Prof Martin Lowe BSc, PhD

Professor

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Research interests

Membrane Traffic in the Secretory and Endocytic Pathways

Our research is focussed on membrane traffic and how defects in this fundamental process lead to disease. Our work can be split into 2 main areas: 1.) the structure and function of the Golgi apparatus; and 2.) regulation of membrane traffic in the endocytic pathway.

1.) The Golgi apparatus lies at the heart of the secretory pathway and plays a major role in the modification, sorting and trafficking of protein and lipid cargo molecules. Defects in these fundamental processes lead to numerous diseases and they are also important during infection by intracellular pathogens. Key players in Golgi structure and trafficking are the golgin family of coiled-coil proteins found on the cytoplasmic surface of the Golgi membrane. We are currently investigating the mechanisms by which members of this family contribute to Golgi function in healthy cells, as well as how their loss leads to pathological changes at the cellular and organismal level. We are also interested in identifying Golgi-associated proteins that regulate mitosis, since this process is often defective in cancer.

2.) We are studying how membrane traffic in the endocytic pathway is regulated. Endocytosis is the process by which cells internalise many proteins such as growth factors and hormones, and is important for a variety of cellular functions including growth factor signalling. We are particularly interested in two lipid metabolising enzymes that are located on endosomes, called INPP5B and OCRL1. Mutation of OCRL1 causes the rare X-linked disorder known as Lowe syndrome, which is characterised by defects in the central nervous system, eyes and kidneys. We are investigating how INPP5B and OCRL1 regulate endocytic trafficking and how loss of OCRL1 leads to the symptoms of Lowe syndrome, using both mammalian cell culture and zebrafish embryo model systems.  

 

Projects

Research and projects

No current projects are available for public display