Zobrazeno 1 - 2
of 2
pro vyhledávání: '"Loren A. Eng"'
Autor:
Chien-Ping Ko, Luca Santarelli, Hasane Ratni, Roland Schmucki, Maureen S. Lynes, Josephine Sheedy, Sergey Paushkin, Chang-Sun Lee, Irene Gerlach, Jesse L. Mull, Nanjing Zhang, Zhihua Feng, Anthony Turpoff, Anuradha Bhattacharyya, Paulo Fontoura, Priya Vazirani, Panayiota Trifillis, Gary Mitchell Karp, Joseph M. Colacino, Martin Ebeling, Kathleen D. McCarthy, John Babiak, Woll Matthew G, Hongyan Qi, Nikolai Naryshkin, Manaswini Sivaramakrishnan, Lee L. Rubin, Jana Narasimhan, Neil Gregory Almstead, Vijayalakshmi Gabbeta, Amal Dakka, Loren A. Eng, Xin Zhao, Nicole Risher, Young-Choon Moon, Marla Weetall, Jiyuan Ma, Karen K. Y. Ling, Stuart W. Peltz, Ellen Welch, Friedrich Metzger, Guangming Chen, Bansri Furia, Daniel Haehnke, Ronald Kong, Anirvan Ghosh, Xiaoyan Zhang, Karen S. Chen
Publikováno v:
Science. 345:688-693
Drugs that provide the splice of life Motor neurons relay signals from the nervous system to muscle fibers. In patients with spinal muscular atrophy, a protein required for the survival of these neurons is deficient or missing altogether, so the neur
Autor:
Nikolai A, Naryshkin, Marla, Weetall, Amal, Dakka, Jana, Narasimhan, Xin, Zhao, Zhihua, Feng, Karen K Y, Ling, Gary M, Karp, Hongyan, Qi, Matthew G, Woll, Guangming, Chen, Nanjing, Zhang, Vijayalakshmi, Gabbeta, Priya, Vazirani, Anuradha, Bhattacharyya, Bansri, Furia, Nicole, Risher, Josephine, Sheedy, Ronald, Kong, Jiyuan, Ma, Anthony, Turpoff, Chang-Sun, Lee, Xiaoyan, Zhang, Young-Choon, Moon, Panayiota, Trifillis, Ellen M, Welch, Joseph M, Colacino, John, Babiak, Neil G, Almstead, Stuart W, Peltz, Loren A, Eng, Karen S, Chen, Jesse L, Mull, Maureen S, Lynes, Lee L, Rubin, Paulo, Fontoura, Luca, Santarelli, Daniel, Haehnke, Kathleen D, McCarthy, Roland, Schmucki, Martin, Ebeling, Manaswini, Sivaramakrishnan, Chien-Ping, Ko, Sergey V, Paushkin, Hasane, Ratni, Irene, Gerlach, Anirvan, Ghosh, Friedrich, Metzger
Publikováno v:
Science (New York, N.Y.). 345(6197)
Spinal muscular atrophy (SMA) is a genetic disease caused by mutation or deletion of the survival of motor neuron 1 (SMN1) gene. A paralogous gene in humans, SMN2, produces low, insufficient levels of functional SMN protein due to alternative splicin