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Effect of obestatin, its N-terminal fragment and fragment analog Nt8U on mice epididymal tissue

ABSTRACT: mRNA profiling of epididymal tissue of mice treated with obestatin, its N-terminal fragment residues 1-13 and a N-terminal fragment analog Nt8U

ORGANISM(S): Mus musculus

PROVIDER: GSE35588 | GEO | 2012/02/08

SECONDARY ACCESSION(S): PRJNA152659

REPOSITORIES: GEO

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Effect of obestatin, its N-terminal fragment and fragment analog Nt8U on mice epididymal tissue

Project description:mRNA profiling of epididymal tissue of mice treated with obestatin, its N-terminal fragment residues 1-13 and a N-terminal fragment analog Nt8U Four groups of six mice each were placed in individual metabolic cages and acclamatised to fasting from 6AM to 6PM and ad libitum water. The mice were administered 80ng/kg of the respective peptides intraperitoneally for 8 days and the epididymal tissue was subjected to mRNA extraction and microarray analysis.

2012-02-08 | E-GEOD-35588 | biostudies-arrayexpress

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Project description:Neuroligins (NLGNs) are one of the autism susceptibility genes, however, the mechanism that how dysfunction of NLGNs leads to Autism remains unclear. More and more studies have shown that the transcriptome alteration may be one of the important factors to generate Autism. Therefore, we are very concerned about whether Neuroligins would affect transcriptional regulation, which may at last lead to Autism. As a single-transmembrane receptor, proteolytic cleavage is one of the most important posttranslational modifications of NLGN proteins. In this study, we demonstrated the existence of DNlg3 C-terminal fragment. Studies in the S2 cells and 293T cells showed the evidence for nuclear access of the DNlg3 C-terminal fragment. Then we identified the possible targets of DNlg3 C-terminal fragment after its nuclear access by RNA-seq. The bioinformatics analysis indicated the transcriptome alteration between dnlg3 null flies and wild type flies focused on genes for the innate immune responses. These results were consistent with the infection hypotheses for autism. Our study revealed the nuclear access ability of DNlg3 c-terminal fragment and its possible function in transcriptional regulation of the innate immune response genes. This work provides the new links between synaptic adhesion molecule NLGNs and immune activation, which may help us to get a deeper understanding on the relationship between NLGNs and Autism.

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Effects of polyglutamine expansion and subcellular localization of C-terminal fragment of Cav2.1 in PC12 rat pheochromocytoma cells

Project description:Polyglutamine(polyQ) expansion of ?1A voltage-dependent calcium channel (Cav2.1) is the causative mutation of spinocerebellar ataxia type 6 (SCA6). The C-terminal fragment (CTF) of Cav2.1 makes aggregates in the cytoplasm of SCA6 Purkinje cells and may relate to the pathogenesis. In order to identify genes associated with polyQ expansion and subcellular localization of CTF, we analyzed gene expression profiles of PC12 rat pheochromocytoma cells using Tet-off system. We exmined gene expression profiles of Tet-off PC12 cells using the following four recombinant C-terminal fragments (rCTFs): rCTF-Q13-NLS, rCTF-Q13-NES, rCTF-Q28-NLS and rCTF-Q28-NES. We obtained gene expression data of both Dox (+) and Dox (-) conditions for each CTF. All assays were performed in duplicate.

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Effects of polyglutamine expansion and subcellular localization of C-terminal fragment of Cav2.1 in PC12 rat pheochromocytoma cells

Project description:Polyglutamine(polyQ) expansion of α1A voltage-dependent calcium channel (Cav2.1) is the causative mutation of spinocerebellar ataxia type 6 (SCA6). The C-terminal fragment (CTF) of Cav2.1 makes aggregates in the cytoplasm of SCA6 Purkinje cells and may relate to the pathogenesis. In order to identify genes associated with polyQ expansion and subcellular localization of CTF, we analyzed gene expression profiles of PC12 rat pheochromocytoma cells using Tet-off system.

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Project description:This study assessed the effects of amino terminal ApoE4 fragments (residues 1-151) on modulating the transcriptome of BV2 microglial cells. Treatment with amino terminal ApoE4 fragments caused the upregulation of nearly four-thousand genes, and further analysis revealed a significant upregulation of genes related to the inflammatory immune response. As a control, an amino terminal ApoE3 fragment was tested and produced a similar but reduced level of upregulation of an identical set of genes. This set of genes affected pathways including Toll receptor signaling, chemokine/cytokine signaling and apoptosis signaling. Additionally, each treatment regulated a unique set of genes. Amino terminal ApoE3 fragments uniquely regulated 14 times as many genes (1,674), many of which are involved in physiological functions within microglia. Amino terminal ApoE4 fragments uniquely upregulated 119 genes, with many of the top upregulated genes having unknown functions. Our results suggest that while amino terminal ApoE3 fragments may serve a more physiological role in microglia amino terminal ApoE4 fragments may activate genes with a more pathological purpose. These data support the hypothesis that the link between harboring the APOE4 allele and dementia risk could be enhanced inflammation through activation of microglia.

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