Literatura académica sobre el tema "Scd6 C-terminal"
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Artículos de revistas sobre el tema "Scd6 C-terminal"
Chang, Eric, Geoffrey Bartholomeusz, Ruth Pimental, Jing Chen, Hong Lai, Li-hua L. Wang, Peirong Yang y Stevan Marcus. "Direct Binding and In Vivo Regulation of the Fission Yeast p21-Activated Kinase Shk1 by the SH3 Domain Protein Scd2". Molecular and Cellular Biology 19, n.º 12 (1 de diciembre de 1999): 8066–74. http://dx.doi.org/10.1128/mcb.19.12.8066.
Texto completoNelson, K. K., M. Holmer y S. K. Lemmon. "SCD5, a suppressor of clathrin deficiency, encodes a novel protein with a late secretory function in yeast." Molecular Biology of the Cell 7, n.º 2 (febrero de 1996): 245–60. http://dx.doi.org/10.1091/mbc.7.2.245.
Texto completoChristiansen, Dale, Patricia Devaux, Brigitte Réveil, Alexey Evlashev, Branka Horvat, Josette Lamy, Chantal Rabourdin-Combe, Jacques H. M. Cohen y Denis Gerlier. "Octamerization Enables Soluble CD46 Receptor To Neutralize Measles Virus In Vitro and In Vivo". Journal of Virology 74, n.º 10 (15 de mayo de 2000): 4672–78. http://dx.doi.org/10.1128/jvi.74.10.4672-4678.2000.
Texto completoZhao, Xiaoyang, Min Wang, Jingjing Liu y Xiong Su. "Stearoyl CoA Desaturase 1 and Inositol-Requiring Protein 1α Determine the Efficiency of Oleic Acid in Alleviating Silica Nanoparticle-Induced Insulin Resistance". Journal of Biomedical Nanotechnology 17, n.º 7 (1 de julio de 2021): 1349–63. http://dx.doi.org/10.1166/jbn.2021.3109.
Texto completoJha, Archana, Malini Ahuja, József Maléth, Claudia M. Moreno, Joseph P. Yuan, Min Seuk Kim y Shmuel Muallem. "The STIM1 CTID domain determines access of SARAF to SOAR to regulate Orai1 channel function". Journal of Cell Biology 202, n.º 1 (1 de julio de 2013): 71–79. http://dx.doi.org/10.1083/jcb.201301148.
Texto completoHenry, Kenneth R., Kathleen D'Hondt, JiSuk Chang, Thomas Newpher, Kristen Huang, R. Tod Hudson, Howard Riezman y Sandra K. Lemmon. "Scd5p and Clathrin Function Are Important for Cortical Actin Organization, Endocytosis, and Localization of Sla2p in Yeast". Molecular Biology of the Cell 13, n.º 8 (agosto de 2002): 2607–25. http://dx.doi.org/10.1091/mbc.e02-01-0012.
Texto completoPapadaki, Piyi, Véronique Pizon, Brian Onken y Eric C. Chang. "Two Ras Pathways in Fission Yeast Are Differentially Regulated by Two Ras Guanine Nucleotide Exchange Factors". Molecular and Cellular Biology 22, n.º 13 (1 de julio de 2002): 4598–606. http://dx.doi.org/10.1128/mcb.22.13.4598-4606.2002.
Texto completoZhuang, Zhen-Jie, Chao-Wen Shan, Bo Li, Min-Xia Pang, Han Wang, Yan Luo, Yin-lan Liu et al. "Linarin Enriched Extract Attenuates Liver Injury and Inflammation Induced by High-Fat High-Cholesterol Diet in Rats". Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4701570.
Texto completoYu, Wenjie, Cheng-Zhen Chen, Yanxia Peng, Ze Li, Yan Gao, Shuang Liang, Bao Yuan, Nam-Hyung Kim, Hao Jiang y Jia-Bao Zhang. "KRAS Affects Adipogenic Differentiation by Regulating Autophagy and MAPK Activation in 3T3-L1 and C2C12 Cells". International Journal of Molecular Sciences 22, n.º 24 (20 de diciembre de 2021): 13630. http://dx.doi.org/10.3390/ijms222413630.
Texto completoJung, Tae Woo, Sun-Young Kim, Da-Som Kim, Eui-Cheol Shin, Yong Bae Park y Kyoung-Tae Lee. "Euodia daniellii Hemsl. (Bee-Bee Tree) Oil Attenuates Palmitate-Induced Lipid Accumulation and Apoptosis in Hepatocytes". Pharmacology 101, n.º 5-6 (2018): 298–308. http://dx.doi.org/10.1159/000487892.
Texto completoTesis sobre el tema "Scd6 C-terminal"
Tsou, Wei-Ling y 鄒瑋玲. "Analyzing C-terminal alternative splicing of Cav2.1and developing the Splice-Isoform-Specific RNAi as apotential therapeutic strategy for SCA6". Thesis, 2011. http://ndltd.ncl.edu.tw/handle/67428207508990682896.
Texto completo國立陽明大學
神經科學研究所
99
Spinocerebellar ataxia type 6 (SCA6) is an inherited neurodegenerative disorder characterized by the preferential degeneration of cerebellar Purkinje cells. SCA6 is caused by a polyglutamine (polyQ)-coding CAG repeat expansion in the 3’ end of the CACNA1A gene, which encodes the P/Q-type voltage-gated calcium channel alpha1A subunit Cav2.1. Purkinje cells express two major Cav2.1 mRNA splice isoforms (protein variants). The “long” variant (V2) contains the pathogenic polyglutamine expansion in the C-terminal tail, whereas the “short” variant (V1) lacks the polyglutamine tract. No effective treatments are currently available to combat this relentlessly progressive disorder; therefore, there is a pressing need to develop safe and efficacious therapies for preventing the neurodegeneration associated with SCA6. RNA interference is a promising therapeutic approach for neurodegenerative diseases, including various autosomal dominant spinocerebellar ataxias. Taking advantage of alternative splicing near the 3’ end of Cav2.1 transcripts, we designed splice isoform-specific (SIS)-RNAi molecules to selectively suppress expression of the polyQ-coding variant (V2). Embedding anti-SCA6 siRNAs within the context of a modified, brain-specific human miR-124 led to improved splice-specific target suppression compared to first generation shRNA platforms. We identified 3’ end base pair modifications in fully processed anti-SCA6 guide strands, supporting the proper recognition of these novel artificial miR124-based constructs by the cellular RNAi machinery. In the Cav2.1 mini-gene reporter system, CAG expansions were also found to enhance splicing activity at the 3’ end of Cav2.1, leading to a selective increase in the levels of polyQ-containing Cav2.1 variants, which may contribute to SCA6 disease pathogenesis. We cloned U6-miR124 expression cassettes into a recombinant adeno-associated viral (rAAV) vector for in vivo testing. Laser capture microdissection (LCM) of mouse Purkinje cells for Cav2.1 mRNA quantification revealed that the injection of mice with a low dose of rAAV-miR124 significantly reduced endogenous Cav2.1 expression. Unexpectedly, injection of high levels of rAAV induced significant neurotoxicity in mouse Purkinje neurons. Our results support the preclinical development of SIS-RNAi as a novel therapeutic approach for the treatment of SCA6; however, improper levels of rAAV-mediated delivery could be a potential concern. The long-term safety and efficacy of rAAV-mediated miRNA delivery should be further investigated in mouse models.