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9 results on '"Ramos, Daniel"'

1. Presynaptic autophagy is coupled to the synaptic vesicle cycle via ATG-9

Author

Yang, Sisi, primary, Park, Daehun, additional, Manning, Laura, additional, Hill, Sarah E., additional, Cao, Mian, additional, Xuan, Zhao, additional, Gonzalez, Ian, additional, Dong, Yongming, additional, Clark, Benjamin, additional, Shao, Lin, additional, Okeke, Ifechukwu, additional, Almoril-Porras, Agustin, additional, Bai, Jihong, additional, De Camilli, Pietro, additional, and Colón-Ramos, Daniel A., additional

Published
2022
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4. Integration of Plasticity Mechanisms within a Single Sensory Neuron of C. elegans Actuates a Memory

Author

Hawk, Josh D., primary, Calvo, Ana C., additional, Liu, Ping, additional, Almoril-Porras, Agustin, additional, Aljobeh, Ahmad, additional, Torruella-Suárez, María Luisa, additional, Ren, Ivy, additional, Cook, Nathan, additional, Greenwood, Joel, additional, Luo, Linjiao, additional, Wang, Zhao-Wen, additional, Samuel, Aravinthan D.T., additional, and Colón-Ramos, Daniel A., additional

Published
2018
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5. The Antisense Transcript SMN-AS1 Regulates SMN Expression and Is a Novel Therapeutic Target for Spinal Muscular Atrophy

Author

d’Ydewalle, Constantin, primary, Ramos, Daniel M., additional, Pyles, Noah J., additional, Ng, Shi-Yan, additional, Gorz, Mariusz, additional, Pilato, Celeste M., additional, Ling, Karen, additional, Kong, Lingling, additional, Ward, Amanda J., additional, Rubin, Lee L., additional, Rigo, Frank, additional, Bennett, C. Frank, additional, and Sumner, Charlotte J., additional

Published
2017
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7. Dynamic Encoding of Perception, Memory, and Movement in a C. elegans Chemotaxis Circuit

Author

Luo, Linjiao, primary, Wen, Quan, additional, Ren, Jing, additional, Hendricks, Michael, additional, Gershow, Marc, additional, Qin, Yuqi, additional, Greenwood, Joel, additional, Soucy, Edward R., additional, Klein, Mason, additional, Smith-Parker, Heidi K., additional, Calvo, Ana C., additional, Colón-Ramos, Daniel A., additional, Samuel, Aravinthan D.T., additional, and Zhang, Yun, additional

Published
2014
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9. The Antisense Transcript SMN-AS1 Regulates SMN Expression and Is a Novel Therapeutic Target for Spinal Muscular Atrophy.

Author

d'Ydewalle C, Ramos DM, Pyles NJ, Ng SY, Gorz M, Pilato CM, Ling K, Kong L, Ward AJ, Rubin LL, Rigo F, Bennett CF, and Sumner CJ

Subjects
Animals, Blotting, Western, Cells, Cultured, Cerebral Cortex cytology, Chromatin Immunoprecipitation, Disease Models, Animal, Humans, Induced Pluripotent Stem Cells, Mice, Muscular Atrophy, Spinal metabolism, Neurons metabolism, Oligonucleotides, Antisense pharmacology, Polycomb Repressive Complex 2 metabolism, Promoter Regions, Genetic, RNA Splicing, RNA, Antisense drug effects, RNA, Antisense metabolism, RNA, Long Noncoding drug effects, RNA, Long Noncoding metabolism, Real-Time Polymerase Chain Reaction, Survival of Motor Neuron 1 Protein metabolism, Survival of Motor Neuron 2 Protein metabolism, Gene Expression Regulation, Motor Neurons metabolism, Muscular Atrophy, Spinal genetics, RNA, Antisense genetics, RNA, Long Noncoding genetics, Survival of Motor Neuron 1 Protein genetics, Survival of Motor Neuron 2 Protein genetics
Abstract

The neuromuscular disorder spinal muscular atrophy (SMA), the most common inherited killer of infants, is caused by insufficient expression of survival motor neuron (SMN) protein. SMA therapeutics development efforts have focused on identifying strategies to increase SMN expression. We identified a long non-coding RNA (lncRNA) that arises from the antisense strand of SMN, SMN-AS1, which is enriched in neurons and transcriptionally represses SMN expression by recruiting the epigenetic Polycomb repressive complex-2. Targeted degradation of SMN-AS1 with antisense oligonucleotides (ASOs) increases SMN expression in patient-derived cells, cultured neurons, and the mouse central nervous system. SMN-AS1 ASOs delivered together with SMN2 splice-switching oligonucleotides additively increase SMN expression and improve survival of severe SMA mice. This study is the first proof of concept that targeting a lncRNA to transcriptionally activate SMN2 can be combined with SMN2 splicing modification to ameliorate SMA and demonstrates the promise of combinatorial ASOs for the treatment of neurogenetic disorders., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Published
2017
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