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Items: 1 to 20 of 96

1.

Characterizing pathogenic processes in Batten disease: use of small eukaryotic model systems.

Phillips SN, Muzaffar N, Codlin S, Korey CA, Taschner PE, de Voer G, Mole SE, Pearce DA.

Biochim Biophys Acta. 2006 Oct;1762(10):906-19. Epub 2006 Sep 1. Review.

2.

Caenorhabditis elegans homologues of the CLN3 gene, mutated in juvenile neuronal ceroid lipofuscinosis.

De Voer G, Jansen G, van Ommen GJ, Peters DJ, Taschner PE.

Eur J Paediatr Neurol. 2001;5 Suppl A:115-20.

PMID:
11588981
4.

Experimental models of NCL: the yeast model.

Pearce DA.

Adv Genet. 2001;45:205-16. Review. No abstract available.

PMID:
11332774
5.

Cross-species homology of the CLN3 gene.

Taschner PE, de Vos N, Breuning MH.

Neuropediatrics. 1997 Feb;28(1):18-20.

PMID:
9151313
7.

btn1, the Schizosaccharomyces pombe homologue of the human Batten disease gene CLN3, regulates vacuole homeostasis.

Gachet Y, Codlin S, Hyams JS, Mole SE.

J Cell Sci. 2005 Dec 1;118(Pt 23):5525-36. Epub 2005 Nov 15.

9.

The subcellular location of the yeast Saccharomyces cerevisiae homologue of the protein defective in the juvenile form of Batten disease.

Croopnick JB, Choi HC, Mueller DM.

Biochem Biophys Res Commun. 1998 Sep 18;250(2):335-41.

PMID:
9753630
10.

Bacteria, yeast, worms, and flies: exploiting simple model organisms to investigate human mitochondrial diseases.

Rea SL, Graham BH, Nakamaru-Ogiso E, Kar A, Falk MJ.

Dev Disabil Res Rev. 2010;16(2):200-18. doi: 10.1002/ddrr.114. Review.

11.
12.

Myb-related Schizosaccharomyces pombe cdc5p is structurally and functionally conserved in eukaryotes.

Ohi R, Feoktistova A, McCann S, Valentine V, Look AT, Lipsick JS, Gould KL.

Mol Cell Biol. 1998 Jul;18(7):4097-108. Erratum in: Mol Cell Biol 1998 Oct;18(10):6164.

13.

Genetic basis and phenotypic correlations of the neuronal ceroid lipofusinoses.

Warrier V, Vieira M, Mole SE.

Biochim Biophys Acta. 2013 Nov;1832(11):1827-30. doi: 10.1016/j.bbadis.2013.03.017. Epub 2013 Mar 28. Review.

14.
15.

Deletion of btn1, an orthologue of CLN3, increases glycolysis and perturbs amino acid metabolism in the fission yeast model of Batten disease.

Pears MR, Codlin S, Haines RL, White IJ, Mortishire-Smith RJ, Mole SE, Griffin JL.

Mol Biosyst. 2010 Jun;6(6):1093-102. doi: 10.1039/b915670d. Epub 2010 Mar 17.

PMID:
20485751
16.

Neurodegenerative diseases: Lessons from genome-wide screens in small model organisms.

van Ham TJ, Breitling R, Swertz MA, Nollen EA.

EMBO Mol Med. 2009 Nov;1(8-9):360-70. doi: 10.1002/emmm.200900051. Review.

17.

Genomic structure of three CLN3-like genes in Caenorhabditis elegans.

Mitchell WA, Porter M, Kuwabara P, Mole SE.

Eur J Paediatr Neurol. 2001;5 Suppl A:121-5.

PMID:
11588982
18.

Bioinformatic perspectives in the neuronal ceroid lipofuscinoses.

Kmoch S, Stránecký V, Emes RD, Mitchison HM.

Biochim Biophys Acta. 2013 Nov;1832(11):1831-41. doi: 10.1016/j.bbadis.2012.12.010. Epub 2012 Dec 26. Review.

19.

The function of CLN3P, the Batten disease protein.

Rakheja D, Narayan SB, Bennett MJ.

Mol Genet Metab. 2008 Mar;93(3):269-74. Review. No abstract available. Erratum in: Mol Genet Metab. 2008 Jun;94(2):270.

PMID:
18688960
20.

Cathepsin D-deficient Drosophila recapitulate the key features of neuronal ceroid lipofuscinoses.

Myllykangas L, Tyynelä J, Page-McCaw A, Rubin GM, Haltia MJ, Feany MB.

Neurobiol Dis. 2005 Jun-Jul;19(1-2):194-9.

PMID:
15837574

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