Yu-Wen Lin, Ph.D.
Affiliations: | Life Sciences | Tunghai University, Taiwan |
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Publications
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| Wu SY, Chen WH, Hsieh CL, et al. (2014) 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 |
| Arakel EC, Brandenburg S, Uchida K, et al. (2014) Tuning the electrical properties of the heart by differential trafficking of KATP ion channel complexes. Journal of Cell Science. 127: 2106-19 |
| Zhang HX, Silva JR, Lin YW, et al. (2013) Heterogeneity and function of K(ATP) channels in canine hearts. Heart Rhythm : the Official Journal of the Heart Rhythm Society. 10: 1576-83 |
| Lin YW, Li A, Grasso V, et al. (2013) 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 |
| Battaglia D, Lin YW, Brogna C, et al. (2012) 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 |
| Lin YW, Akrouh A, Hsu Y, et al. (2012) 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 |
| Pinney SE, MacMullen C, Becker S, et al. (2008) Clinical characteristics and biochemical mechanisms of congenital hyperinsulinism associated with dominant KATP channel mutations. The Journal of Clinical Investigation. 118: 2877-86 |
| Lin YW, Bushman JD, Yan FF, et al. (2008) Destabilization of ATP-sensitive potassium channel activity by novel KCNJ11 mutations identified in congenital hyperinsulinism. The Journal of Biological Chemistry. 283: 9146-56 |
| Yan FF, Lin YW, MacMullen C, et al. (2007) Congenital hyperinsulinism associated ABCC8 mutations that cause defective trafficking of ATP-sensitive K+ channels: identification and rescue. Diabetes. 56: 2339-48 |
| Lin CW, Lin YW, Yan FF, et al. (2006) 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 |