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The family-specific α4-helix of the kinesin-13, MCAK, is critical to microtubule end recognition (2016)
Journal Article
Patel, J. T., Belsham, H. R., Rathbone, A. J., Wickstead, B., Gell, C., & Friel, C. T. (2016). The family-specific α4-helix of the kinesin-13, MCAK, is critical to microtubule end recognition. Open Biology, 6(10), doi:10.1098/rsob.160223. ISSN 2046-2441

Kinesins that influence the dynamics of microtubule growth and shrinkage require the ability to distinguish between the microtubule end and the microtubule lattice. The microtubule depolymerizing kinesin MCAK has been shown to specifically recognize... Read More

Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD
Journal Article
Goode, A., Butler, K., Long, J., Cavey, J., Scott, D., Shaw, B., …Layfield, R. (2016). Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD. Autophagy, ISSN 1554-8627

Growing evidence implicates impairment of autophagy as a candidate pathogenic mechanism in the spectrum of neurodegenerative disorders which includes amyotrophic lateral sclerosis and frontotemporal lobar degeneration (ALS-FTLD). SQSTM1, which encode... Read More