Amira Klip

Summary

Affiliation: The Hospital for Sick Children
Country: Canada

Publications

  1. doi Signal transduction meets vesicle traffic: the software and hardware of GLUT4 translocation
    Amira Klip
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada and Department of Biochemistry, The University of Toronto, Ontario, Canada
    Am J Physiol Cell Physiol 306:C879-86. 2014
  2. 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
  3. 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
  4. doi 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
  5. doi 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
  6. ncbi 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
  7. ncbi 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
  8. ncbi 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
  9. ncbi 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
  10. 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

Collaborators

Detail Information

Publications71

  1. doi Signal transduction meets vesicle traffic: the software and hardware of GLUT4 translocation
    Amira Klip
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada and Department of Biochemistry, The University of Toronto, Ontario, Canada
    Am J Physiol Cell Physiol 306:C879-86. 2014
    ..Finally, we illustrate how actin filaments interact with myosin 1c and α-Actinin4 to promote vesicle tethering as preamble to fusion with the membrane...
  2. 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...
  3. 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...
  4. doi 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...
  5. doi 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
    ....
  6. ncbi 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
    ....
  7. ncbi 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...
  8. ncbi 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
    ....
  9. ncbi 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...
  10. 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...
  11. ncbi 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
    ....
  12. ncbi 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...
  13. ncbi 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...
  14. 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...
  15. doi 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...
  16. doi 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...
  17. ncbi 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...
  18. ncbi 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...
  19. 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...
  20. doi 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
    ....
  21. ncbi 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...
  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. doi 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
    ....
  24. ncbi 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...
  25. 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...
  26. 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...
  27. doi 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
    ....
  28. doi 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...
  29. doi 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...
  30. 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
    ....
  31. doi 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
    ....
  32. ncbi 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...
  33. doi 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...
  34. ncbi 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
    ....
  35. 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...
  36. pmc Myosin Va mediates Rab8A-regulated GLUT4 vesicle exocytosis in insulin-stimulated muscle cells
    Yi Sun
    Cell Biology Program, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada
    Mol Biol Cell 25:1159-70. 2014
    ..Hence insulin signaling to the molecular switch Rab8A connects with the motor protein MyoVa to mobilize GLUT4 vesicles toward the muscle cell plasma membrane. ..
  37. doi 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...
  38. ncbi 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...
  39. ncbi 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...
  40. 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...
  41. doi 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...
  42. doi 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...
  43. doi 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...
  44. ncbi 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
    ....
  45. doi 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 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
    ....
  47. ncbi 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. doi 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
    ....
  49. ncbi 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...
  50. ncbi 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. ncbi 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
    ....
  52. doi 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...
  53. ncbi 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...
  54. doi 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
    ....
  55. pmc Palmitoleate Reverses High Fat-induced Proinflammatory Macrophage Polarization via AMP-activated Protein Kinase (AMPK)
    Kenny L Chan
    From the Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada, The Department of Physiology, University of Toronto, Toronto, Ontario M5S 1A8, Canada, and
    J Biol Chem 290:16979-88. 2015
    ..These findings could have applicability to reverse obesity-linked inflammation in metabolically relevant tissues. ..
  56. 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...
  57. doi Palmitate-induced inflammatory pathways in human adipose microvascular endothelial cells promote monocyte adhesion and impair insulin transcytosis
    Nicolas J Pillon
    Cell Biology Program, The Hospital for Sick Children, Toronto, Ontario, Canada
    Am J Physiol Endocrinol Metab 309:E35-44. 2015
    ..This behavior may contribute in vivo to reduced tissue insulin action and enhanced tissue infiltration by immune cells. ..
  58. doi Nucleotides released from palmitate-challenged muscle cells through pannexin-3 attract monocytes
    Nicolas J Pillon
    Program in Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada
    Diabetes 63:3815-26. 2014
    ..These findings identify pannexins as new targets of saturated fatty acid-induced inflammation in myotubes, and point to nucleotides as possible mediators of immune cell chemoattraction toward muscle in the context of obesity. ..
  59. doi Pro-inflammatory macrophages increase in skeletal muscle of high fat-fed mice and correlate with metabolic risk markers in humans
    Lisbeth N Fink
    Cell Biology Program, The Hospital for Sick Children, Toronto, Canada Diabetes Research Unit, Novo Nordisk A S, Måløv, Denmark
    Obesity (Silver Spring) 22:747-57. 2014
    ..Skeletal muscle is the major tissue of insulin-dependent glucose disposal, and indices of muscle inflammation arise during obesity, but whether and which immune cells increase in muscle remain unclear...
  60. doi 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...
  61. ncbi 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...
  62. pmc Reciprocal regulation of endocytosis and metabolism
    Costin N Antonescu
    Department of Chemistry and Biology, Ryerson University, Toronto, Ontario M5B 2K3, Canada
    Cold Spring Harb Perspect Biol 6:a016964. 2014
    ..Here, we examine how the endocytosis of nutrient transporters and carriers as well as signaling receptors governs cellular metabolism and thereby systemic (whole-body) metabolite homeostasis. ..
  63. doi Mice lacking NOX2 are hyperphagic and store fat preferentially in the liver
    Sheila R Costford
    The Hospital for Sick Children, Toronto, Ontario, Canada
    Am J Physiol Endocrinol Metab 306:E1341-53. 2014
    ..We propose that NOX2 participates in food intake control and lipid distribution in mice...
  64. ncbi 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...
  65. ncbi 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
    ....
  66. ncbi 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
    ....
  67. ncbi 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...
  68. 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...
  69. ncbi 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
    ....
  70. ncbi Muscle, liver, and pancreas: Three Musketeers fighting to control glycemia
    Amira Klip
    Am J Physiol Endocrinol Metab 291:E1141-3. 2006
  71. ncbi Kei on GSK: a contribution by the 2007 recipient of the Young Scientist Award
    Amira Klip
    Am J Physiol Endocrinol Metab 294:E27. 2008