N(epsilon)-(gamma-L-glutamyl)-L-lysine (GGEL) is increased in cerebrospinal fluid of patients with Huntington's disease.

@article{Jeitner2001NepsilongammaLglutamylLlysineI,
  title={N(epsilon)-(gamma-L-glutamyl)-L-lysine (GGEL) is increased in cerebrospinal fluid of patients with Huntington's disease.},
  author={Thomas M. Jeitner and Mikhail B. Bogdanov and Wayne R. Matson and Yevgeny Daikhin and Marc Yudkoff and John E. Folk and Lawrence Steinman and Susan E. Browne and Myron Flint Beal and John P. Blass and Arthur J. L. Cooper},
  journal={Journal of neurochemistry},
  year={2001},
  volume={79 5},
  pages={1109-12}
}
Pathological-length polyglutamine (Q(n)) expansions, such as those that occur in the huntingtin protein (htt) in Huntington's disease (HD), are excellent substrates for tissue transglutaminase in vitro, and transglutaminase activity is increased in post-mortem HD brain. However, direct evidence for the participation of tissue transglutaminase (or other transglutaminases) in HD patients in vivo is scarce. We now report that levels of N(epsilon)-(gamma-L-glutamyl)-L-lysine (GGEL)--a 'marker… CONTINUE READING