| Year |
Citation |
Score |
| 2014 |
Wu SY, Chen WH, Hsieh CL, Lin YW. Abundant expression and functional participation of TRPV1 at Zusanli acupoint (ST36) in mice: mechanosensitive TRPV1 as an "acupuncture-responding channel". Bmc Complementary and Alternative Medicine. 14: 96. PMID 24612851 DOI: 10.1186/1472-6882-14-96 |
0.43 |
|
| 2014 |
Arakel EC, Brandenburg S, Uchida K, Zhang H, Lin YW, Kohl T, Schrul B, Sulkin MS, Efimov IR, Nichols CG, Lehnart SE, Schwappach B. Tuning the electrical properties of the heart by differential trafficking of KATP ion channel complexes. Journal of Cell Science. 127: 2106-19. PMID 24569881 DOI: 10.1242/Jcs.141440 |
0.621 |
|
| 2013 |
Zhang HX, Silva JR, Lin YW, Verbsky JW, Lee US, Kanter EM, Yamada KA, Schuessler RB, Nichols CG. Heterogeneity and function of K(ATP) channels in canine hearts. Heart Rhythm : the Official Journal of the Heart Rhythm Society. 10: 1576-83. PMID 23871704 DOI: 10.1016/J.Hrthm.2013.07.020 |
0.568 |
|
| 2013 |
Lin YW, Li A, Grasso V, Battaglia D, Crinò A, Colombo C, Barbetti F, Nichols CG. Functional characterization of a novel KCNJ11 in frame mutation-deletion associated with infancy-onset diabetes and a mild form of intermediate DEND: a battle between K(ATP) gain of channel activity and loss of channel expression. Plos One. 8: e63758. PMID 23667671 DOI: 10.1371/journal.pone.0063758 |
0.731 |
|
| 2012 |
Battaglia D, Lin YW, Brogna C, Crinò A, Grasso V, Mozzi AF, Russo L, Spera S, Colombo C, Ricci S, Nichols CG, Mercuri E, Barbetti F. Glyburide ameliorates motor coordination and glucose homeostasis in a child with diabetes associated with the KCNJ11/S225T, del226-232 mutation. Pediatric Diabetes. 13: 656-60. PMID 22694282 DOI: 10.1111/j.1399-5448.2012.00874.x |
0.538 |
|
| 2012 |
Lin YW, Akrouh A, Hsu Y, Hughes N, Nichols CG, De León DD. Compound heterozygous mutations in the SUR1 (ABCC 8) subunit of pancreatic K(ATP) channels cause neonatal diabetes by perturbing the coupling between Kir6.2 and SUR1 subunits. Channels (Austin, Tex.). 6: 133-8. PMID 22562119 DOI: 10.4161/chan.19980 |
0.715 |
|
| 2008 |
Pinney SE, MacMullen C, Becker S, Lin YW, Hanna C, Thornton P, Ganguly A, Shyng SL, Stanley CA. Clinical characteristics and biochemical mechanisms of congenital hyperinsulinism associated with dominant KATP channel mutations. The Journal of Clinical Investigation. 118: 2877-86. PMID 18596924 DOI: 10.1172/JCI35414 |
0.732 |
|
| 2008 |
Lin YW, Bushman JD, Yan FF, Haidar S, MacMullen C, Ganguly A, Stanley CA, Shyng SL. Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism. The Journal of Biological Chemistry. 283: 9146-56. PMID 18250167 DOI: 10.1074/jbc.M708798200 |
0.7 |
|
| 2007 |
Yan FF, Lin YW, MacMullen C, Ganguly A, Stanley CA, Shyng SL. Congenital hyperinsulinism associated ABCC8 mutations that cause defective trafficking of ATP-sensitive K+ channels: identification and rescue. Diabetes. 56: 2339-48. PMID 17575084 DOI: 10.2337/db07-0150 |
0.754 |
|
| 2006 |
Lin CW, Lin YW, Yan FF, Casey J, Kochhar M, Pratt EB, Shyng SL. Kir6.2 mutations associated with neonatal diabetes reduce expression of ATP-sensitive K+ channels: implications in disease mechanism and sulfonylurea therapy. Diabetes. 55: 1738-46. PMID 16731837 DOI: 10.2337/Db05-1571 |
0.734 |
|
| 2006 |
Lin YW, MacMullen C, Ganguly A, Stanley CA, Shyng SL. A novel KCNJ11 mutation associated with congenital hyperinsulinism reduces the intrinsic open probability of beta-cell ATP-sensitive potassium channels. The Journal of Biological Chemistry. 281: 3006-12. PMID 16332676 DOI: 10.1074/jbc.M511875200 |
0.763 |
|
| 2003 |
Lin YW, Jia T, Weinsoft AM, Shyng SL. Stabilization of the activity of ATP-sensitive potassium channels by ion pairs formed between adjacent Kir6.2 subunits. The Journal of General Physiology. 122: 225-37. PMID 12885877 DOI: 10.1085/jgp.200308822 |
0.682 |
|
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