein and nuclear hormone receptor genes with SPTB. Several orthogonal datasets supported roles for SEC63, HSPA1L, SACS, RORA, and AR in susceptibility to SPTB. We propose that suppression of specific heat shock proteins promotes maintenance of pregnancy, whereas activation of specific heat shock protein mediated signaling may disturb maternal-fetal tolerance and promote labor.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Reproduktionsmedicin och gynekologi0 (SwePub)302202 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Obstetrics, Gynaecology and Reproductive Medicine0 (SwePub)302202 hsv//eng
700a Tiensuu, Heli4 aut
700a Haapalainen, Antti M4 aut
700a Pasanen, Anu4 aut
700a Tissarinen, Pinja4 aut
700a Karjalainen, Minna K4 aut
700a Zhang, Ge4 aut
700a Christensen, Kaare4 aut
700a Ryckman, Kelli K4 aut
700a Jacobsson, Bo,d 1960u Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi,Institute of Clinical Sciences, Department of Obstetrics and Gynecology4 aut0 (Swepub:gu)xjacbo
700a Murray, Jeffrey C4 aut
700a Kingsmore, Stephen F4 aut
700a Hallman, Mikko4 aut
700a Muglia, Louis J4 aut
700a Rämet, Mika4 aut
710a Göteborgs universitetb Institutionen för kliniska vetenskaper, Avdelningen för obstetrik och gynekologi4 org
773t Scientific reportsd : Springer Science and Business Media LLCg 11:1q 11:1x 2045-2322
856u https://www.nature.com/articles/s41598-021-96374-9.pdf
8564 8u https://gup.ub.gu.se/publication/306845
8564 8u https://doi.org/10.1038/s41598-021-96374-9

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