Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice

By L. Klaman, O. Boss, O. Peroni, Jason K. Kim, Jennifer L. Martino, J. Zabolotny, N. Moghal, M. Lubkin, Young-Bum Kim, Arlene H. Sharpe and 4 more. Molecular and Cellular Biology, 2000

1,247 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/f4adeb05d58bd57d914bc982d076deecbc0247ad

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Citations in the corpus

Oxidation state of the active-site cysteine in protein tyrosine phosphatase 1B (2003, background): “Here we report the crystal structures of the regulatory sulphenic and irreversible sulphinic and sulphonic acids of protein tyrosine phosphatase 1B (PTP1B), an important enzyme in the negative regulation of the insulin recepto”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “Overexpression of PTP1B in mouse muscle or myocytes led to impaired insulin signal transduction of reduced glucose uptake and glycogen deposition (173, 720).”
Protein tyrosine phosphatase 1B inhibitors for diabetes (2002, background): “The disclosure that Ptp1b-deficient mice have increased insulin sensitivity and are resistant to weight gain on a high-fat diet, but are otherwise normal, addressed many of these concern”
Obesity and insulin resistance. (2000, background): “Interestingly, the insulin sensitivity is present in muscle and liver but not in adipocytes (18, 19).”
Structural and Evolutionary Relationships among Protein Tyrosine Phosphatase Domains (2001, background): “Recently, studies with PTP1B knockout mice (17, 44) and PTP1B antisense oligonucleotides have provided compelling evidence that inhibition of PTP1B may be an effective approach for the treatment of diabetes and obesity (53).”
Thermogenic mechanisms and their hormonal regulation. (2006, background): “Despite PTP-1B being expressed in many tissues, WAT among them, insulin-stimulated glucose uptake was not increased in this latter (132), suggesting that muscle responsiveness to insulin is a major determinant in the partition of energy.”
The Human Obesity Gene Map: The 2005 Update (2006, background): “2 PTPN1 Protein tyrosine phosphatase, nonreceptor type 1 Reduced adiposity (532,533)”
Redox regulation of protein tyrosine phosphatase 1B involves a sulphenyl-amide intermediate (2003, background): “with the kinase domain of the insulin receptor (IRK), a physiological substrate of PTP1”
Increased Insulin Sensitivity and Reduced Adiposity in Phosphatidylinositol 5-Phosphate 4-Kinase β−/− Mice (2004, background): “In addition, mice lacking protein tyrosine phosphatase 1B, which dephosphorylates the insulin receptor and insulin receptor substrates (15), are lean and have enhanced insulin sensitivity in vivo (13, 20).”
BMAL1 and CLOCK, Two Essential Components of the Circadian Clock, Are Involved in Glucose Homeostasis (2004, methodology): “Tests were performed as described (Klaman et al. 2000) with a diminution in the glucose bolus (0.”