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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003705naa a2200385 4500
001oai:DiVA.org:uu-168429
003SwePub
008120210s2011 | |||||||||||000 ||eng|
0247 a https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1684292 URI
0247 a https://doi.org/10.1186/1471-2202-12-1172 DOI
040 a (SwePub)uu
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Rask-Andersen, Mathiasu Uppsala universitet,Funktionell farmakologi4 aut0 (Swepub:uu)matra895
2451 0a Functional coupling analysis suggests link between the obesity gene FTO and the BDNF-NTRK2 signaling pathway
264 c 2011-11-16
264 1b Springer Science and Business Media LLC,c 2011
338 a electronic2 rdacarrier
520 a Background: The Fat mass and obesity gene (FTO) has been identified through genome wide association studies as an important genetic factor contributing to a higher body mass index (BMI). However, the molecular context in which this effect is mediated has yet to be determined. We investigated the potential molecular network for FTO by analyzing co-expression and protein-protein interaction databases, Coxpresdb and IntAct, as well as the functional coupling predicting multi-source database, FunCoup. Hypothalamic expression of FTO-linked genes defined with this bioinformatics approach was subsequently studied using quantitative real time-PCR in mouse feeding models known to affect FTO expression.Results: We identified several candidate genes for functional coupling to FTO through database studies and selected nine for further study in animal models. We observed hypothalamic expression of Profilin 2 (Pfn2), cAMP-dependent protein kinase catalytic subunit beta (Prkacb), Brain derived neurotrophic factor (Bdnf), neurotrophic tyrosine kinase, receptor, type 2 (Ntrk2), Signal transducer and activator of transcription 3 (Stat3), and Btbd12 to be co-regulated in concert with Fto. Pfn2 and Prkacb have previously not been linked to feeding regulation.Conclusions: Gene expression studies validate several candidates generated through database studies of possible FTO-interactors. We speculate about a wider functional role for FTO in the context of current and recent findings, such as in extracellular ligand-induced neuronal plasticity via NTRK2/BDNF, possibly via interaction with the transcription factor CCAAT/enhancer binding protein beta (C/EBP beta)
7001 a Sällman Almén, Markusu Uppsala universitet,Funktionell farmakologi4 aut0 (Swepub:uu)marsa340
7001 a Olausen, Hans R.u Uppsala universitet,Funktionell farmakologi4 aut
7001 a Olszewski, Pawel K.u Uppsala universitet,Funktionell farmakologi4 aut0 (Swepub:uu)pawol865
7001 a Eriksson, Jennyu Uppsala universitet,Funktionell farmakologi4 aut
7001 a Chavan, Rohit A.u Uppsala universitet,Funktionell farmakologi4 aut
7001 a Levine, Allen S.4 aut
7001 a Fredriksson, Robertu Uppsala universitet,Funktionell farmakologi4 aut0 (Swepub:uu)rfr20930
7001 a Schiöth, Helgi Bu Uppsala universitet,Funktionell farmakologi4 aut0 (Swepub:uu)helgschi
7102 a Uppsala universitetb Funktionell farmakologi4 org
7730 t BMC Neuroscienced : Springer Science and Business Media LLCg 12, s. 117-q 12<117-x 1471-2202
8564 u https://uu.diva-portal.org/smash/get/diva2:497157/FULLTEXT01.pdfx primaryx Raw objecty fulltext:print
8564 u https://bmcneurosci.biomedcentral.com/track/pdf/10.1186/1471-2202-12-117
8564 8u https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-168429
8564 8u https://doi.org/10.1186/1471-2202-12-117

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