Amira Klip

Summary

Affiliation: The Hospital for Sick Children
Country: Canada

Publications

  1. pmc Muscle cells challenged with saturated fatty acids mount an autonomous inflammatory response that activates macrophages
    Nicolas J Pillon
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada
    Cell Commun Signal 10:30. 2012
  2. pmc Desperately seeking sugar: glial cells as hypoglycemia sensors
    Amira Klip
    Cell Biology Programme, The Hospital for Sick Children, Toronto, Ontario, Canada
    J Clin Invest 115:3403-5. 2005
  3. doi request reprint The many ways to regulate glucose transporter 4
    Amira Klip
    Cell Biology Program, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, ON M5G 1X8, Canada
    Appl Physiol Nutr Metab 34:481-7. 2009
  4. doi request reprint Regulation of glucose transporter 4 traffic by energy deprivation from mitochondrial compromise
    A Klip
    Cell Biology Program, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada
    Acta Physiol (Oxf) 196:27-35. 2009
  5. ncbi request reprint Skeletal muscle cells and adipocytes differ in their reliance on TC10 and Rac for insulin-induced actin remodeling
    Lellean Jebailey
    Programme in Cell Biology, Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8
    Mol Endocrinol 18:359-72. 2004
  6. ncbi request reprint Insulin but not PDGF relies on actin remodeling and on VAMP2 for GLUT4 translocation in myoblasts
    Dora Torok
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada
    J Cell Sci 117:5447-55. 2004
  7. ncbi request reprint Differential contribution of insulin receptor substrates 1 versus 2 to insulin signaling and glucose uptake in l6 myotubes
    Carol Huang
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 280:19426-35. 2005
  8. ncbi request reprint Maturation of the regulation of GLUT4 activity by p38 MAPK during L6 cell myogenesis
    Wenyan Niu
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 278:17953-62. 2003
  9. ncbi request reprint A dominant-negative p38 MAPK mutant and novel selective inhibitors of p38 MAPK reduce insulin-stimulated glucose uptake in 3T3-L1 adipocytes without affecting GLUT4 translocation
    Romel Somwar
    Programme in Cell Biology, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 277:50386-95. 2002
  10. ncbi request reprint Intracellular delivery of phosphatidylinositol (3,4,5)-trisphosphate causes incorporation of glucose transporter 4 into the plasma membrane of muscle and fat cells without increasing glucose uptake
    Gary Sweeney
    Programme in Cell Biology, Hospital for Sick Children, and Department of Biology, York University, Toronto, Ontario, Canada
    J Biol Chem 279:32233-42. 2004

Collaborators

Detail Information

Publications63

  1. pmc Muscle cells challenged with saturated fatty acids mount an autonomous inflammatory response that activates macrophages
    Nicolas J Pillon
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada
    Cell Commun Signal 10:30. 2012
    ..We hypothesize that saturated fat-induced, low-grade muscle cell inflammation may trigger resident skeletal muscle macrophage polarization, possibly contributing to insulin resistance in vivo...
  2. pmc Desperately seeking sugar: glial cells as hypoglycemia sensors
    Amira Klip
    Cell Biology Programme, The Hospital for Sick Children, Toronto, Ontario, Canada
    J Clin Invest 115:3403-5. 2005
    ..report that glucose sensing and consequent pancreatic glucagon secretion are restored by re-expression of GLUT2 in glial but not neuronal cells. A new, glucose-sensing role is ascribed to GLUT2-expressing glial cells...
  3. doi request reprint The many ways to regulate glucose transporter 4
    Amira Klip
    Cell Biology Program, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, ON M5G 1X8, Canada
    Appl Physiol Nutr Metab 34:481-7. 2009
    ..The glycolytic enzymes glyceraldehyde-3-dehydrogenase and hexokinase II contribute to such regulation, through differential binding to GLUT4...
  4. doi request reprint Regulation of glucose transporter 4 traffic by energy deprivation from mitochondrial compromise
    A Klip
    Cell Biology Program, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada
    Acta Physiol (Oxf) 196:27-35. 2009
    ....
  5. ncbi request reprint Skeletal muscle cells and adipocytes differ in their reliance on TC10 and Rac for insulin-induced actin remodeling
    Lellean Jebailey
    Programme in Cell Biology, Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8
    Mol Endocrinol 18:359-72. 2004
    ....
  6. ncbi request reprint Insulin but not PDGF relies on actin remodeling and on VAMP2 for GLUT4 translocation in myoblasts
    Dora Torok
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, M5G 1X8, Canada
    J Cell Sci 117:5447-55. 2004
    ..These results suggest that insulin and PDGF rely differently on the actin cytoskeleton and on tetanus-toxin-sensitive VAMPs for mobilizing GLUT4...
  7. ncbi request reprint Differential contribution of insulin receptor substrates 1 versus 2 to insulin signaling and glucose uptake in l6 myotubes
    Carol Huang
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 280:19426-35. 2005
    ....
  8. ncbi request reprint Maturation of the regulation of GLUT4 activity by p38 MAPK during L6 cell myogenesis
    Wenyan Niu
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 278:17953-62. 2003
    ..Regulation of GLUT4 activity by insulin develops upon muscle cell differentiation and correlates with p38 MAPK activation by insulin...
  9. ncbi request reprint A dominant-negative p38 MAPK mutant and novel selective inhibitors of p38 MAPK reduce insulin-stimulated glucose uptake in 3T3-L1 adipocytes without affecting GLUT4 translocation
    Romel Somwar
    Programme in Cell Biology, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 277:50386-95. 2002
    ..We propose that p38 contributes to enhancing GLUT4 activity, thereby increasing glucose uptake. In addition, the azaazulene class of inhibitors described will be useful to decipher cellular actions of p38 and JNK...
  10. ncbi request reprint Intracellular delivery of phosphatidylinositol (3,4,5)-trisphosphate causes incorporation of glucose transporter 4 into the plasma membrane of muscle and fat cells without increasing glucose uptake
    Gary Sweeney
    Programme in Cell Biology, Hospital for Sick Children, and Department of Biology, York University, Toronto, Ontario, Canada
    J Biol Chem 279:32233-42. 2004
    ....
  11. pmc Myo1c binding to submembrane actin mediates insulin-induced tethering of GLUT4 vesicles
    Shlomit Boguslavsky
    Cell Biology Program, Hospital for Sick Children, Toronto, ON M5G 1X8, Canada
    Mol Biol Cell 23:4065-78. 2012
    ..Thus we propose that interaction of vesicular Myo1c with cortical actin filaments is required for insulin-mediated tethering of GLUT4 vesicles and for efficient GLUT4 surface delivery in muscle cells...
  12. ncbi request reprint Need for GLUT4 activation to reach maximum effect of insulin-mediated glucose uptake in brown adipocytes isolated from GLUT4myc-expressing mice
    Daniel Konrad
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Diabetes 51:2719-26. 2002
    ..Using this animal model, we found that stimulation of glucose uptake into brown adipocytes involves both GLUT4 translocation and activation...
  13. doi request reprint Selective regulation of the perinuclear distribution of glucose transporter 4 (GLUT4) by insulin signals in muscle cells
    Chandrasagar B Dugani
    Cell Biology Program, The Hospital for Sick Children, Toronto, ON, Canada
    Eur J Cell Biol 87:337-51. 2008
    ..We propose that insulin causes selective, dynamic relocalization of perinuclear GLUT4myc and VAMP2 and perinuclear GLUT4myc redistribution is a direct target of insulin-derived signals...
  14. ncbi request reprint Activation of the glucose transporter GLUT4 by insulin
    L Michelle Furtado
    Programme in Cell Biology, Hospital for Sick Children, University of Toronto, ON, Canada
    Biochem Cell Biol 80:569-78. 2002
    ..This review discusses the evidence for the divergence of GLUT4 translocation and activity and proposed mechanisms for the regulation of GLUT4...
  15. ncbi request reprint Ceramide- and oxidant-induced insulin resistance involve loss of insulin-dependent Rac-activation and actin remodeling in muscle cells
    Lellean Jebailey
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
    Diabetes 56:394-403. 2007
    ..We propose that ceramide and oxidative stress can each affect two independent arms of insulin signaling to GLUT4 at distinct steps, Rac-GTP loading and Akt phosphorylation...
  16. pmc Rab8A and Rab13 are activated by insulin and regulate GLUT4 translocation in muscle cells
    Yi Sun
    Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8
    Proc Natl Acad Sci U S A 107:19909-14. 2010
    ..These findings close in on the series of events regulating muscle GLUT4 traffic in response to insulin, crucial for whole-body glucose homeostasis...
  17. doi request reprint NOD2 activation induces muscle cell-autonomous innate immune responses and insulin resistance
    Akhilesh K Tamrakar
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Endocrinology 151:5624-37. 2010
    ....
  18. pmc Intracellular segregation of phosphatidylinositol-3,4,5-trisphosphate by insulin-dependent actin remodeling in L6 skeletal muscle cells
    Nish Patel
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada M5G 1X8
    Mol Cell Biol 23:4611-26. 2003
    ..Insulin-stimulated actin remodeling may spatially coordinate the localized generation of PI-3,4,5-P(3) and recruitment of Akt, ultimately leading to GLUT4 insertion at the plasma membrane...
  19. ncbi request reprint Insulin regulates the membrane arrival, fusion, and C-terminal unmasking of glucose transporter-4 via distinct phosphoinositides
    Manabu Ishiki
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8
    J Biol Chem 280:28792-802. 2005
    ..PI(3,4,5)P(3) causes arrival and fusion without unmasking, whereas PI3P causes arrival and unmasking without fusion...
  20. ncbi request reprint Opposite effect of JAK2 on insulin-dependent activation of mitogen-activated protein kinases and Akt in muscle cells: possible target to ameliorate insulin resistance
    Ana C P Thirone
    The Hospital for Sick Children, 555 University Ave, Toronto, Ontario, Canada M5G 1X8
    Diabetes 55:942-51. 2006
    ..These results suggest that JAK2 may depress the Akt to glucose uptake signaling axis selectively in insulin-resistant states. Inhibition of JAK2 may be a useful strategy to relieve insulin resistance of metabolic outcomes...
  21. doi request reprint GLUT4 vesicle recruitment and fusion are differentially regulated by Rac, AS160, and Rab8A in muscle cells
    Varinder K Randhawa
    Program in Cell Biology, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 283:27208-19. 2008
    ....
  22. pmc Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance
    Tim Ting Chiu
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    J Biol Chem 288:17520-31. 2013
    ..We propose that potent elevation of Rac-1 activation alone suffices to drive insulin-independent GLUT4 translocation in muscle cells, and such a strategy might be exploited to bypass signaling defects during insulin resistance...
  23. pmc Insulin and hypertonicity recruit GLUT4 to the plasma membrane of muscle cells by using N-ethylmaleimide-sensitive factor-dependent SNARE mechanisms but different v-SNAREs: role of TI-VAMP
    Varinder K Randhawa
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    Mol Biol Cell 15:5565-73. 2004
    ..The insulin effect was abolished by DN-NSF, but only partly reduced by TI-VAMP siRNA. We propose that insulin and hypertonicity recruit GLUT4myc from partly overlapping, but distinct sources defined by VAMP2 and TI-VAMP, respectively...
  24. doi request reprint Muscle cells engage Rab8A and myosin Vb in insulin-dependent GLUT4 translocation
    Shuhei Ishikura
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, M5G 1X8, Canada
    Am J Physiol Cell Physiol 295:C1016-25. 2008
    ..These results support a model whereby AS160, Rab8A, and myosin Vb are required for insulin-induced GLUT4 translocation in muscle cells, potentially as part of a linear signaling cascade...
  25. doi request reprint A transgenic mouse model to study glucose transporter 4myc regulation in skeletal muscle
    Jonathan D Schertzer
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada
    Endocrinology 150:1935-40. 2009
    ....
  26. pmc Arp2/3- and cofilin-coordinated actin dynamics is required for insulin-mediated GLUT4 translocation to the surface of muscle cells
    Tim Ting Chiu
    Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada
    Mol Biol Cell 21:3529-39. 2010
    ..We propose that Arp2/3 and cofilin coordinate a dynamic cycle of actin branching and severing at the cell cortex, essential for insulin-mediated GLUT4 translocation in muscle cells...
  27. doi request reprint Contraction-related stimuli regulate GLUT4 traffic in C2C12-GLUT4myc skeletal muscle cells
    Wenyan Niu
    Program in Cell Biology, The Hospital for Sick Children, 555 University Ave, Toronto, ON, M5G 1X8, Canada
    Am J Physiol Endocrinol Metab 298:E1058-71. 2010
    ..This system will be ideal to further analyze the underlying molecular events of contraction-regulated GLUT4 traffic...
  28. pmc NOD1 activators link innate immunity to insulin resistance
    Jonathan D Schertzer
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Diabetes 60:2206-15. 2011
    ....
  29. ncbi request reprint The Rab GTPase-activating protein AS160 integrates Akt, protein kinase C, and AMP-activated protein kinase signals regulating GLUT4 traffic
    Farah S L Thong
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
    Diabetes 56:414-23. 2007
    ..Collectively, these results indicate that activation of Akt, c/n PKC, or alpha2-AMPK intersect at AS160 to regulate GLUT4 traffic, as well as highlight the potential of AS160 as a therapy target to increase muscle glucose uptake...
  30. doi request reprint GAPDH binds GLUT4 reciprocally to hexokinase-II and regulates glucose transport activity
    Hilal Zaid
    Program in Cell Biology, Hospital for Sick Children, Toronto, ON, Canada M5G 1X8
    Biochem J 419:475-84. 2009
    ..The results show that GAPDH and HKII reciprocally interact with GLUT4 and suggest that these interactions regulate GLUT4 intrinsic activity in response to insulin...
  31. doi request reprint Alpha-actinin-4 is selectively required for insulin-induced GLUT4 translocation
    Ilana Talior-Volodarsky
    Program in Cell Biology, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada
    J Biol Chem 283:25115-23. 2008
    ..We propose that ACTN4 contributes to GLUT4 traffic, likely by tethering GLUT4 vesicles to the cortical actin cytoskeleton...
  32. ncbi request reprint Dissecting GLUT4 traffic components in L6 myocytes by fluorescence-based, single-cell assays
    Costin N Antonescu
    Hospital for Sick Children, Toronto, Ontario, Canada
    Methods Mol Biol 457:367-78. 2008
    ....
  33. doi request reprint Insulin action on glucose transporters through molecular switches, tracks and tethers
    Hilal Zaid
    Program in Cell Biology, Hospital for Sick Children, Toronto, ON M5G 1X8, Canada
    Biochem J 413:201-15. 2008
    ....
  34. pmc Palmitate-activated macrophages confer insulin resistance to muscle cells by a mechanism involving protein kinase C θ and ε
    Girish Kewalramani
    Cell Biology Program, The Hospital for Sick Children, Toronto, Canada
    PLoS ONE 6:e26947. 2011
    ..However, the mechanism whereby CM-PA confers this negative response onto muscle cells remains unknown...
  35. doi request reprint Rac1 signalling towards GLUT4/glucose uptake in skeletal muscle
    Tim T Chiu
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Canada
    Cell Signal 23:1546-54. 2011
    ..This review summarises the current thinking on the regulation of Rac1 by insulin, the role of Rac-dependent cortical actin remodelling in GLUT4 traffic, and the impact of Rac1 towards insulin resistance in skeletal muscle...
  36. ncbi request reprint Muscle cell depolarization induces a gain in surface GLUT4 via reduced endocytosis independently of AMPK
    Nadeeja Wijesekara
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Ave, Toronto, ON, Canada M5G 1X8
    Am J Physiol Endocrinol Metab 290:E1276-86. 2006
    ..We propose that K+ depolarization reduces GLUT4 internalization through signals and mechanisms distinct from those engaged by insulin. Such a pathway(s) is largely independent of PI3K, Akt, AMPK, and CaMKII but may involve PKC...
  37. doi request reprint Documenting GLUT4 exocytosis and endocytosis in muscle cell monolayers
    Shuhei Ishikura
    Program in Cell Biology, The Hospital for Sick Children, Ontario, Canada
    Curr Protoc Cell Biol . 2010
    ..Here, we describe cell population-based assays to measure the steady-state levels of GLUT4 at the cell surface, as well as to separately measure the rates of GLUT4 endocytosis and endocytosis...
  38. doi request reprint Palmitate- and lipopolysaccharide-activated macrophages evoke contrasting insulin responses in muscle cells
    Victor Samokhvalov
    Cell Biology Program, The Hospital for Sick Children, 555 University Ave, Toronto, ON, M5G 1X8 Canada
    Am J Physiol Endocrinol Metab 296:E37-46. 2009
    ..Macrophages may be an integral element in glucose homeostasis in vivo, relaying effects of circulating factors to skeletal muscle...
  39. pmc Muscle-specific Pten deletion protects against insulin resistance and diabetes
    Nadeeja Wijesekara
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada M5G 2N9
    Mol Cell Biol 25:1135-45. 2005
    ..Muscle Pten may be a potential target for treatment or prevention of insulin resistance and diabetes...
  40. ncbi request reprint Sustained exposure of L6 myotubes to high glucose and insulin decreases insulin-stimulated GLUT4 translocation but upregulates GLUT4 activity
    Carol Huang
    Programme in Cell Biology, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8
    Diabetes 51:2090-8. 2002
    ..In addition, basal state GLUT4 activity was augmented to partially compensate for the translocation defect, resulting in a more robust glucose uptake than what would be predicted from the amount of cell surface GLUT4 alone...
  41. doi request reprint Cross-talk between skeletal muscle and immune cells: muscle-derived mediators and metabolic implications
    Nicolas J Pillon
    Program in Cell Biology, Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    Am J Physiol Endocrinol Metab 304:E453-65. 2013
    ....
  42. ncbi request reprint Rabs 8A and 14 are targets of the insulin-regulated Rab-GAP AS160 regulating GLUT4 traffic in muscle cells
    Shuhei Ishikura
    Program in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ont, Canada M5G 1X8
    Biochem Biophys Res Commun 353:1074-9. 2007
    ..In contrast, neither wild-type nor constitutively active GFP-tagged Rab10 restored GLUT4 translocation. These results suggest that Rab8A and possibly Rab14 may be targets of AS160 leading to GLUT4 translocation in L6 muscle cells...
  43. ncbi request reprint Exercise- and insulin-stimulated muscle glucose transport: distinct mechanisms of regulation
    Zayna A Khayat
    Programme in Cell Biology, Hospital for Sick Children, Toronto, ON
    Can J Appl Physiol 27:129-51. 2002
    ....
  44. doi request reprint Direct and macrophage-mediated actions of fatty acids causing insulin resistance in muscle cells
    Phillip J Bilan
    Cell Biology Program, The Hospital for Sick Children, Toronto, Canada
    Arch Physiol Biochem 115:176-90. 2009
    ..This review summarizes our observations that fatty acids evoke the release of pro-inflammatory factors from macrophages that consequently induce insulin resistance in muscle cells...
  45. doi request reprint Muscle insulin resistance: assault by lipids, cytokines and local macrophages
    Girish Kewalramani
    The Hospital for Sick Children, Toronto, Ontario, Canada
    Curr Opin Clin Nutr Metab Care 13:382-90. 2010
    ..The present review outlines possible mechanisms by which high fatty acids, associated with high-fat diet and obesity, impose insulin resistance on glucose uptake into skeletal muscle...
  46. doi request reprint Ready, set, internalize: mechanisms and regulation of GLUT4 endocytosis
    Costin N Antonescu
    Program in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, ON, Canada, M5G 1X8
    Biosci Rep 29:1-11. 2009
    ....
  47. ncbi request reprint Intracellular traffic and activation of the muscle glucose transporter
    Amira Klip
    Cell Biology Programme, The Hospital for Sick Children, Toronto, Canada
    J Muscle Res Cell Motil 25:595-6. 2004
  48. ncbi request reprint Turning signals on and off: GLUT4 traffic in the insulin-signaling highway
    Farah S L Thong
    Programme in Cell Biology, The Hospital for Sick Children, Ontario, Canada
    Physiology (Bethesda) 20:271-84. 2005
    ..The round trip of GLUT4 is intricately regulated by diverse signaling molecules impinging on specific compartments. Here we highlight the key molecular signals that are turned on and off by insulin to accomplish this task...
  49. doi request reprint Endocytosis, recycling, and regulated exocytosis of glucose transporter 4
    Kevin Foley
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M4G 1X8, Canada
    Biochemistry 50:3048-61. 2011
    ....
  50. ncbi request reprint Cellular location of insulin-triggered signals and implications for glucose uptake
    Nish Patel
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Pflugers Arch 451:499-510. 2006
    ..We summarize evidence suggesting that spatial localization of signals is critical for efficient insulin action, and that the cytoskeleton may act as a scaffold to promote efficient translocation of GLUT4 to the cell surface...
  51. doi request reprint Clathrin-dependent and independent endocytosis of glucose transporter 4 (GLUT4) in myoblasts: regulation by mitochondrial uncoupling
    Costin N Antonescu
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Traffic 9:1173-90. 2008
    ..Manipulating GLUT4 endocytosis to maintain surface GLUT4 may bypass insulin resistance...
  52. ncbi request reprint Tissue-specific roles of IRS proteins in insulin signaling and glucose transport
    Ana C P Thirone
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario M5G 1X8, Canada
    Trends Endocrinol Metab 17:72-8. 2006
    ....
  53. pmc Glucose transporter 4: cycling, compartments and controversies
    Chandrasagar B Dugani
    Programme in Cell Biology, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8, Canada
    EMBO Rep 6:1137-42. 2005
    ..The localization of the insulin-sensitive GLUT4 compartment and the precise target of insulin-derived signals remain open for future investigation...
  54. doi request reprint A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death
    Tabitha E Wood
    Princess Margaret Hospital, Ontario Cancer Institute, 610 University Avenue, Toronto, Ontario, Canada
    Mol Cancer Ther 7:3546-55. 2008
    ..Thus, fasentin is a novel inhibitor of glucose transport that blocks glucose uptake and highlights a new mechanism to sensitize cells to death ligands...
  55. ncbi request reprint Minireview: recent developments in the regulation of glucose transporter-4 traffic: new signals, locations, and partners
    Manabu Ishiki
    Programme in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Endocrinology 146:5071-8. 2005
    ..Vesicle tethering and fusion are regulated by insulin through input from class IA PI 3-kinase...
  56. ncbi request reprint The AMP-activated protein kinase activator AICAR does not induce GLUT4 translocation to transverse tubules but stimulates glucose uptake and p38 mitogen-activated protein kinases alpha and beta in skeletal muscle
    Kathleen Lemieux
    Department of Physiology and Lipid Research Unit, Laval University Hospital Research Center, Ste Foy, Quebec, G1V 4G2, Canada
    FASEB J 17:1658-65. 2003
    ....
  57. ncbi request reprint Agent and cell-type specificity in the induction of insulin resistance by HIV protease inhibitors
    Ronit Ben-Romano
    Department of Clinical Biochemistry, Ben Gurion University of the Negev, Beer Sheva, Israel
    AIDS 17:23-32. 2003
    ..To test agent and cell-type specificity in insulin resistance induced by prolonged exposure to HIV protease inhibitors (HPI), and to assess its relation to the direct, short-term inhibition of insulin-stimulated glucose uptake...
  58. pmc The pleckstrin homology (PH) domain-interacting protein couples the insulin receptor substrate 1 PH domain to insulin signaling pathways leading to mitogenesis and GLUT4 translocation
    Janet Farhang-Fallah
    Department of Biology Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario L8N 3Z5, Canada
    Mol Cell Biol 22:7325-36. 2002
    ..Our results are consistent with the hypothesis that PHIP represents a physiological protein ligand of the IRS-1 PH domain, which plays an important role in insulin receptor-mediated mitogenic and metabolic signal transduction...
  59. ncbi request reprint The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6
    Nerea Roher
    Departament de Fisiologia, Facultat de Biologia, Universitat de Barcelona, Barcelona, Spain
    Endocrinology 149:1880-9. 2008
    ....
  60. ncbi request reprint Insulin-dependent interactions of proteins with GLUT4 revealed through stable isotope labeling by amino acids in cell culture (SILAC)
    Leonard J Foster
    Center for Experimental Bioinformatics CEBI, Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, DK 5230 Odense M, Denmark
    J Proteome Res 5:64-75. 2006
    ....
  61. ncbi request reprint Fish glucose transporter (GLUT)-4 differs from rat GLUT4 in its traffic characteristics but can translocate to the cell surface in response to insulin in skeletal muscle cells
    Monica Diaz
    Departament de Fisiologia, Facultat de Biologia, Universitat de Barcelona, 08028, Barcelona, Spain
    Endocrinology 148:5248-57. 2007
    ..Our data suggest that btGLUT4 is subjected to a different intracellular traffic from rat-GLUT4 and may explain the relative glucose intolerance observed in fish...
  62. ncbi request reprint Muscle, liver, and pancreas: Three Musketeers fighting to control glycemia
    Amira Klip
    Am J Physiol Endocrinol Metab 291:E1141-3. 2006
  63. ncbi request reprint Kei on GSK: a contribution by the 2007 recipient of the Young Scientist Award
    Amira Klip
    Am J Physiol Endocrinol Metab 294:E27. 2008