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  • 1
    Electronic Resource
    Electronic Resource
    Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease (1999)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 399 (1999), S. 263-267 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Huntington's disease is an autosomal-dominant progressive neurodegenerative disorder resulting in specific neuronal loss and dysfunction in the striatum and cortex. The disease is universally fatal, with a mean survival following onset of 15–20 years and, at present, there is no ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/20446
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  • 2
    Electronic Resource
    Electronic Resource
    Genomic structure of human anion exchanger 3 and its potential role in hereditary neurological disease (1998)
    Springer
    Neurogenetics 1 (1998), S. 289-292 
    Details
    ISSN: 1364-6753
    Keywords: Key words Anion exchanger ; Genomic structure ; Paroxysmal dyskinesia ; Polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: ABSTRACT Alterations in ion channel permeability or selectivity have been shown to cause neurological defects in humans. Anion exchanger isoform 3 (AE3) is prominently expressed in the brain and performs an electroneutral exchange of chloride and bicarbonate ions. In order to study the potential role of AE3 in human neurological disease, we characterized AE3 genomic structure and performed mutational analysis on patients with an episodic movement disorder that maps to the same genetic locus. AE3 genomic organization, including the nucleotide sequence of the 5′-untranslated region and intron/exon boundaries, is highly conserved between humans and homologs from mouse and rat. Mutational analysis revealed no disease-causing defect in patients with familial paroxysmal dyskinesia, although several benign polymorphisms were identified. AE3 variation may prove useful for further genetic studies, such as finer resolution mapping. Characterization of genomic structure will facilitate mutational analysis of AE3 in studies of neurological diseases mapped to the same locus.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100480050043
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  • 3
    Electronic Resource
    Electronic Resource
    Functional evidence for a role of combined CDKN2A (p16-p14ARF)/CDKN2B (p15) gene inactivation in malignant gliomas (1999)
    Springer
    Acta neuropathologica 98 (1999), S. 444-452 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glioblastoma ; p16 ; p15 ; p14ARF ; Tetracycline-controlled operator
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Homozygous chromosome 9p deletions in gliomas commonly include the CDKN2A and CDKN2B genes, which code for the structurally highly homologous cdk inhibitors/tumor suppressors p16 and p15, respectively. Alternative splicing of the CDKN2A gene results in the expression of p14ARF. Interestingly, not only p16 and p15, but also the structurally unrelated p14ARF appear to function as negative cell cycle regulators. Concerted inactivation of p16, p15 and p14ARF could be demonstrated in seven of nine glioblastoma cell lines. Strong suppression of tumorigenicity after transfection with p16 and p15 alone or in combination was seen in cell lines containing neither endogenous p16 nor p15 but functional pRB. Significantly weaker growth suppression was observed in tumors either retaining expression of both p16 and p15 or p15 only. p14ARF proved to be a potent tumor suppressor in the presence of wild-type p53, while mutant p53 substantially reduced growth inhibition by p14ARF. No differences between p16 and p15 effects could be observed, suggesting a largely overlapping function of p16 and p15. To facilitate further research into p16/p15 effects, three cell lines with conditional, tetracycline-controlled p16 expression were established. Reversible growth suppression mediated by p16 was observed in these models. Combined inactivation of CDKN2A and CDKN2B, i.e., loss of both p16 and p15 as well as p14ARF, results in disruption of two major growth control pathways involving pRB and p53 in malignant gliomas. Therefore, homozygous co-deletions of CDKN2A and CDKN2B rather than mutations targeting individual transcripts are frequently selected for in these tumors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010051107
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition of angiogenesis and growth of human non-malignant and malignant meningiomas by TNP-470 (1995)
    Springer
    Journal of neuro-oncology 23 (1995), S. 23-29 
    Details
    ISSN: 1573-7373
    Keywords: meningioma ; angiogenesis ; tumor growth ; metastasis ; TNP-470, AGM-1470
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Meningiomas are relatively common (22%) vascular brain tumors. 3–11% of meningiomas are malignant, and defy currently available therapy. Inhibition of neovascularization is one potential strategy for treating these hypervascular tumors. Inhibition of tumor-induced angiogenesis by TNP-470 (previously termed AGM-1470), a synthetic analogue of fumagillin, was tested on the growth of human non-malignant and malignant meningiomas in nude mice. TNP-470 significantly inhibited tumor neovascularization and tumor growth of both non-malignant and malignant meningiomas. TNP-470 is now in human trial and should be tested for efficacy in treating malignant or recurrent aggressive meningiomas.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01058456
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  • 5
    Electronic Resource
    Electronic Resource
    Cloning and characterization of murine Aqp5: evidence for a conserved aquaporin gene cluster (1999)
    Springer
    Mammalian genome 10 (1999), S. 498-505 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Aquaporin 5 (Aqp5), a member of the aquaporin family of membrane water channels, is thought to modulate the osmolality of fluids in the eye, lung, and salivary gland. Here, we report the cloning and genomic characterization of murine Aqp5 and its expression in relevant mouse tissues. This gene, comprised of four exons encoding 265 amino acids (121, 55, 28, and 61 amino acids respectively), is transcribed into an approximate 1.8-kb mRNA detected in lung, parotid, submandibular, sublingual, and lacrimal tissues. Aqp5 encodes a protein that is 98% identical to rat Aqp5. An Aqp5 antibody detects an approximately 27-kDa protein band in mouse lung, and an additional 29 kDa band in salivary gland. Cloning and physical mapping genomic fragments contiguous with Aqp5 revealed two other members of the aquaporin family: Aqp2 and Aqp6, arrayed head to tail in the order Aqp2–Aqp5–Aqp6, and provides evidence of a gene cluster conserved in order and orientation in both mice and humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003359901030
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    Paper (German National Licenses)
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