Genetic Disruption of Protein Kinase STK25 Ameliorates Metabolic Defects in a Diet-Induced Type 2 Diabetes Model.
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Silencing of FABP1 ameliorates hepatic steatosis, inflammation, and oxidative stress in mice with nonalcoholic fatty liver disease.Overexpressing the novel autocrine/endocrine adipokine WISP2 induces hyperplasia of the heart, white and brown adipose tissues and prevents insulin resistanceProtein kinase STK25 aggravates the severity of non-alcoholic fatty pancreas disease in mice.The MST3/STK24 kinase mediates impaired fasting blood glucose after a high-fat diet.Overexpression of protein kinase STK25 in mice exacerbates ectopic lipid accumulation, mitochondrial dysfunction and insulin resistance in skeletal muscle.Serine/threonine protein kinase 25 antisense oligonucleotide treatment reverses glucose intolerance, insulin resistance, and nonalcoholic fatty liver disease in mice.
P2860
Genetic Disruption of Protein Kinase STK25 Ameliorates Metabolic Defects in a Diet-Induced Type 2 Diabetes Model.
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2015年の論文
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name
Genetic Disruption of Protein ...... Induced Type 2 Diabetes Model.
@en
type
label
Genetic Disruption of Protein ...... Induced Type 2 Diabetes Model.
@en
prefLabel
Genetic Disruption of Protein ...... Induced Type 2 Diabetes Model.
@en
P2093
P2860
P50
P356
P1433
P1476
Genetic Disruption of Protein ...... Induced Type 2 Diabetes Model.
@en
P2093
Anna Wickman
Belén Chanclón
Emmelie Cansby
Esther Nuñez-Durán
Louise Mannerås-Holm
Urszula Chursa
Vincent Fridén
P2860
P304
P356
10.2337/DB15-0060
P407
P577
2015-04-06T00:00:00Z