Unknown,Transcriptomics,Genomics,Proteomics

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Gene expression in wild type and mENT1 knock out mice

ABSTRACT: To investigate the functional importance of a nucleoside transporter, the mENT1 (Slc29a1) was knocked out in mice. The gene expression profile was compared between wildtype and mENT1 knock out mice in two tissues. RNA was isolated from heart and kidney from 3 mENT1 knockout and 3 wildtype (FVB/N) mice.Gene expression profiles were compared between the knockout and wild type tissues.

ORGANISM(S): Mus musculus

SUBMITTER: Kathryn Graham

PROVIDER: E-GEOD-22565 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Nucleoside transporter gene expression in wild-type and mENT1 knockout mice.

Graham Kathryn K Yao Sylvia S Johnson Lorelei L Mowles Delores D Ng Amy A Wilkinson Jodi J Young James D JD Cass Carol E CE

Biochemistry and cell biology = Biochimie et biologie cellulaire 20110401 2

Owing to the overlapping and redundant roles of the seven mammalian nucleoside transporters (NTs), which belong to two protein families (ENTs and CNTs), the physiological importance of individual NTs has been difficult to assess. Mice that have NT genes knocked out can be a valuable tool in gaining an understanding of the NT proteins. We have generated a strain of mice that is homozygous for a disruption mutation between exons 2 and 3 of the mouse equilibrative nucleoside transporter, mENT1. We ...[more]

PMID: 21455274

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Project description:Genomic radiation signature illuminates low-dose effects with sharply reflected transcriptome in Ptch1-deficient medulloblastomas. Cancer risks of low-dose radiation are of great concern especially in relation to rapidly increasing medical exposures; however, their accurate assessments cope with many challenges and difficulties, partly due to the inability to distinguish radiation-induced tumors from spontaneous ones. Here, we analyzed the dose-dependent effect of radiation on medulloblastoma development in Ptch1 heterozygous mice on C3B6F1 background. The incidence and latency of medulloblastoma increased and shortened with increasing radiation dose, respectively. Amazingly, radiation contributed to tumorigenesis even at 50 mGy and 100% of mice got medulloblastoma with 1.5 Gy. Loss of heterozygosity (LOH) analysis on a total of 164 tumors indicated that spontaneous tumors showed LOH in broad regions on chromosome 13, including Ptch1 and distally-extending telomeric portion (S-type). In contrast, tumors developed after 3 Gy irradiation exhibited interstitial losses around Ptch1 (R-type). A clear dose-dependent increase in the proportion of R-type tumor at intermediate doses suggested R-type to be a reliable radiation signature. Array-CGH analysis indicated the R-type-specific copy-number reduction around Ptch1 and LOH-type-independent frequent gains of whole chromosome 6. Integrated expression microarray analysis indicated that expression levels of many genes within the altered genomic regions faithfully reflected the genomic copy-number changes. Furthermore, it was also suggested that these expression changes in turn influenced on many other genes, such as Tgfb2 and Tgfb3, on widespread genomic regions. This is the first demonstration that radiation-induced tumors developed after low-dose irradiation can be characterized quite precisely by interstitial deletion of Ptch1 and by associated gene expression profile. Gene expression in 3 normal cerebellum tissues and 12 medulloblastomas was measured.

Dataset Information

Gene expression in wild type and mENT1 knock out mice

Publications

Nucleoside transporter gene expression in wild-type and mENT1 knockout mice.

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