Search Results - "Minn, Alexandra"

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  1. 1

    Thioredoxin-Interacting Protein Is Stimulated by Glucose through a Carbohydrate Response Element and Induces β-Cell Apoptosis by Minn, Alexandra H, Hafele, Christian, Shalev, Anath

    Published in Endocrinology (Philadelphia) (01-05-2005)
    “…Recently, we identified thioredoxin-interacting protein (TXNIP) as the most dramatically glucose-induced gene in our human islet microarray study. TXNIP is a…”
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    Journal Article
  2. 2

    Molecular basis for negative regulation of the glucagon receptor by Koth, Christopher M., Murray, Jeremy M., Mukund, Susmith, Madjidi, Azadeh, Minn, Alexandra, Clarke, Holly J., Wong, Terence, Chiang, Vicki, Luis, Elizabeth, Estevez, Alberto, Rondon, Jesus, Zhang, Yingnan, Hötzel, Isidro, Allan, Bernard B.

    “…Members of the class B family of G protein-coupled receptors (GPCRs) bind peptide hormones and have causal roles in many diseases, ranging from diabetes and…”
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  3. 3

    Exenatide inhibits β-cell apoptosis by decreasing thioredoxin-interacting protein by Chen, Junqin, Couto, Francesca M., Minn, Alexandra H., Shalev, Anath

    “…Exenatide (Ex-4) is a novel anti-diabetic drug that stimulates insulin secretion and enhances β-cell mass, but the mechanisms involved are not fully…”
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  4. 4

    Metabolism-Independent Sugar Effects on Gene Transcription:  The Role of 3-O-Methylglucose by Minn, Alexandra H, Couto, Francesca M, Shalev, Anath

    Published in Biochemistry (Easton) (19-09-2006)
    “…Glucose effects on cellular functions such as gene expression require, in general, glucose metabolism at least to glucose-6-phosphate (G-6-P). However, the…”
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  5. 5

    Gene expression profiling in INS-1 cells overexpressing thioredoxin-interacting protein by Minn, Alexandra H., Pise-Masison, Cynthia A., Radonovich, Michael, Brady, John N., Wang, Ping, Kendziorski, Christina, Shalev, Anath

    “…Thioredoxin-interacting protein (TXNIP) is overexpressed in diabetes and has deleterious effects on pancreatic β-cells and the cardiovascular system. TXNIP is…”
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  6. 6

    Resistin is expressed in pancreatic islets by Minn, Alexandra H, Patterson, Noelle B, Pack, Stephanie, Hoffmann, Steven C, Gavrilova, Oksana, Vinson, Charles, Harlan, David M, Shalev, Anath

    “…Resistin, a recently described adipocyte factor, is regulated by peroxisome proliferator-activated receptor gamma (PPARγ) agonists. While resistin has been…”
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  7. 7

    Phylogenetics of Paniceae (Poaceae) by Duvall, Melvin R., Noll, Jeffrey D., Minn, Alexandra H.

    Published in American journal of botany (01-11-2001)
    “…Paniceae demonstrate unique variability of photosynthetic physiology and anatomy, including both non-Kranz and Kranz species and all subtypes of the latter…”
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  8. 8

    Exenatide blocks JAK1-STAT1 in pancreatic beta cells by Couto, Francesca M, Minn, Alexandra H, Pise-Masison, Cynthia A, Radonovich, Mike, Brady, John N, Hanson, Matthew, Fernandez, Luis A, Wang, Ping, Kendziorski, Christina, Shalev, Anath

    Published in Metabolism, clinical and experimental (01-07-2007)
    “…Abstract Exenatide (Ex-4) is an antidiabetic drug that acts through the glucagon-like peptide 1 receptor and has recently been approved for the treatment of…”
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  9. 9

    Increased Insulin Translation from an Insulin Splice-Variant Overexpressed in Diabetes, Obesity, and Insulin Resistance by Minn, Alexandra H, Lan, Hong, Rabaglia, Mary E, Harlan, David M, Peculis, Brenda A, Attie, Alan D, Shalev, Anath

    Published in Molecular endocrinology (Baltimore, Md.) (01-03-2005)
    “…Type 2 diabetes occurs when pancreatic β-cells become unable to compensate for the underlying insulin resistance. Insulin secretion requires β-cell insulin…”
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  10. 10

    Insulinomas and expression of an insulin splice variant by Minn, Alexandra H, Kayton, Mark, Lorang, Dominique, Hoffmann, Steven C, Harlan, David M, Libutti, Steven K, Shalev, Anath

    Published in The Lancet (British edition) (31-01-2004)
    “…Insulinomas are β-cell tumours characterised by uncontrolled insulin secretion even in the presence of hypoglycaemia. However, the mechanisms allowing such…”
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