Buyandelger, ByambajavByambajavBuyandelgerMansfield, CatherineCatherineMansfieldKostin, SawaSawaKostinChoi, OnjeeOnjeeChoiRoberts, Angharad M.Angharad M.RobertsWare, James S.James S.WareMazzarotto, FrancescoFrancescoMazzarottoPesce, FrancescoFrancescoPesceBuchan, RachelRachelBuchanIsaacson, Rivka L.Rivka L.IsaacsonVouffo, JoseeJoseeVouffoGunkel, SylviaSylviaGunkelKnoll, GudrunGudrunKnollMcSweeney, Sara J.Sara J.McSweeneyWei, HemingHemingWeiPerrot, AndreasAndreasPerrotPfeiffer, ConnyConnyPfeifferToliat, Mohammad RezaMohammad RezaToliatIlieva, KristinaKristinaIlievaKrysztofinska, EwelinaEwelinaKrysztofinskaLopez-Olaneta, Marina M.Marina M.Lopez-OlanetaGomez-Salinero, Jesus M.Jesus M.Gomez-SalineroSchmidt, AlbrechtAlbrechtSchmidtNg, Keat-EngKeat-EngNgTeucher, NielsNielsTeucherChen, JuJuChenTeichmann, MartinMartinTeichmannEilers, MartinMartinEilersHaverkamp, WilhelmWilhelmHaverkampRegitz-Zagrosek, VeraVeraRegitz-ZagrosekHasenfuß, GerdGerdHasenfußBraun, ThomasThomasBraunPennell, Dudley J.Dudley J.PennellGould, IanIanGouldBarton, Paul J. R.Paul J. R.BartonLara-Pezzi, EnriqueEnriqueLara-PezziSchaefer, SebastianSebastianSchaeferHübner, NorbertNorbertHübnerFelkin, Leanne E.Leanne E.FelkinO’Regan, D. P.D. P.O’ReganBrand, ThomasThomasBrandMilting, HendrikHendrikMiltingNürnberg, PeterPeterNürnbergSchneider, Michael D.Michael D.SchneiderPrasad, SanjaySanjayPrasadPetretto, EnricoEnricoPetrettoKnoll, RalphRalphKnoll2017-09-072017-09-072015https://resolver.sub.uni-goettingen.de/purl?gro-2/1379Background Mutations in sarcomeric and cytoskeletal proteins are a major cause of hereditary cardiomyopathies, but our knowledge remains incomplete as to how the genetic defects execute their effects. Methods and Results We used cysteine and glycine-rich protein 3, a known cardiomyopathy gene, in a yeast 2-hybrid screen and identified zinc-finger and BTB domain-containing protein 17 (ZBTB17) as a novel interacting partner. ZBTB17 is a transcription factor that contains the peak association signal (rs10927875) at the replicated 1p36 cardiomyopathy locus. ZBTB17 expression protected cardiac myocytes from apoptosis in vitro and in a mouse model with cardiac myocyte-specific deletion of Zbtb17, which develops cardiomyopathy and fibrosis after biomechanical stress. ZBTB17 also regulated cardiac myocyte hypertrophy in vitro and in vivo in a calcineurin-dependent manner. Conclusions We revealed new functions for ZBTB17 in the heart, a transcription factor that may play a role as a novel cardiomyopathy gene.journal_article10.1161/CIRCGENETICS.113.000690261755290003633738000033141815