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Journal Abstract Search

583 related items for PubMed ID: 23877479

  • 21.
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  • 22. Synapse alterations precede neuronal damage and storage pathology in a human cerebral organoid model of CLN3-juvenile neuronal ceroid lipofuscinosis.
    Gomez-Giro G, Arias-Fuenzalida J, Jarazo J, Zeuschner D, Ali M, Possemis N, Bolognin S, Halder R, Jäger C, Kuper WFE, van Hasselt PM, Zaehres H, Del Sol A, van der Putten H, Schöler HR, Schwamborn JC.
    Acta Neuropathol Commun; 2019 Dec 30; 7(1):222. PubMed ID: 31888773
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  • 23. Molecular mechanisms of the juvenile form of Batten disease: important role of MAPK signaling pathways (ERK1/ERK2, JNK and p38) in pathogenesis of the malady.
    Shematorova EK, Shpakovski DG, Chernysheva AD, Shpakovski GV.
    Biol Direct; 2018 Sep 25; 13(1):19. PubMed ID: 30621751
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  • 24. Strategy for mutation detection in CLN3: characterisation of two Finnish mutations.
    Munroe PB, O'Rawe AM, Mitchison HM, Järvelä IE, Santavuori P, Lerner TJ, Taschner PE, Gardiner RM, Mole SE.
    Neuropediatrics; 1997 Feb 25; 28(1):15-7. PubMed ID: 9151312
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  • 25. Altered arginine metabolism in the central nervous system (CNS) of the Cln3-/- mouse model of juvenile Batten disease.
    Chan CH, Ramirez-Montealegre D, Pearce DA.
    Neuropathol Appl Neurobiol; 2009 Apr 25; 35(2):189-207. PubMed ID: 19284480
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  • 29. A novel mutation af Cln3 associated with delayed-classic juvenile ceroid lipofuscinois and autophagic vacuolar myopathy.
    Licchetta L, Bisulli F, Fietz M, Valentino ML, Morbin M, Mostacci B, Oliver KL, Berkovic SF, Tinuper P.
    Eur J Med Genet; 2015 Oct 25; 58(10):540-4. PubMed ID: 26360874
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  • 30.
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  • 31. Deletion of the Caenorhabditis elegans homologues of the CLN3 gene, involved in human juvenile neuronal ceroid lipofuscinosis, causes a mild progeric phenotype.
    de Voer G, van der Bent P, Rodrigues AJ, van Ommen GJ, Peters DJ, Taschner PE.
    J Inherit Metab Dis; 2005 Oct 25; 28(6):1065-80. PubMed ID: 16435200
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  • 33. Glial cells are functionally impaired in juvenile neuronal ceroid lipofuscinosis and detrimental to neurons.
    Parviainen L, Dihanich S, Anderson GW, Wong AM, Brooks HR, Abeti R, Rezaie P, Lalli G, Pope S, Heales SJ, Mitchison HM, Williams BP, Cooper JD.
    Acta Neuropathol Commun; 2017 Oct 17; 5(1):74. PubMed ID: 29041969
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  • 34. First case of genetically confirmed CLN3 disease in Chinese with cDNA sequencing revealing pathogenicity of a novel splice site variant.
    Lau NKC, Ching CK, Lee HHC, Chak WKM, Kwan Shing N, Hanchard NA, Mak CM.
    Clin Chim Acta; 2018 Nov 17; 486():151-155. PubMed ID: 30053402
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  • 36. Altered gene expression in the eye of a mouse model for batten disease.
    Chattopadhyay S, Kingsley E, Serour A, Curran TM, Brooks AI, Pearce DA.
    Invest Ophthalmol Vis Sci; 2004 Sep 17; 45(9):2893-905. PubMed ID: 15326100
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  • 37. [From gene to disease; from CLN1, CLN2 and CLN3 to neuronal ceroid lipofuscinosis].
    Taschner PE, Losekoot M, Breuning MH, Hofman I, van Diggelen OP.
    Ned Tijdschr Geneeskd; 2005 Feb 05; 149(6):300-3. PubMed ID: 15730038
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  • 38. The Batten disease gene CLN3 confers resistance to endoplasmic reticulum stress induced by tunicamycin.
    Wu D, Liu J, Wu B, Tu B, Zhu W, Luo J.
    Biochem Biophys Res Commun; 2014 Apr 25; 447(1):115-20. PubMed ID: 24699413
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  • 39. Modulation of Kv4.2/KChIP3 interaction by the ceroid lipofuscinosis neuronal 3 protein CLN3.
    Seifert C, Storch S, Bähring R.
    J Biol Chem; 2020 Aug 21; 295(34):12099-12110. PubMed ID: 32641494
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  • 40. A novel deletion variant in CLN3 with highly variable expressivity is responsible for juvenile neuronal ceroid lipofuscinoses.
    Gilani N, Razmara E, Ozaslan M, Abdulzahra IK, Arzhang S, Tavasoli AR, Garshasbi M.
    Acta Neurol Belg; 2021 Jun 21; 121(3):737-748. PubMed ID: 33783722
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