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Muqit, M.M.K., Davidson, S.M., Smith, M.D.P., MacCormac, L.P., Kahns, S., Jensen, P.H., Wood, N.W. and Latchman, D.S. (2004) Parkin is recruited into aggresomes in a stress-specific manner: Over-expression of parkin reduces aggresome formation but can be dissociated from parkin’s effect on neuronal survival. Human Molecular Genetics, 13, 117-135. doi:10.1093/hmg/ddh012

has been cited by the following article:

• TITLE: Tyrosine hydroxylase and Lewy body molecules immunoreactivity in the SNC neurons of an AS/AGU mutantrat

  AUTHORS: A. G. Al-Kushi, D. Russell, A. P. Payne

  KEYWORDS: PKC-Gamma; Tyrosine Hydroxylase;Ubiquitin; Parkin

  JOURNAL NAME: World Journal of Neuroscience, Vol.2 No.3, August 23, 2012

  ABSTRACT: The AS/AGU rat has a recessive single point mutation in the gene coding for the gamma isoform of protein kinase C (PKC-γ) resulting in a failure to release dopamine in the striatum and impaired movement including a staggering gait, difficulty in initiating movement and a slight whole body tremor. This study examined the levels tyrosine hydroxylase, ubiquitin and parkin in individual SNC cell bodies, there was no evidence of a reduction in tyrosine hydroxylase levels although levels of ubiquitin and parkin were elevated in the cytoplasm. The findings support the hypothesis that the initial bar to dopamine availability in the striatum is reduced release, with substantia nigra cell death being a later phenomenon.