Search Results - "Baptista, Melisa"

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    Mutant SOD1 alters the motor neuronal transcriptome: implications for familial ALS by Kirby, Janine, Halligan, Eugene, Baptista, Melisa J., Allen, Simon, Heath, Paul R., Holden, Hazel, Barber, Sian C., Loynes, Catherine A., Wood-Allum, Clare A., Lunec, Joseph, Shaw, Pamela J.

    Published in Brain (London, England : 1878) (01-07-2005)
    “…Familial amyotrophic lateral sclerosis (FALS) is caused, in 20% of cases, by mutations in the Cu/Zn superoxide dismutase gene (SOD1). Although motor neuron…”
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    Co‐ordinate transcriptional regulation of dopamine synthesis genes by α‐synuclein in human neuroblastoma cell lines by Baptista, Melisa J., O'Farrell, Casey, Daya, Sneha, Ahmad, Rili, Miller, David W., Hardy, John, Farrer, Matthew J., Cookson, Mark R.

    Published in Journal of neurochemistry (01-05-2003)
    “…Abnormal accumulation of α‐synuclein in Lewy bodies is a neuropathological hallmark of both sporadic and familial Parkinson's disease (PD). Although mutations…”
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    Microarray analysis reveals induction of heat shock proteins mRNAs by the torsion dystonia protein, TorsinA by Baptista, Melisa J., O'Farrell, Casey, Hardy, John, Cookson, Mark R.

    Published in Neuroscience letters (29-05-2003)
    “…An in-frame deletion (ΔE302/303) in the TorsinA gene has been demonstrated to be responsible for primary torsion dystonia, showing dominant inheritance with…”
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    Parkin and alpha-synuclein: opponent actions in the pathogenesis of Parkinson's disease by Baptista, Melisa J, Cookson, Mark R, Miller, David W

    Published in The Neuroscientist (Baltimore, Md.) (01-02-2004)
    “…Dominant mutations in the gene for alpha-synuclein, a small presynaptic protein, can cause Parkinson's disease. Although there is still substantial debate…”
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    Heterotrisomy, a significant contributing factor to ventricular septal defect associated with Down syndrome? by BAPTISTA, Melisa J, FAIRBROTHER, Una L, KESSLING, Anna M, HOWARD, Catherine M, FARRER, Matthew J, DAVIES, Gail E, TRIKKA, Dimitra, MARATOU, Klio, REDINGTON, Andrew, GREVE, Gottfried, NJØLSTAD, Pal Rasmus

    Published in Human genetics (01-11-2000)
    “…Down syndrome (DS; trisomy 21) is associated with a wide range of variable clinical features, one of the most common being congenital heart defects (CHD). We…”
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    Parkin Protects against the Toxicity Associated with Mutant α-Synuclein: Proteasome Dysfunction Selectively Affects Catecholaminergic Neurons by Petrucelli, Leonard, O'Farrell, Casey, Lockhart, Paul J., Baptista, Melisa, Kehoe, Kathryn, Vink, Liselot, Choi, Peter, Wolozin, Benjamin, Farrer, Matthew, Hardy, John, Cookson, Mark R.

    Published in Neuron (Cambridge, Mass.) (19-12-2002)
    “…One hypothesis for the etiology of Parkinson's disease (PD) is that subsets of neurons are vulnerable to a failure in proteasome-mediated protein turnover…”
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    Parkin and -Synuclein: Opponent Actions in The Pathogenesis of Parkinson’S Disease by Baptista, Melisa J., Cookson, Mark R., Miller, David W.

    Published in The Neuroscientist (Baltimore, Md.) (01-02-2004)
    “…Dominant mutations in the gene for •-synuclein, a small presynaptic protein, can cause Parkinson’s disease. Although there is still substantial debate about…”
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    An In Vitro Model of Parkinson's Disease: Linking Mitochondrial Impairment to Altered alpha -Synuclein Metabolism and Oxidative Damage by Sherer, Todd B, Betarbet, Ranjita, Stout, Amy K, Lund, Serena, Baptista, Melisa, Panov, Alexander V, Cookson, Mark R, Greenamyre, J. Timothy

    Published in The Journal of neuroscience (15-08-2002)
    “…Chronic systemic complex I inhibition caused by rotenone exposure induces features of Parkinson's disease (PD) in rats, including selective nigrostriatal…”
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    Parkin and &b.alpha; -Synuclein: Opponent Actions in The Pathogenesis of Parkinson'S Disease by Baptista, Melisa J, Cookson, Mark R, Miller, David W

    Published in The Neuroscientist (Baltimore, Md.) (01-02-2004)
    “…Dominant mutations in the gene for times -synuclein, a small presynaptic protein, can cause Parkinson's disease. Although there is still substantial debate…”
    Get full text
    Journal Article
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