Cpd-1 Null Mice Display a Subtle Neurological Phenotype

Kular, Rupinder; Gogliotti, Rocky G.; Opal, Puneet

doi:10.1371/journal.pone.0012649

Cited by 6 publications

(9 citation statements)

References 28 publications

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“…Consistent with previous results in mixed-bred populations [27], [28], the C57BL/6-congenic Anp32e deficiency segregated at normal Mendelian ratios (Table S1). At ages between 16–20 weeks old, we performed an array of established motor tests.…”

Section: Resultssupporting

confidence: 91%

“…Mice homozygous for the targeted allele demonstrated no motor deficiency in qualitative analysis or in an accelerating rotorod analysis [27]. The “gene-trapped” allele carrying a “β-Geo” promoter trap insertion in intron 3, on the other hand, was analysed more thoroughly for movement disorders and was likewise normal in accelerating rotorod behaviour but had subtle phenotypes in balance beam and limb-clasp testing [28].…”

Section: Introductionmentioning

confidence: 99%

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Targeted ANP32E Mutant Mice Do Not Demonstrate Obvious Movement Defects

et al. 2013

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BackgroundThe ANP32 family of proteins have been implicated in neuronal function through biochemical and cellular biology studies in neurons, as well as by recent behavioural studies of a gene-trapped loss-of-function mutation of Anp32e in mice, particularly with respect to fine motor function. A second targeted allele of the Anp32e, however, did not appear to demonstrate neurological phenotypes.Methodology/Principal FindingsUsing a stringently controlled cohort of ten-generation backcrossed, co-caged, sex-matched, littermate pairs, we assayed for potential motor defects in the targeted ANP32E-deficient mice. We found no phenotypic difference in any assays.ConclusionSince it is unlikely that the gene-trap is a more complete loss-of-function, our results suggest that ANP32E has no appreciable effect on motor functions and that genetic background differences most likely account for the gene-trap phenomena.

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Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Targeted ANP32E Mutant Mice Do Not Demonstrate Obvious Movement Defects

et al. 2013

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“…The rat pheochromocytoma PC12 cell line was grown in Dulbecco's modified Eagle's medium containing 8% horse serum and 8% fetal bovine serum (FBS) (Kular et al, 2010). PC12 cells were induced to differentiate and extend neurites by the addition of 100 ng/ml Nerve Growth Factor (NGF; Sigma) and by reducing the serum in the media (1% FBS and no horse serum).…”

Section: Methodsmentioning

confidence: 99%

“…Mice were placed on the rotating rod (Ugo Basile) which accelerates from 4 rpm to 40 rpm for the first 5 min followed by constant speed of 40 rpm (Kular et al, 2010). The time it takes for a mouse to fall off the rotating rod is noted to a maximum of 10 min (the duration of each run).…”

Section: Methodsmentioning

confidence: 99%

LANP mediates neuritic pathology in Spinocerebellar ataxia type 1

Cvetanović

Kular

Opal

2012

Neurobiology of Disease

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Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disease that results from a pathogenic glutamine-repeat expansion in the protein ataxin-1 (ATXN1). Although the functions of ATXN1 are still largely unknown, there is evidence to suggest that ATXN1 plays a role in regulating gene expression, the earliest process known to go awry in SCA1 mouse models. In this study, we show that ATXN1 reduces histone acetylation, a post-translational modification of histones associated with enhanced transcription, and represses histone acetyl transferase-mediated transcription. In addition, we find that depleting the Leucine-rich Acidic Nuclear Protein (LANP)—an ATXN1 binding inhibitor of histone acetylation—reverses aspects of SCA1 neuritic pathology.

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“…ANP32c or ppr32-1 belongs to a family of highly conserved leucine-rich acidic nucleoproteins (LANP) family of genes (Kular et al 2010). The other well-known member of this family of gene is ANP32b (pp32), known to be associated with inhibition of histone acetylation and is an inhibitor of protein phosphatase 2A (Munemasa et al 2008).…”

Section: Discussionmentioning

confidence: 99%

Differential Display RT-PCR Reveals Genes Associated with Lithium-Induced Neuritogenesis in SK-N-MC Cells

Italia¹,

Mukhopadhyaya

Rajadhyaksha³

2011

Cell Mol Neurobiol

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Lithium is shown to be neurotrophic and protective against variety of environmental stresses both in vitro as well as in vivo. In view of the wider clinical applications, it is necessary to examine alterations in levels of expression of genes affected by lithium. Lithium induces neuritogenesis in human neuroblastoma cell line SK-N-MC. Our aim was to elucidate genes involved in lithium-induced neuritogenesis using SK-N-MC cells. The differential display reverse transcriptase polymerase chain reaction (DD-RT-PCR) technique was used to study gene expression profiles in SK-N-MC cells undergoing lithium-induced neuritogenesis. Differential expression of genes in control and lithium (2.5 mM, 24 h)-treated cells was compared by display of cDNAs generated by reverse transcription of mRNA followed by PCR using arbitrary primers. Expression of four genes was altered in lithium-treated cells. Real-time PCR was done to confirm the levels of expression of each of these genes using specific primers. Lithium significantly up-regulated NCAM, a molecule known to stimulate neuritogenesis, occludin, a molecule participating in tight junctions and PKD2, a molecule known to modulate calcium transport. ANP 32c, a gene whose function is not fully known yet, was found to be down-regulated by lithium. This is the first report demonstrating altered levels of expression of these genes in lithium-induced neuritogenesis and contributes four hitherto unreported candidates possibly involved in the process.

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Cpd-1 Null Mice Display a Subtle Neurological Phenotype

Cited by 6 publications

References 28 publications

Targeted ANP32E Mutant Mice Do Not Demonstrate Obvious Movement Defects

Targeted ANP32E Mutant Mice Do Not Demonstrate Obvious Movement Defects

LANP mediates neuritic pathology in Spinocerebellar ataxia type 1

Differential Display RT-PCR Reveals Genes Associated with Lithium-Induced Neuritogenesis in SK-N-MC Cells

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