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Displaying 20 of 21 results for "SLC2A2"
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  1. Integrative analysis of pathology, mRNA and microRNA in a polygenic diabetes model, NONcNZO10/LtJ mice ArrayExpress

    ID: E-GEOD-83241

    Description: sis (Slc30a8, Mt1 and Mt2) or glucose metabolism (Slc2a2) was suggested as being the candidate mechanism of pancreas failure in NONcNZO10/LtJ mice. These results demonstrate NONcNZO10/LtJ mice have a complex pathogenic mechanism of diabetes, and moreover, this fundamental information of NONcNZO10/LtJ mice would offer the opportunity for research and development of a novel antidiabetic drug. To identify the diabetes related genes that changed expression during the development of T2D in NONcNZO10/LtJ mice, we analyzed gene expression profiles of 7-, 13-, and 22-week old NONcNZO10/LtJ mice using GeneChip Mouse Gene 2.0 ST Arrays. On the other hand, we compared gene expres...

  2. Integrative analysis of pathology, mRNA and microRNA in a polygenic diabetes model, NONcNZO10/LtJ mice BioProject

    ID: PRJNA325351

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: sis (Slc30a8, Mt1 and Mt2) or glucose metabolism (Slc2a2) was suggested as being the candidate mechanism of pancreas failure in NONcNZO10/LtJ mice. These results demonstrate NONcNZO10/LtJ mice have a complex pathogenic mechanism of diabetes, and moreover, this fundamental information of NONcNZO10/LtJ mice would offer the opportunity for research and development of a novel antidiabetic drug. Overall design: To identify the diabetes related genes that changed expression during the development of T2D in NONcNZO10/LtJ mice, we analyzed gene expression profiles of 7-, 13-, and 22-week old NONcNZO10/LtJ mice using GeneChip Mouse Gene 2.0 ST Arrays. On the other hand, we comp...
  3. Pancreas-specific Sirt1-deficiency in mice compromises beta-cell function without development of hyperglycemia ArrayExpress

    ID: E-GEOD-67239

    Description: a decreased expression of the glucose transporter Slc2A2/Glut2 and of the Glucagon like peptide-1 receptor (Glp1r) as well as with a marked down regulation of endoplasmic reticulum (ER) chaperones that participate in the Unfolded Protein Response (UPR) pathway. Counter intuitively, the Sirt1-deficient mice did not develop hyperglycemia. Pancreatic polypeptide (PP) cells were the only other islet cells affected, with reduced numbers in the Sirt1-deficient pancreas. This study provides new mechanistic insights showing that beta-cell function in Sirt1-deficient pancreas is affected due to altered glucose sensing and deregulation of the UPR pathway. Interestingly, we uncover a context in which impaired beta-cell function is not accompanied by increased glycemia. This points to a unique compensatory mechanism. Given the reduction in PP, investigation of its role in the control of blood glucose is warranted. To uncover other Sirt1-regulated mechanisms, we performed a gene expression microarray ...

  4. Metabolic and gene expression changes induced by the naturally occurring deltaNp53 isoform link mTOR pathway and mitochondrial alterations to the prog... ArrayExpress

    ID: E-GEOD-37271

    Description: P3K1, FGF5) and regulators of glucose metabolism (SLC2A2, CRYAB, LRCH1). Expression of other key metabolic genes were also altered in cells expressing ΔNp53:WTp53 tetramers, suggesting that global me tabolic changes might contribute to ΔNp53:WTp53 pathology. In collaboration with Metabolon (Durham, NC), we identified approximately one hundred metabolites that were significantly up- or down-regulated in H1299 cells expressing ΔNp53:WTp53. The metabolome analysis was a powerful complement to the gene expression data, and further suggested that the mTOR pathway (e.g. across-the-board up-regulation of amino acid levels) and mitochondrial function (e.g. up-regulation of carnitine, important for a-oxidation of fatty acids) was altered in cells expressing ΔNp53:WTp53. These findings were subsequently validated using biochemical and cell-based approaches. Furthermore, whereas equal expression of ΔNp53 and WTp53 cause accelerated aging in mammals, due to alternative splicing and translation initiation ΔNp53 is a naturally-occurring isoform whose expression levels can change throughout the lifetime. Thus, the cellular and molecular mechanisms identified from this work will likely reflect changes common to normal, physiological aging. Comparison of global gene expression profiles in WTp53 or ΔNp53:WTp53 expressed H1299 RNA from FACS sorted GFP positive hybrid to Affymatrix Gene The exp 0, exp 4 and exp 5 are independent replicate/transfections/biological experiments. The exp d, exp e and exp f are control experiments....

  5. Pancreas-specific Sirt1-deficiency in mice compromises beta-cell function without development of hyperglycemia BioProject

    ID: PRJNA279307

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: a decreased expression of the glucose transporter Slc2A2/Glut2 and of the Glucagon like peptide-1 receptor (Glp1r) as well as with a marked down regulation of endoplasmic reticulum (ER) chaperones that participate in the Unfolded Protein Response (UPR) pathway. Counter intuitively, the Sirt1-deficient mice did not develop hyperglycemia. Pancreatic polypeptide (PP) cells were the only other islet cells affected, with reduced numbers in the Sirt1-deficient pancreas. This study provides new mechanistic insights showing that beta-cell function in Sirt1-deficient pancreas is affected due to altered glucose sensing and deregulation of the UPR pathway. Interestingly, we uncover a context in which impaired beta-cell function is not accompanied by increased glycemia. This points to a unique compensatory mechanism. Given the reduction in PP, investigation of its role in the control of blood glucose is warranted. Overall design: To uncover other Sirt1-regulated mechanisms, we performed a gene expres...
  6. Glis3 regulates pancreatic beta cells development and maturation ArrayExpress

    ID: E-GEOD-67238

    Description: Glis3 is expressed in pancreatic beta and PP cells. To identify down stream target genes of Glis3, we performed microarray analysis using pancreas tot...

  7. Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet ArrayExpress

    ID: E-GEOD-38138

    Description: Phloridzin is a dihydrochalcone typically contained in apples. A diet containing 0.5 % phloridzin significantly improves hyperglycemia but not hypoins...

  8. Glis3 regulates pancreatic beta cells development and maturation BioProject

    ID: PRJNA279305

    Keywords: Transcriptome or Gene expression

    Access Type: download

  9. Transcription profiling of rainbow trout cells following anoxia exposure ArrayExpress

    ID: E-MAXD-41

    Description: The rainbow trout, Oncorhynchus mykiss, is relatively sensitive to hypoxia and does not survive deep hypoxia or anoxia. Given this lack of hypoxia-to...

  10. Hepatic glucose sensing is required to preserve beta-cell glucose competence ArrayExpress

    ID: E-GEOD-43581

    Description: We assessed the impact of glucose transporter Glut2 gene inactivation in adult mouse liver (LG2KO mice). This suppressed hepatic glucose uptake but no...

  11. Pancreas-specific Sirt1-deficiency in mice compromises beta-cell function without development of hyperglycemia OmicsDI

    ID: E-GEOD-67239

    Date Released: 03-06-2016

    Description: a decreased expression of the glucose transporter Slc2A2/Glut2 and of the Glucagon like peptide-1 receptor (Glp1r) as well as with a marked down regulation of endoplasmic reticulum (ER) chaperones that participate in the Unfolded Protein Response (UPR) pathway. Counter intuitively, the Sirt1-deficient mice did not develop hyperglycemia. Pancreatic polypeptide (PP) cells were the only other islet cells affected, with reduced numbers in the Sirt1-deficient pancreas. This study provides new mechanistic insights showing that beta-cell function in Sirt1-deficient pancreas is affected due to altered glucose sensing and deregulation of the UPR pathway. Interestingly, we uncover a context in which impaired beta-cell function is not accompanied by increased glycemia. This points to a unique compensatory mechanism. Given the reduction in PP, investigation of its role in the control of blood glucose is warranted. To uncover other Sirt1-regulated mechanisms, we performed a gene expression microarray ...

  12. Integrative analysis of pathology, mRNA and microRNA in a polygenic diabetes model, NONcNZO10/LtJ mice OmicsDI

    ID: E-GEOD-83241

    Date Released: 07-02-2016

    Description: sis (Slc30a8, Mt1 and Mt2) or glucose metabolism (Slc2a2) was suggested as being the candidate mechanism of pancreas failure in NONcNZO10/LtJ mice. These results demonstrate NONcNZO10/LtJ mice have a complex pathogenic mechanism of diabetes, and moreover, this fundamental information of NONcNZO10/LtJ mice would offer the opportunity for research and development of a novel antidiabetic drug. To identify the diabetes related genes that changed expression during the development of T2D in NONcNZO10/LtJ mice, we analyzed gene expression profiles of 7-, 13-, and 22-week old NONcNZO10/LtJ mice using GeneChip Mouse Gene 2.0 ST Arrays. On the other hand, we compared gene expres...

  13. Metabolic and gene expression changes induced by the naturally occurring ΔNp53 isoform link mTOR pathway and mitochondrial alterations to the progero... BioProject

    ID: PRJNA159167

    Keywords: Transcriptome or Gene expression

    Access Type: download

    dataset.description: P3K1, FGF5) and regulators of glucose metabolism (SLC2A2, CRYAB, LRCH1). Expression of other key metabolic genes were also altered in cells expressing ΔNp53:WTp53 tetramers, suggesting that global me tabolic changes might contribute to ΔNp53:WTp53 pathology. In collaboration with Metabolon (Durham, NC), we identified approximately one hundred metabolites that were significantly up- or down-regulated in H1299 cells expressing ΔNp53:WTp53. The metabolome analysis was a powerful complement to the gene expression data, and further suggested that the mTOR pathway (e.g. across-the-board up-regulation of amino acid levels) and mitochondrial function (e.g. up-regulation of carnitine, important for a-oxidation of fatty acids) was altered in cells expressing ΔNp53:WTp53. These findings were subsequently validated using biochemical and cell-based approaches. Furthermore, whereas equal expression of ΔNp53 and WTp53 cause accelerated aging in mammals, due to alternative splicing and translation initiation ΔNp53 is a naturally-occurring isoform whose expression levels can change throughout the lifetime. Thus, the cellular and molecular mechanisms identified from this work will likely reflect changes common to normal, physiological aging. Overall design: Comparison of global gene expression profiles in WTp53 or ΔNp53:WTp53 expressed H1299 RNA from FACS sorted GFP positive hybrid to Affymatrix Gene The exp 0, exp 4 and exp 5 are independent replicate/transfections/biological experiments. The exp d, exp e and exp f are control experiments....
  14. Hepatic gene expression in streptozotocin-induced diabetic mice fed a phloridzin diet BioProject

    ID: PRJNA167276

    Keywords: Transcriptome or Gene expression

    Access Type: download

  15. Diabetes Enhances the Proliferation of Adult Pancreatic Multipotent Progenitor Cells and Biases Their Differentiation to More Beta-Cell Production BioProject

    ID: PRJNA278022

    Keywords: Transcriptome or Gene expression

    Access Type: download

  16. Hepatic glucose sensing is required to preserve beta-cell glucose competence BioProject

    ID: PRJNA186754

    Keywords: Transcriptome or Gene expression

    Access Type: download

  17. Targeting evasion from Antiangiogenic therapy BioProject

    ID: PRJNA318902

    Keywords: Transcriptome or Gene expression

    Access Type: download

  18. Metabolic and gene expression changes induced by the naturally occurring deltaNp53 isoform link mTOR pathway and mitochondrial alterations to the prog... OmicsDI

    ID: E-GEOD-37271

    Date Released: 08-18-2015

    Description: P3K1, FGF5) and regulators of glucose metabolism (SLC2A2, CRYAB, LRCH1). Expression of other key metabolic genes were also altered in cells expressing ΔNp53:WTp53 tetramers, suggesting that global me tabolic changes might contribute to ΔNp53:WTp53 pathology. In collaboration with Metabolon (Durham, NC), we identified approximately one hundred metabolites that were significantly up- or down-regulated in H1299 cells expressing ΔNp53:WTp53. The metabolome analysis was a powerful complement to the gene expression data, and further suggested that the mTOR pathway (e.g. across-the-board up-regulation of amino acid levels) and mitochondrial function (e.g. up-regulation of carnitine, important for a-oxidation of fatty acids) was altered in cells expressing ΔNp53:WTp53. These findings were subsequently validated using biochemical and cell-based approaches. Furthermore, whereas equal expression of ΔNp53 and WTp53 cause accelerated aging in mammals, due to alternative splicing and translation initiation ΔNp53 is a naturally-occurring isoform whose expression levels can change throughout the lifetime. Thus, the cellular and molecular mechanisms identified from this work will likely reflect changes common to normal, physiological aging. Comparison of global gene expression profiles in WTp53 or ΔNp53:WTp53 expressed H1299 RNA from FACS sorted GFP positive hybrid to Affymatrix Gene The exp 0, exp 4 and exp 5 are independent replicate/transfections/biological experiments. The exp d, exp e and exp f are control experiments....

  19. Transcriptomic effects of GLUT2 knock-down in zebrafish embryos ArrayExpress

    ID: E-GEOD-57836

    Description: Glucose transporter 2 (GLUT2) is a key player in the regulation of glucose dynamics in organs central to metabolism, namely the liver, pancreas and in...

  20. Transcriptomic effects of GLUT2 knock-down in zebrafish embryos BioProject

    ID: PRJNA248211

    Keywords: Transcriptome or Gene expression

    Access Type: download


Displaying 20 of 21 results for "SLC2A2"