Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
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Contact

 

+44 (0)013 34621727m.d.schneider Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Buyandelger:2015:10.1161/CIRCGENETICS.113.000690,
author = {Buyandelger, B and Mansfield, C and Kostin, S and Choi, O and Roberts, AM and Ware, JS and Mazzarotto, F and Pesce, F and Buchan, R and Isaacson, RL and Vouffo, J and Gunkel, S and Knöll, G and McSweeney, SJ and Wei, H and Perrot, A and Pfeiffer, C and Toliat, MR and Ilieva, K and Krysztofinska, E and López-Olañeta, MM and Gómez-Salinero, JM and Schmidt, A and Ng, KE and Teucher, N and Chen, J and Teichmann, M and Eilers, M and Haverkamp, W and Regitz-Zagrosek, V and Hasenfuss, G and Braun, T and Pennell, DJ and Gould, I and Barton, PJ and Lara-Pezzi, E and Schafer, S and Hübner, N and Felkin, LE and O'Regan, DP and Petretto, E and Brand, T and Milting, H and Nürnberg, P and Schneider, MD and Prasad, S and Knöll, R},
doi = {10.1161/CIRCGENETICS.113.000690},
journal = {Circulation. Cardiovascular Genetics},
pages = {643--652},
title = {ZBTB17 (MIZ1) Is Important for the Cardiac Stress Response and a Novel Candidate Gene for Cardiomyopathy and Heart Failure.},
url = {http://dx.doi.org/10.1161/CIRCGENETICS.113.000690},
volume = {8},
year = {2015}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - BACKGROUND: -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 (CSRP3), a known cardiomyopathy gene, in a yeast two-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 which may play a role as a novel cardiomyopathy gene.
AU - Buyandelger,B
AU - Mansfield,C
AU - Kostin,S
AU - Choi,O
AU - Roberts,AM
AU - Ware,JS
AU - Mazzarotto,F
AU - Pesce,F
AU - Buchan,R
AU - Isaacson,RL
AU - Vouffo,J
AU - Gunkel,S
AU - Knöll,G
AU - McSweeney,SJ
AU - Wei,H
AU - Perrot,A
AU - Pfeiffer,C
AU - Toliat,MR
AU - Ilieva,K
AU - Krysztofinska,E
AU - López-Olañeta,MM
AU - Gómez-Salinero,JM
AU - Schmidt,A
AU - Ng,KE
AU - Teucher,N
AU - Chen,J
AU - Teichmann,M
AU - Eilers,M
AU - Haverkamp,W
AU - Regitz-Zagrosek,V
AU - Hasenfuss,G
AU - Braun,T
AU - Pennell,DJ
AU - Gould,I
AU - Barton,PJ
AU - Lara-Pezzi,E
AU - Schafer,S
AU - Hübner,N
AU - Felkin,LE
AU - O'Regan,DP
AU - Petretto,E
AU - Brand,T
AU - Milting,H
AU - Nürnberg,P
AU - Schneider,MD
AU - Prasad,S
AU - Knöll,R
DO - 10.1161/CIRCGENETICS.113.000690
EP - 652
PY - 2015///
SN - 1942-3268
SP - 643
TI - ZBTB17 (MIZ1) Is Important for the Cardiac Stress Response and a Novel Candidate Gene for Cardiomyopathy and Heart Failure.
T2 - Circulation. Cardiovascular Genetics
UR - http://dx.doi.org/10.1161/CIRCGENETICS.113.000690
UR - http://hdl.handle.net/10044/1/25683
VL - 8
ER -