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About me

I have a background in growth plate biology from my PhD at the University of Manchester and Roslin Institute (Edinburgh, UK), and read Biochemistry as an undergraduate at University College London. I am currently working as a postdoctoral researcher with Professor Lars Sävendahl (Department of Women's and Children's Health) and Asst. Professor Andrei Chagin (Department of Physiology and Pharmacology).

Research description

The growth plate is a very interesting tissue. It is made up of highly organised columns of cells (chondrocytes) which participate in causing the growth of our long bones. Long-bone growth is very important as it ultimately determines how tall we become. This process must be very tightly controlled so that our bones continue to grow in proportion to each other and so that we grow similarly to our peers.

My research aims to understand the fundamental aspects of long-bone growth at the cellular level and to unravel in more details what signaling pathways control our final height. By coupling clinical samples with basic research at the lab bench we endeavour to have a patient-oriented approach.

Selected publications:

Pharmacological inhibition of lysosomes activates the mTORC1 signaling pathway in chondrocytes in an autophagy-independent manner

Phillip T Newton, Karuna K Vuppalapati, Thibault Bouderlique, and Andrei S Chagin; Autophagy (2015).

Chondrogenic ATDC5 cells: An optimised model for rapid and physiological matrix mineralisation

Phillip T. Newton, Katherine A. Staines, Lyudmila Spevak, Adele L. Boskey, Cristina C. Teixeira, Vicky E. MacRae, Ann E. Canfield, Colin Farquharson; International Journal of Molecular Medicine (2012).

Targeted deletion of autophagy genes Atg5 or Atg7 in the chondrocytes impairs cell viability and inhibits skeletal growth.

Karuna K Vuppalapati, Thibault Bouderlique, Vitaliy O Kaminskyy, Phillip Newton, Henrik Wehtje, Lars Sävendahl, Boris Zhivotovsky and Andrei S Chagin; Journal of Bone and Mineral Research, J. Am. Soc. Bone Miner. Res. (2015).

Targeted deletion of Atg5 in chondrocytes promotes age-related osteoarthritis.

Thibault Bouderlique, Karuna K Vuppalapati, Phillip T Newton, Lei Li, Björn Barenius, Andrei S Chagin; Ann. Rheum (2015).

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