Atp6ap2 deletion causes extensive vacuolation that consumes the insulin content of pancreatic beta cells
Katrina J Binger, Martin Neukam, Sudhir Gopal Tattikota, Fatimunnisa Qadri, Dmytro Puchkov, Diana M Willmes, Sabrina Wurmsee, Sabrina Geisberger, Ralf Dechend, Klemens Raile, Thomas Kurth, Genevieve Nguyen, Matthew N Poy, Michele Solimena, Dominik N Muller, Andreas L Birkenfeld
Proceedings of the National Academy of Sciences | NATL ACAD SCIENCES | Published : 2019
Awarded by Australian National Health Medical Research Council (NHMRC) fellowship
Awarded by German Research Foundation
Awarded by German Research Foundation (DFG)
Awarded by German-Israeli Foundation
We thank Jana Czychi, Ilona Kamer, Francesca Spagnoli, and Thomas Rathjen (all MDC-Berlin), Prof. Gil Leibowitz (The Hebrew University of Jerusalem), Prof. Paul Gleeson (The University of Melbourne), and Anthony Rousselle for generously providing the Atp6ap2flox/+; R26YFPflox/flox mice (MDC-Berlin). K.J.B. was funded for this study by an Australian National Health Medical Research Council (NHMRC) fellowship (APP1037633). A.L.B. and D.M.W. were supported by the German Research Foundation (BI1292/4-2, BI1292/9-1, BI1292/10-1, BI1292/12-1, and IRTG2251). D.N.M. was supported by the German Research Foundation (DFG; 394046635 -SFB1365) and the German Center for Cardiovascular Research. M. N. was supported by a Dresden International Graduate School for Biomedicine and Bioengineering (DIGS-BB) PhD fellowship. M. S. was supported by the German Federal Ministry of Education and Research (BMBF) to the German Center for Diabetes Research and by the German-Israeli Foundation (I-1429-201.2/2017).