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Professor Rob Layfield's Outputs (3)

Contribution of Ref(2)p to regulation of Drosophila notum epithelial cell apico-basal polarity and phenotype (2015)
Presentation / Conference Contribution
Shohayeb, B., Georgiou, M., & Layfield, R. Contribution of Ref(2)p to regulation of Drosophila notum epithelial cell apico-basal polarity and phenotype. Presented at 78th Harden Conference: Protein Kinases in Health and Disease

Cell polarity impacts on the maintenance of cell shape, cell-cell junction integrity, and protrusion formation and dynamics. Further, polarity additionally regulates cell movement, proliferation and differentiation. Conversely when cells lose their p... Read More about Contribution of Ref(2)p to regulation of Drosophila notum epithelial cell apico-basal polarity and phenotype.

Ion mobility-mass spectrometry reveals conformational flexibility in the deubiquitinating enzyme USP5 (2015)
Journal Article
Scott, D., Layfield, R., & Oldham, N. J. (2015). Ion mobility-mass spectrometry reveals conformational flexibility in the deubiquitinating enzyme USP5. Proteomics, 15(16), https://doi.org/10.1002/pmic.201400457

Many proteins exhibit conformation flexibility as part of their biological function, whether through the presence of a series of well-defined states or by the existence of intrinsic disorder. Ion mobility spectrometry, in combination with MS (IM–MS),... Read More about Ion mobility-mass spectrometry reveals conformational flexibility in the deubiquitinating enzyme USP5.

Autophagy receptor defects and ALS-FTLD (2015)
Journal Article
Majchera, V., Goode, A., James, V., & Layfield, R. (2015). Autophagy receptor defects and ALS-FTLD. Molecular and Cellular Neuroscience, 66(A), 43-52. https://doi.org/10.1016/j.mcn.2015.01.002

Various pathophysiological mechanisms have been implicated in the ALS-FTLD clinicopathological spectrum of neurodegenerative disorders. Here we focus on the role of autophagy, an intracellular catabolic pathway, in these conditions. Growing evidence... Read More about Autophagy receptor defects and ALS-FTLD.