David Nicholls, senior advisor
David Nicholls is one of three senior researchers in within LUDC. Davids main research base at the Buck Institute for Research on Aging, Novato (near San Fransisco). David was one of the founding Faculty there and since 2008 have continued on a part-time basis, spending 3-4 months a year at the bench developing techniques for investigating mitochondrial bioenergetics in intact cells. You can find out more about David on the Buck website http://www.buckinstitute.org/nichollsLab.
For the remaining part of the year David is based in Lund and have a part-time position with the LUDC. Davids career has been devoted to mitochondrial bioenergetics, with an emphasis at different times on chemiosmotic coupling of ATP synthesis (David co-author the standard textbook on the subject and is currently writing the 4th edition), brown fat metabolism (uncoupling protein 1), calcium transport, exocytosis from synaptosomes (isolated nerve terminals), neuronal bioenergetics and most recently mitochondrial control of plasma membrane potential and clacium channels in insulinoma cell lines.
This last David is investigating at the Buck and in LUDC in collaboration with Hindrik´s group.
David has helped to establish the Seahorse technology in LUDC to monitor cell function, together with a range of live-cell confocal fluorescent imaging techniques (plasma membrane potential, mitochondrial membrane potential, cytoplasmic Ca2+ etc).
David also help to run bioenergetic teaching courses around the world.
David is happy to help and collaborate with any group within the LUDC. Feel free to contact his using the Buch email
dnicholls [at] buckinstitute.org
Retrieved from Lund University's publications database
- A lipotoxicity model in the INS-1 832/13 beta cell line and the epigenetic alterations induced by it
- Mitochondrial ion circuits.
- Stochastic aspects of transmitter release and bioenergetic dysfunction in isolated nerve terminals
- The membrane potential response is altered in pancreatic beta cells chronically exposed to high glucose
- Differences in metabolic regulation between glucose responsive INS-1 832/13 and its glucose non-responsive INS-1 832/2 sister clonal rat beta cell line decides their beta cell functionality
- Mitochondrial spare respiratory capacity and the life and death of neurons
- Spare respiratory capacity, oxidative stress and excitotoxicity
- Tight coupling between glucose and mitochondrial metabolism in clonal beta-cells is required for robust insulin secretion.