Role of AE3 and NHE1 for cardiomyocyte homeostasis and remodeling
Christian Hübner and Andreas Gal,
Institute of Human Genetics, UKE
Contact:
c.huebner@uke.uni-hamburg.de
Objectives
- What is the role of AE3/NHE1* for cardiac pHi regulation?
- Does loss of AE3 in the heart cause cardiac dysfunction?
- How does loss of AE3 interfere with established models
- of cardiac hypertrophy?
- Can overexpression of NHE1 and/or AE3 induce
- cardiac hypertrophy or modulate cardiac remodeling?
*AE3 (SLC4A3): Cl-/HCO3- Exchanger 3; NHE1 (SLC9A1): Sodium/Hydrogen Exchanger 1
Selected publications
- Boettger T*, Hübner CA*, Maier H, Rust MB, Beck FX, Jentsch TJ: Deafness and renal tubular acidosis in mice lacking K-Cl co-transporter Kcc4. Nature, 2002, 416: 874- 8 *shared first authorship
- Hübner CA, Hentschke M, Jackobs S, Hermans-Borgmeyer I. Expression of the sodium-dependent chloride-bicarbonate exchanger NCBE during early mouse development. Mechanisms of development, 2004, 5: 219-23
- Kurth I, Hentschke M, Hentschke S, Borgmeyer U, Gal A, Hübner CA. Foxi1 directly activates the anion exchanger AE4. Biochemical Journal, 2006, 393: 277-83
- Hentschke M, Wiemann M, Hentschke S, Kurth I, Seidenbecher T, Hermans-Borgmeyer I, Jentsch TJ, Gal A, Hübner CA. Mice with a targeted disruption of the Cl-/HCO3- exchanger AE3 display a reduced seizure threshold. Molecular and Cellular Biology, 2006, 26: 182-91
- Rust MB, Faulhaber J, Budack M, Pfeffer C, Maritzen T, Didié M, Beck FX, Boettger T, Schubert R, Ehmke H, Jentsch TJ, Hübner CA. Neurogenic mechanisms contribute to hypertension in mice with disruption of the K-Cl-cotransporter KCC3. Circulation Research, im Druck
