All Outputs (2)

The family-specific ?4-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 ?4-helix of the kinesin-13, MCAK, is critical to microtubule end recognition. Open Biology, 6(10), Article 160223. https://doi.org/10.1098/rsob.160223

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 about The family-specific ?4-helix of the kinesin-13, MCAK, is critical to microtubule end recognition.

Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD (2016)
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, 12(7), 1094-1104. https://doi.org/10.1080/15548627.2016.1170257

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 about Defective recognition of LC3B by mutant SQSTM1/p62 implicates impairment of autophagy as a pathogenic mechanism in ALS-FTLD.