Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues - Wikidata - wikimedia - TriplyDB

Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues

Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues

http://www.wikidata.org/entity/Q41818058

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BMP8B increases brown adipose tissue thermogenesis through both central and peripheral actions The brain and brown fat Protein-Induced Pluripotent Stem Cells Ameliorate Cognitive Dysfunction and Reduce Aβ Deposition in a Mouse Model of Alzheimer's Disease.Enhanced retinal insulin receptor-activated neuroprotective survival signal in mice lacking the protein-tyrosine phosphatase-1B gene.Regulation of brown fat adipogenesis by protein tyrosine phosphatase 1B Metabolic regulation by protein tyrosine phosphatases.Macrophage alpha1 AMP-activated protein kinase (alpha1AMPK) antagonizes fatty acid-induced inflammation through SIRT1 Ventromedial hypothalamus-specific Ptpn1 deletion exacerbates diet-induced obesity in female mice.Protein tyrosine phosphatase 1B inhibitors: a molecular level legitimate approach for the management of diabetes mellitus.Regulation of insulin and leptin signaling by muscle suppressor of cytokine signaling 3 (SOCS3).Chronic sleep fragmentation during the sleep period induces hypothalamic endoplasmic reticulum stress and PTP1b-mediated leptin resistance in male mice.Adrenergic regulation of AMP-activated protein kinase in brown adipose tissue in vivo Deficiency of PTP1B in POMC neurons leads to alterations in energy balance and homeostatic response to cold exposure.Protein-tyrosine phosphatase 1B substrates and metabolic regulation Endogenously determined restriction of food intake overcomes excitation-contraction uncoupling in JP45KO mice with aging.Nicotine induces negative energy balance through hypothalamic AMP-activated protein kinase.Transgenic mouse models resistant to diet-induced metabolic disease: is energy balance the key?Deficiency of PTP1B in leptin receptor-expressing neurons leads to decreased body weight and adiposity in mice.Exercise-mimetic AICAR transiently benefits brain function.Histone Deacetylase 1 (HDAC1) Negatively Regulates Thermogenic Program in Brown Adipocytes via Coordinated Regulation of Histone H3 Lysine 27 (H3K27) Deacetylation and Methylation.Thiamine deficiency induces anorexia by inhibiting hypothalamic AMPK.PTP1B: a double agent in metabolism and oncogenesis.Hypothalamic AMP-activated protein kinase as a mediator of whole body energy balance.Altered hypothalamic function in diet-induced obesity.Redox control of enzymatic functions: The electronics of life's circuitry.PTP1B inhibitors for type 2 diabetes treatment: a patent review (2011 - 2014).Leptin signalling pathways in hypothalamic neurons.Hypothalamic AMPK: a canonical regulator of whole-body energy balance.Recent advances in the development of protein tyrosine phosphatase 1B inhibitors for Type 2 diabetes.Biogenesis, characterization, and the effect of vicenin-gold nanoparticles on glucose utilization in 3T3-L1 adipocytes: a bioinformatic approach to illuminate its interaction with PTP 1B and AMPK.Deletion of ghrelin prevents aging-associated obesity and muscle dysfunction without affecting longevity.Targeting adipose tissue.Neuroprotective role of protein tyrosine phosphatase-1B in rod photoreceptor neurons.Protein tyrosine phosphatase 1B deficiency in podocytes mitigates hyperglycemia-induced renal injury.Protein-altering variants associated with body mass index implicate pathways that control energy intake and expenditure in obesity.Protein-Tyrosine Phosphatase-1B Mediates Sleep Fragmentation-Induced Insulin Resistance and Visceral Adipose Tissue Inflammation in Mice.PAS kinase is a nutrient and energy sensor in hypothalamic areas required for the normal function of AMPK and mTOR/S6K1.

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Neuronal protein tyrosine phosphatase 1B deficiency results in inhibition of hypothalamic AMPK and isoform-specific activation of AMPK in peripheral tissues

http://www.wikidata.org/entity/Q41818058

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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name

Neuronal protein tyrosine phos ...... of AMPK in peripheral tissues

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Neuronal protein tyrosine phos ...... of AMPK in peripheral tissues

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Molecular and Cellular Biology

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Neuronal protein tyrosine phos ...... of AMPK in peripheral tissues

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Anna Lee

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Barbara B Kahn

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Benjamin G Neel

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Bingzhong Xue

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Fawaz Haj

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Huamei He

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Incoronata Murano

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James A Balschi

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Karyn J Catalano

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Kenji Asakura

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P2860

Complexes between the LKB1 tumor suppressor, STRAD alpha/beta and MO25 alpha/beta are upstream kinases in the AMP-activated protein kinase cascade

Tyrosine dephosphorylation and deactivation of insulin receptor substrate-1 by protein-tyrosine phosphatase 1B. Possible facilitation by the formation of a ternary complex with the Grb2 adaptor protein

Role of AMP-activated protein kinase in mechanism of metformin action

Mice overexpressing human uncoupling protein-3 in skeletal muscle are hyperphagic and lean

TYK2 and JAK2 are substrates of protein-tyrosine phosphatase 1B

PTP1B regulates leptin signal transduction in vivo

Mechanism of protein tyrosine phosphatase 1B-mediated inhibition of leptin signalling

Downregulation of AMP-activated protein kinase by Cidea-mediated ubiquitination and degradation in brown adipose tissue

AMP kinase is required for mitochondrial biogenesis in skeletal muscle in response to chronic energy deprivation.

Increased energy expenditure, decreased adiposity, and tissue-specific insulin sensitivity in protein-tyrosine phosphatase 1B-deficient mice

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4563-4573

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10.1128/MCB.01914-08

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16

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29

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Thomas Pulinilkunnil

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2009-06-15T00:00:00Z

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26293759

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