Endogenous SHIP2 does not localize in lipid rafts in 3T3‐L1 adipocytes

@article{Jacobs2004EndogenousSD,
  title={Endogenous SHIP2 does not localize in lipid rafts in 3T3‐L1 adipocytes},
  author={Christine Jacobs and Sheela Onnockx and Isabelle Vandenbroere and Isabelle Pirson},
  journal={FEBS Letters},
  year={2004},
  volume={565}
}
Regulation of Insulin Signaling by the Phosphatidylinositol 3,4,5-Triphosphate Phosphatase SKIP through the Scaffolding Function of Pak1
TLDR
The first report of the mechanisms by which SKIP specifically suppresses insulin signaling and the subsequent glucose uptake is presented, which are the foundation of the specific and prominent role of SKIP in the regulation of insulin signaling.
SHIP2: Structure, Function and Inhibition
TLDR
Inhibitors of SHIP2 activity have been designed to interact with the catalytic domain with sub‐micromolar IC50 values: these come from a range of structural classes and have been shown to have in vivo effects consistent withSHIP2 inhibition.
Lipid Raft Association and Cholesterol Sensitivity of P2X1-4 Receptors for ATP
TLDR
It is suggested that cholesterol is normally needed to facilitate the opening/gating of ATP-bound P2X1 receptor channels, and mutations in the pre-first transmembrane segment region remove this requirement.
Involvement of JNK/NFκB Signaling Pathways in the Lipopolysaccharide-Induced Modulation of Aquaglyceroporin Expression in 3T3-L1 Cells Differentiated into Adipocytes
TLDR
Results clearly show that many AQPs are expressed in murine 3T3-L1 adipocytes, and in DCs, LPS led to decreased AQP7 and AQP11 mRNA levels but to increased AQP3 mRNA levels, resulting from the Toll-like receptor 4 (TLR4)-induced activation of JNK and/or NFκB pathway.
ABCG1 and ABCG4 Suppress γ-Secretase Activity and Amyloid β Production
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Results suggest that ABCG1 and ABCG4 alter the distribution of γ-secretase on the plasma membrane, leading to the decreasedγ- secretase activity and suppressed Aβ secretion, which may inhibit the development of Alzheimer’s disease.
Lipopolysaccharide Modifies Glycerol Permeability and Metabolism in 3T3-L1 Adipocytes
TLDR
These findings provide novel insights in understanding the LPS-induced adipocyte hypertrophy that accompanies obesity.
Pituitary Adenylate Cyclase Activating Peptide (PACAP) Participates in Adipogenesis by Activating ERK Signaling Pathway
TLDR
It is speculated that ERK1/2 activation is crucial for the activation of CCAAT/enhancer- binding protein β (C/EBPβ) in adipogenesis in 3T3-L1 cell line.
Murine 3T3-L1 Adipocyte Cell Differentiation Model: Validated Reference Genes for qPCR Gene Expression Analysis
TLDR
It is observed that the number and the stability of potential RGs vary significantly during differentiation of 3T3-L1 cells into adipocytes, and for the first time, that during mitotic clonal expansion, the most suitable RGs are ATP-5b, NoNo, RPL, ACTB and Ywhaz.
ABCA1, ABCG1, and ABCG4 Are Distributed to Distinct Membrane Meso-Domains and Disturb Detergent-Resistant Domains on the Plasma Membrane
TLDR
The results suggest that ABCA1, ABCG1, and ABCG4 are localized to distinct membrane meso-domains and disturb the mese-domain structures by reorganizing lipids on the plasma membrane; collectively, these observations may explain the different substrate profiles and lipid efflux roles of these transporters.
Tobacco Smoke-Induced Alterations in Hepatic Lipid Profiles Demonstrated by Imaging Mass Spectrometry
TLDR
Several of the CS-induced lipid profile alterations persisted after air recovery, suggesting that the responses had become permanent, whereas others worsened with CS exposure duration and were either sustained or revered with recovery.
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TLDR
It is shown that SHIP2, which is recruited in anti-phosphotyrosine immunoprecipitates in insulin-stimulated cells, accounts for the insulin sensitivity or apparent increase in activity reported by Guilherme et al.
The SH2-containing inositol polyphosphate 5-phosphatase, SHIP-2, binds filamin and regulates submembraneous actin
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It is demonstrated that filamin-dependent SHIP-2 localization critically regulates phosphatidylinositol 3 kinase signaling to the actin cytoskeleton.
An SH2 Domain-Containing 5′ Inositolphosphatase Inhibits Insulin-Induced GLUT4 Translocation and Growth Factor-Induced Actin Filament Rearrangement
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Results show that expression of SHIP inhibits insulin-induced GLUT4 translocation, growth factor-induced membrane ruffling, and DNA synthesis, indicating that PtdIns 3,4,5-P3 is the key phospholipid product mediating these biological actions.
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The results indicate that SHIP2 negatively regulates metabolic signaling of insulin via the 5′-phosphatase activity and that PI(3,4,5)P3 rather than PI( 3,4)P2 is important for in vivo regulation of insulin-induced activation of downstream molecules of PI 3-kinase leading to glucose uptake and glycogen synthesis.
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Caveolae-DIG may operate as signalosomes for insulin-independent positive cross talk to metabolic insulin signaling downstream of the insulin receptor based on redistribution and accompanying activation of nonreceptor tyrosine kinases.
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