Галерея 2757796
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Proc Natl Acad Sci U S A
v.106(39); 2009 Sep 29
PMC2757796
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Proc Natl Acad Sci U S A. 2009 Sep 29; 106(39): 16669–16674.
Published online 2009 Sep 15. doi: 10.1073/pnas.0907138106
a Department of Internal Medicine, Division of Cardiology;
b Department of Molecular Physiology and Biophysics; and University of Iowa Carver College of Medicine, Iowa City, IA 52242; and
c Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110
1 To whom correspondence should be addressed. E-mail: ude.awoiu@relhom-retep
Edited by Andrew R. Marks, Columbia University College of Physicians and Surgeons, New York, NY, and approved August 10, 2009
GUID: 43FCE80D-B735-4F86-A9EC-9C32AE11692E
GUID: B09D5C93-212B-4030-982A-7772776989D6
GUID: 4EB83123-3140-4929-B43F-783D21B97BD4
Keywords: ankyrin, cytoskeleton, diabetes, Kir6.2
1. Seino S. ATP-sensitive potassium channels: A model of heteromultimeric potassium channel/receptor assemblies. Annu Rev Physiol. 1999; 61 :337–362. [ PubMed ] [ Google Scholar ]
2. Nichols CG. KATP channels as molecular sensors of cellular metabolism. Nature. 2006; 440 :470–476. [ PubMed ] [ Google Scholar ]
3. Gloyn AL, Siddiqui J, Ellard S. Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2006; 27 :220–231. [ PubMed ] [ Google Scholar ]
4. Bahi-Buisson N, et al. Infantile spasms as an epileptic feature of DEND syndrome associated with an activating mutation in the potassium adenosine triphosphate (ATP) channel, Kir6.2. J Child Neurol. 2007; 22 :1147–1150. [ PubMed ] [ Google Scholar ]
5. Bienengraeber M, et al. ABCC9 mutations identified in human dilated cardiomyopathy disrupt catalytic KATP channel gating. Nat Genet. 2004; 36 :382–387. [ PMC free article ] [ PubMed ] [ Google Scholar ]
6. Garrido JJ, et al. A targeting motif involved in sodium channel clustering at the axonal initial segment. Science. 2003; 300 :2091–2094. [ PubMed ] [ Google Scholar ]
7. Lowe JS, et al. Voltage-gated Nav channel targeting in the heart requires an ankyrin-G dependent cellular pathway. J Cell Biol. 2008; 180 :173–186. [ PMC free article ] [ PubMed ] [ Google Scholar ]
8. Mohler PJ, et al. Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes. Proc Natl Acad Sci USA. 2004; 101 :17533–17538. [ PMC free article ] [ PubMed ] [ Google Scholar ]
9. Chung HJ, Jan YN, Jan LY. Polarized axonal surface expression of neuronal KCNQ channels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminal domains. Proc Natl Acad Sci USA. 2006; 103 :8870–8875. [ PMC free article ] [ PubMed ] [ Google Scholar ]
10. Hill AS, et al. Ion channel clustering at the axon initial segment and node of ranvier evolved sequentially in early chordates. PLoS Genet. 2008; 4 :e1000317. [ PMC free article ] [ PubMed ] [ Google Scholar ]
11. Mohler PJ, et al. Ankyrin-B syndrome: Enhanced cardiac function balanced by risk of cardiac death and premature senescence. PLoS ONE. 2007; 2 :e1051. [ PMC free article ] [ PubMed ] [ Google Scholar ]
12. Mohler PJ, et al. Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death. Nature. 2003; 421 :634–639. [ PubMed ] [ Google Scholar ]
13. Hamilton-Shield JP. Overview of neonatal diabetes. Endocr Dev. 2007; 12 :12–23. [ PubMed ] [ Google Scholar ]
14. Vaxillaire M, et al. Kir6.2 mutations are a common cause of permanent neonatal diabetes in a large cohort of French patients. Diabetes. 2004; 53 :2719–2722. [ PubMed ] [ Google Scholar ]
15. Bennett V, Baines AJ. Spectrin and ankyrin-based pathways: Metazoan inventions for integrating cells into tissues. Physiol Rev. 2001; 81 :1353–1392. [ PubMed ] [ Google Scholar ]
16. Remedi MS, et al. Hyperinsulinism in mice with heterozygous loss of K(ATP) channels. Diabetologia. 2006; 49 :2368–2378. [ PubMed ] [ Google Scholar ]
17. Tarasov AI, et al. Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes. Diabetes Obes Metab. 2007; 9 (Suppl 2):46–55. [ PubMed ] [ Google Scholar ]
18. Koster JC, Marshall BA, Ensor N, Corbett JA, Nichols CG. Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes. Cell. 2000; 100 :645–654. [ PubMed ] [ Google Scholar ]
19. Lin CW, et al. Kir6.2 mutations associated with neonatal diabetes reduce expression of ATP-sensitive K+ channels: Implications in disease mechanism and sulfonylurea therapy. Diabetes. 2006; 55 :1738–1746. [ PubMed ] [ Google Scholar ]
20. Inagaki N, et al. Reconstitution of IKATP: An inward rectifier subunit plus the sulfonylurea receptor. Science. 1995; 270 :1166–1170. [ PubMed ] [ Google Scholar ]
21. Proks P, Girard C, Baevre H, Njolstad PR, Ashcroft FM. Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy. Diabetes. 2006; 55 :1731–1737. [ PubMed ] [ Google Scholar ]
22. Tammaro P, Proks P, Ashcroft FM. Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels. J Physiol. 2006; 571 :3–14. [ PMC free article ] [ PubMed ] [ Google Scholar ]
23. Schwappach B, Zerangue N, Jan YN, Jan LY. Molecular basis for K(ATP) assembly: Transmembrane interactions mediate association of a K+ channel with an ABC transporter. Neuron. 2000; 26 :155–167. [ PubMed ] [ Google Scholar ]
24. Furukawa T, Yamane T, Terai T, Katayama Y, Hiraoka M. Functional linkage of the cardiac ATP-sensitive K+ channel to the actin cytoskeleton. Pflugers Arch. 1996; 431 :504–512. [ PubMed ] [ Google Scholar ]
25. Brady PA, Alekseev AE, Aleksandrova LA, Gomez LA, Terzic A. A disrupter of actin microfilaments impairs sulfonylurea-inhibitory gating of cardiac KATP channels. Am J Physiol. 1996; 271 :H2710–H2716. [ PubMed ] [ Google Scholar ]
26. Terzic A, Kurachi Y. Actin microfilament disrupters enhance K(ATP) channel opening in patches from guinea-pig cardiomyocytes. J Physiol. 1996; 492 :395–404. [ PMC free article ] [ PubMed ] [ Google Scholar ]
27. Zerangue N, Schwappach B, Jan YN, Jan LY. A new ER trafficking signal regulates the subunit stoichiometry of plasma membrane K(ATP) channels. Neuron. 1999; 22 :537–548. [ PubMed ] [ Google Scholar ]
28. Hough E, Beech DJ, Sivaprasadarao A. Identification of molecular regions responsible for the membrane trafficking of Kir6.2. Pflugers Arch. 2000; 440 :481–487. [ PubMed ] [ Google Scholar ]
29. Makhina EN, Nichols CG. Independent trafficking of KATP channel subunits to the plasma membrane. J Biol Chem. 1998; 273 :3369–3374. [ PubMed ] [ Google Scholar ]
30. Gumina RJ, et al. Knockout of Kir6.2 negates ischemic preconditioning-induced protection of myocardial energetics. Am J Physiol Heart Circ Physiol. 2003; 284 :H2106–H2113. [ PubMed ] [ Google Scholar ]
31. Miki T, et al. Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1. Nat Med. 2002; 8 :466–472. [ PubMed ] [ Google Scholar ]
32. Morrissey A, et al. Immunolocalization of KATP channel subunits in mouse and rat cardiac myocytes and the coronary vasculature. BMC Physiol. 2005; 5 :1. [ PMC free article ] [ PubMed ] [ Google Scholar ]
33. Zhou M, et al. ATP-sensitive K+-channel subunits on the mitochondria and endoplasmic reticulum of rat cardiomyocytes. J Histochem Cytochem. 2005; 53 :1491–1500. [ PMC free article ] [ PubMed ] [ Google Scholar ]
34. Gloyn AL, et al. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med. 2004; 350 :1838–1849. [ PubMed ] [ Google Scholar ]
35. Riedel MJ, Steckley DC, Light PE. Current status of the E23K Kir6.2 polymorphism: Implications for type-2 diabetes. Hum Genet. 2005; 116 :133–145. [ PubMed ] [ Google Scholar ]
Articles from Proceedings of the National Academy of Sciences of the United States of America are provided here courtesy of National Academy of Sciences
1. Seino S. ATP-sensitive potassium channels: A model of heteromultimeric potassium channel/receptor assemblies. Annu Rev Physiol. 1999; 61 :337–362. [ PubMed ] [ Google Scholar ] [ Ref list ]
2. Nichols CG. KATP channels as molecular sensors of cellular metabolism. Nature. 2006; 440 :470–476. [ PubMed ] [ Google Scholar ] [ Ref list ]
3. Gloyn AL, Siddiqui J, Ellard S. Mutations in the genes encoding the pancreatic beta-cell KATP channel subunits Kir6.2 (KCNJ11) and SUR1 (ABCC8) in diabetes mellitus and hyperinsulinism. Hum Mutat. 2006; 27 :220–231. [ PubMed ] [ Google Scholar ] [ Ref list ]
4. Bahi-Buisson N, et al. Infantile spasms as an epileptic feature of DEND syndrome associated with an activating mutation in the potassium adenosine triphosphate (ATP) channel, Kir6.2. J Child Neurol. 2007; 22 :1147–1150. [ PubMed ] [ Google Scholar ] [ Ref list ]
5. Bienengraeber M, et al. ABCC9 mutations identified in human dilated cardiomyopathy disrupt catalytic KATP channel gating. Nat Genet. 2004; 36 :382–387. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
6. Garrido JJ, et al. A targeting motif involved in sodium channel clustering at the axonal initial segment. Science. 2003; 300 :2091–2094. [ PubMed ] [ Google Scholar ] [ Ref list ]
7. Lowe JS, et al. Voltage-gated Nav channel targeting in the heart requires an ankyrin-G dependent cellular pathway. J Cell Biol. 2008; 180 :173–186. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
8. Mohler PJ, et al. Nav1.5 E1053K mutation causing Brugada syndrome blocks binding to ankyrin-G and expression of Nav1.5 on the surface of cardiomyocytes. Proc Natl Acad Sci USA. 2004; 101 :17533–17538. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
9. Chung HJ, Jan YN, Jan LY. Polarized axonal surface expression of neuronal KCNQ channels is mediated by multiple signals in the KCNQ2 and KCNQ3 C-terminal domains. Proc Natl Acad Sci USA. 2006; 103 :8870–8875. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
10. Hill AS, et al. Ion channel clustering at the axon initial segment and node of ranvier evolved sequentially in early chordates. PLoS Genet. 2008; 4 :e1000317. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
11. Mohler PJ, et al. Ankyrin-B syndrome: Enhanced cardiac function balanced by risk of cardiac death and premature senescence. PLoS ONE. 2007; 2 :e1051. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
12. Mohler PJ, et al. Ankyrin-B mutation causes type 4 long-QT cardiac arrhythmia and sudden cardiac death. Nature. 2003; 421 :634–639. [ PubMed ] [ Google Scholar ] [ Ref list ]
13. Hamilton-Shield JP. Overview of neonatal diabetes. Endocr Dev. 2007; 12 :12–23. [ PubMed ] [ Google Scholar ] [ Ref list ]
14. Vaxillaire M, et al. Kir6.2 mutations are a common cause of permanent neonatal diabetes in a large cohort of French patients. Diabetes. 2004; 53 :2719–2722. [ PubMed ] [ Google Scholar ] [ Ref list ]
15. Bennett V, Baines AJ. Spectrin and ankyrin-based pathways: Metazoan inventions for integrating cells into tissues. Physiol Rev. 2001; 81 :1353–1392. [ PubMed ] [ Google Scholar ] [ Ref list ]
16. Remedi MS, et al. Hyperinsulinism in mice with heterozygous loss of K(ATP) channels. Diabetologia. 2006; 49 :2368–2378. [ PubMed ] [ Google Scholar ] [ Ref list ]
17. Tarasov AI, et al. Functional analysis of two Kir6.2 (KCNJ11) mutations, K170T and E322K, causing neonatal diabetes. Diabetes Obes Metab. 2007; 9 (Suppl 2):46–55. [ PubMed ] [ Google Scholar ] [ Ref list ]
18. Koster JC, Marshall BA, Ensor N, Corbett JA, Nichols CG. Targeted overactivity of beta cell K(ATP) channels induces profound neonatal diabetes. Cell. 2000; 100 :645–654. [ PubMed ] [ Google Scholar ] [ Ref list ]
19. Lin CW, et al. Kir6.2 mutations associated with neonatal diabetes reduce expression of ATP-sensitive K+ channels: Implications in disease mechanism and sulfonylurea therapy. Diabetes. 2006; 55 :1738–1746. [ PubMed ] [ Google Scholar ] [ Ref list ]
20. Inagaki N, et al. Reconstitution of IKATP: An inward rectifier subunit plus the sulfonylurea receptor. Science. 1995; 270 :1166–1170. [ PubMed ] [ Google Scholar ] [ Ref list ]
21. Proks P, Girard C, Baevre H, Njolstad PR, Ashcroft FM. Functional effects of mutations at F35 in the NH2-terminus of Kir6.2 (KCNJ11), causing neonatal diabetes, and response to sulfonylurea therapy. Diabetes. 2006; 55 :1731–1737. [ PubMed ] [ Google Scholar ] [ Ref list ]
22. Tammaro P, Proks P, Ashcroft FM. Functional effects of naturally occurring KCNJ11 mutations causing neonatal diabetes on cloned cardiac KATP channels. J Physiol. 2006; 571 :3–14. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
23. Schwappach B, Zerangue N, Jan YN, Jan LY. Molecular basis for K(ATP) assembly: Transmembrane interactions mediate association of a K+ channel with an ABC transporter. Neuron. 2000; 26 :155–167. [ PubMed ] [ Google Scholar ] [ Ref list ]
24. Furukawa T, Yamane T, Terai T, Katayama Y, Hiraoka M. Functional linkage of the cardiac ATP-sensitive K+ channel to the actin cytoskeleton. Pflugers Arch. 1996; 431 :504–512. [ PubMed ] [ Google Scholar ] [ Ref list ]
25. Brady PA, Alekseev AE, Aleksandrova LA, Gomez LA, Terzic A. A disrupter of actin microfilaments impairs sulfonylurea-inhibitory gating of cardiac KATP channels. Am J Physiol. 1996; 271 :H2710–H2716. [ PubMed ] [ Google Scholar ] [ Ref list ]
26. Terzic A, Kurachi Y. Actin microfilament disrupters enhance K(ATP) channel opening in patches from guinea-pig cardiomyocytes. J Physiol. 1996; 492 :395–404. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
27. Zerangue N, Schwappach B, Jan YN, Jan LY. A new ER trafficking signal regulates the subunit stoichiometry of plasma membrane K(ATP) channels. Neuron. 1999; 22 :537–548. [ PubMed ] [ Google Scholar ] [ Ref list ]
28. Hough E, Beech DJ, Sivaprasadarao A. Identification of molecular regions responsible for the membrane trafficking of Kir6.2. Pflugers Arch. 2000; 440 :481–487. [ PubMed ] [ Google Scholar ] [ Ref list ]
29. Makhina EN, Nichols CG. Independent trafficking of KATP channel subunits to the plasma membrane. J Biol Chem. 1998; 273 :3369–3374. [ PubMed ] [ Google Scholar ] [ Ref list ]
30. Gumina RJ, et al. Knockout of Kir6.2 negates ischemic preconditioning-induced protection of myocardial energetics. Am J Physiol Heart Circ Physiol. 2003; 284 :H2106–H2113. [ PubMed ] [ Google Scholar ] [ Ref list ]
31. Miki T, et al. Mouse model of Prinzmetal angina by disruption of the inward rectifier Kir6.1. Nat Med. 2002; 8 :466–472. [ PubMed ] [ Google Scholar ] [ Ref list ]
32. Morrissey A, et al. Immunolocalization of KATP channel subunits in mouse and rat cardiac myocytes and the coronary vasculature. BMC Physiol. 2005; 5 :1. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
33. Zhou M, et al. ATP-sensitive K+-channel subunits on the mitochondria and endoplasmic reticulum of rat cardiomyocytes. J Histochem Cytochem. 2005; 53 :1491–1500. [ PMC free article ] [ PubMed ] [ Google Scholar ] [ Ref list ]
34. Gloyn AL, et al. Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes. N Engl J Med. 2004; 350 :1838–1849. [ PubMed ] [ Google Scholar ] [ Ref list ]
35. Riedel MJ, Steckley DC, Light PE. Current status of the E23K Kir6.2 polymorphism: Implications for type-2 diabetes. Hum Genet. 2005; 116 :133–145. [ PubMed ] [ Google Scholar ] [ Ref list ]
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a Department of Internal Medicine, Division of Cardiology;
b Department of Molecular Physiology and Biophysics; and University of Iowa Carver College of Medicine, Iowa City, IA 52242; and
a Department of Internal Medicine, Division of Cardiology;
a Department of Internal Medicine, Division of Cardiology;
a Department of Internal Medicine, Division of Cardiology;
a Department of Internal Medicine, Division of Cardiology;
a Department of Internal Medicine, Division of Cardiology;
a Department of Internal Medicine, Division of Cardiology;
b Department of Molecular Physiology and Biophysics; and University of Iowa Carver College of Medicine, Iowa City, IA 52242; and
c Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110
a Department of Internal Medicine, Division of Cardiology;
b Department of Molecular Physiology and Biophysics; and University of Iowa Carver College of Medicine, Iowa City, IA 52242; and
Author contributions: C.F.K., H.T.K., T.J.H., S.R.C., O.M.K., P.J.W., M.E.A., C.G.N., and P.J.M. designed research; C.F.K., H.T.K., T.J.H., S.R.C., O.M.K., P.J.W., and M.C. performed research; C.F.K., H.T.K., T.J.H., S.R.C., O.M.K., P.J.W., and C.G.N. contributed new reagents/analytic tools; C.F.K., H.T.K., T.J.H., S.R.C., O.M.K., P.J.W., M.C., M.E.A., C.G.N., and P.J.M. analyzed data; and C.F.K., H.T.K., T.J.H., S.R.C., O.M.K., M.E.A., C.G.N., and P.J.M. wrote the paper.
The coordinated sorting of ion channels to specific plasma membrane domains is necessary for excitable cell physiology. K ATP channels, assembled from pore-forming (Kir6.x) and regulatory sulfonylurea receptor subunits, are critical electrical transducers of the metabol
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