択一的スプライシングとは - わかりやすく解説 Weblio辞書

ウィキペディア

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選択的スプライシング

(択一的スプライシングから転送)

出典: フリー百科事典『ウィキペディア（Wikipedia）』 (2023/04/30 14:06 UTC 版)

選択的スプライシング（せんたくてき－、Alternative Splicing）とは、DNAからの転写過程において特定のエクソンをとばしてスプライシングを行うことである。択一的スプライシングとも呼ばれる。

出典

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^ ^a ^b ^c ^d “Aberrant RNA splicing in cancer; expression changes and driver mutations of splicing factor genes”. Oncogene 35 (19): 2413–27. (May 2016). doi:10.1038/onc.2015.318. PMID 26300000.
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^ “Role of RNA structure in regulating pre-mRNA splicing”. Trends in Biochemical Sciences 35 (3): 169–78. (March 2010). doi:10.1016/j.tibs.2009.10.004. PMC 2834840. PMID 19959365.
^ ^a ^b “Next-generation SELEX identifies sequence and structural determinants of splicing factor binding in human pre-mRNA sequence”. RNA 15 (12): 2385–97. (December 2009). doi:10.1261/rna.1821809. PMC 2779669. PMID 19861426.
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^ ^a ^b “Deciphering the splicing code”. Nature 465 (7294): 53–9. (May 2010). Bibcode: 2010Natur.465...53B. doi:10.1038/nature09000. PMID 20445623.
^ “Positive selection acting on splicing motifs reflects compensatory evolution”. Genome Research 18 (4): 533–43. (April 2008). doi:10.1101/gr.070268.107. PMC 2279241. PMID 18204002.
^ “Single nucleotide polymorphism-based validation of exonic splicing enhancers”. PLoS Biology 2 (9): E268. (September 2004). doi:10.1371/journal.pbio.0020268. PMC 514884. PMID 15340491.
^ “The Function of DNA Methylation Marks in Social Insects”. Frontiers in Ecology and Evolution 4: 57. (2016). doi:10.3389/fevo.2016.00057.
^ “Physiological and molecular mechanisms of nutrition in honey bees.”. Advances in insect physiology. 49. Academic Press. (January 2015). pp. 25–58. doi:10.1016/bs.aiip.2015.06.002
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^ “Genome-wide association between DNA methylation and alternative splicing in an invertebrate”. BMC Genomics 13 (1): 480. (September 2012). doi:10.1186/1471-2164-13-480. PMC 3526459. PMID 22978521.
^ “Insights into social insects from the genome of the honeybee Apis mellifera”. Nature 443 (7114): 931–49. (October 2006). Bibcode: 2006Natur.443..931T. doi:10.1038/nature05260. PMC 2048586. PMID 17073008.
^ “RNA interference knockdown of DNA methyl-transferase 3 affects gene alternative splicing in the honey bee”. Proceedings of the National Academy of Sciences of the United States of America 110 (31): 12750–5. (July 2013). Bibcode: 2013PNAS..11012750L. doi:10.1073/pnas.1310735110. PMC 3732956. PMID 23852726.
^ ^a ^b “Assembly of specific SR protein complexes on distinct regulatory elements of the Drosophila doublesex splicing enhancer”. Genes & Development 10 (16): 2089–101. (August 1996). doi:10.1101/gad.10.16.2089. PMID 8769651.
^ “The role of U2AF35 and U2AF65 in enhancer-dependent splicing”. RNA 7 (6): 806–18. (June 2001). doi:10.1017/S1355838201010317. PMC 1370132. PMID 11421359.
^ “Expression of CD95 (Fas) in sun-exposed human skin and cutaneous carcinomas”. Cancer 94 (3): 814–9. (February 2002). doi:10.1002/cncr.10277. PMID 11857317.
^ ^a ^b “Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition”. Molecular Cell 19 (4): 475–84. (August 2005). doi:10.1016/j.molcel.2005.06.015. PMID 16109372.
^ ^a ^b “SC35 and heterogeneous nuclear ribonucleoprotein A/B proteins bind to a juxtaposed exonic splicing enhancer/exonic splicing silencer element to regulate HIV-1 tat exon 2 splicing”. The Journal of Biological Chemistry 279 (11): 10077–84. (March 2004). doi:10.1074/jbc.M312743200. PMID 14703516.
^ “A second exon splicing silencer within human immunodeficiency virus type 1 tat exon 2 represses splicing of Tat mRNA and binds protein hnRNP H”. The Journal of Biological Chemistry 276 (44): 40464–75. (November 2001). doi:10.1074/jbc.M104070200. PMID 11526107.
^ “HHMI Bulletin September 2005: Alternative Splicing”. www.hhmi.org. 2009年6月22日時点のオリジナルよりアーカイブ。2009年5月26日閲覧。
^ “Alternative splicing in concert with protein intrinsic disorder enables increased functional diversity in multicellular organisms”. Proceedings of the National Academy of Sciences of the United States of America 103 (22): 8390–5. (May 2006). Bibcode: 2006PNAS..103.8390R. doi:10.1073/pnas.0507916103. PMC 1482503. PMID 16717195.
^ “The emerging era of genomic data integration for analyzing splice isoform function”. Trends in Genetics 30 (8): 340–7. (August 2014). doi:10.1016/j.tig.2014.05.005. PMC 4112133. PMID 24951248.
^ ^a ^b “Systematically differentiating functions for alternatively spliced isoforms through integrating RNA-seq data”. PLoS Computational Biology 9 (11): e1003314. (Nov 2013). Bibcode: 2013PLSCB...9E3314E. doi:10.1371/journal.pcbi.1003314. PMC 3820534. PMID 24244129.
^ “Functional and evolutionary analysis of alternatively spliced genes is consistent with an early eukaryotic origin of alternative splicing”. BMC Evolutionary Biology 7: 188. (October 2007). doi:10.1186/1471-2148-7-188. PMC 2082043. PMID 17916237.
^ “Analysis of expressed sequence tags indicates 35,000 human genes”. Nature Genetics 25 (2): 232–4. (June 2000). doi:10.1038/76115. PMID 10835644.
^ “Estimate of human gene number provided by genome-wide analysis using Tetraodon nigroviridis DNA sequence”. Nature Genetics 25 (2): 235–8. (June 2000). doi:10.1038/76118. PMID 10835645.
^ “Alternative splicing and genome complexity”. Nature Genetics 30 (1): 29–30. (January 2002). doi:10.1038/ng803. PMID 11743582.
^ “Different levels of alternative splicing among eukaryotes”. Nucleic Acids Research 35 (1): 125–31. (2006). doi:10.1093/nar/gkl924. PMC 1802581. PMID 17158149.
^ “Are splicing mutations the most frequent cause of hereditary disease?”. FEBS Letters 579 (9): 1900–3. (March 2005). doi:10.1016/j.febslet.2005.02.047. PMID 15792793.
^ “The pathobiology of splicing”. The Journal of Pathology 220 (2): 152–63. (January 2010). doi:10.1002/path.2649. PMC 2855871. PMID 19918805.
^ “A new class of protein cancer biomarker candidates: differentially expressed splice variants of ERBB2 (HER2/neu) and ERBB1 (EGFR) in breast cancer cell lines”. Journal of Proteomics 107: 103–12. (July 2014). doi:10.1016/j.jprot.2014.04.012. PMC 4123867. PMID 24802673.
^ “Transcriptome instability as a molecular pan-cancer characteristic of carcinomas”. BMC Genomics 15: 672. (August 2014). doi:10.1186/1471-2164-15-672. PMC 3219073. PMID 25109687.
^ “Transcriptome instability in colorectal cancer identified by exon microarray analyses: Associations with splicing factor expression levels and patient survival”. Genome Medicine 3 (5): 32. (May 2011). doi:10.1186/gm248. PMC 4137096. PMID 21619627.
^ “Abnormal RNA splicing and genomic instability after induction of DNMT3A mutations by CRISPR/Cas9 gene editing”. Blood Cells, Molecules & Diseases 69: 10–22. (March 2018). doi:10.1016/j.bcmd.2017.12.002. PMC 6728079. PMID 29324392.
^ “Insights into the connection between cancer and alternative splicing”. Trends in Genetics 24 (1): 7–10. (January 2008). doi:10.1016/j.tig.2007.10.001. PMID 18054115.
^ ^a ^b “Cell motility is controlled by SF2/ASF through alternative splicing of the Ron protooncogene”. Molecular Cell 20 (6): 881–90. (December 2005). doi:10.1016/j.molcel.2005.10.026. PMID 16364913.
^ “Identification of alternatively spliced mRNA variants related to cancers by genome-wide ESTs alignment”. Oncogene 23 (17): 3013–23. (April 2004). doi:10.1038/sj.onc.1207362. PMID 15048092.
^ “Abnormally spliced beta-globin mRNAs: a single point mutation generates transcripts sensitive and insensitive to nonsense-mediated mRNA decay”. Blood 99 (5): 1811–6. (March 2002). doi:10.1182/blood.V99.5.1811. PMID 11861299.
^ “Cellular basis of memory for addiction”. Dialogues in Clinical Neuroscience 15 (4): 431–43. (December 2013). PMC 3898681. PMID 24459410. "DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement"
^ “Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. The American Journal of Drug and Alcohol Abuse 40 (6): 428–37. (November 2014). doi:10.3109/00952990.2014.933840. PMID 25083822. "ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."
^ “Epigenetic regulation in drug addiction”. Annals of Agricultural and Environmental Medicine 19 (3): 491–6. (2012). PMID 23020045. "For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken"
^ “Natural rewards, neuroplasticity, and non-drug addictions”. Neuropharmacology 61 (7): 1109–22. (December 2011). doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704. PMID 21459101.
^ “Epigenetics in alternative pre-mRNA splicing”. Cell 144 (1): 16–26. (January 2011). doi:10.1016/j.cell.2010.11.056. PMC 3038581. PMID 21215366.
^ “Predictive identification of exonic splicing enhancers in human genes”. Science 297 (5583): 1007–13. (August 2002). Bibcode: 2002Sci...297.1007F. doi:10.1126/science.1073774. PMID 12114529.
^ “Revealing global regulatory features of mammalian alternative splicing using a quantitative microarray platform”. Molecular Cell 16 (6): 929–41. (December 2004). doi:10.1016/j.molcel.2004.12.004. PMID 15610736.
^ “A rapid high-throughput method for mapping ribonucleoproteins (RNPs) on human pre-mRNA”. Journal of Visualized Experiments 34 (34): 1622. (December 2009). doi:10.3791/1622. PMC 3152247. PMID 19956082.
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^ “High-throughput binding analysis determines the binding specificity of ASF/SF2 on alternatively spliced human pre-mRNAs”. Combinatorial Chemistry & High Throughput Screening 13 (3): 242–52. (March 2010). doi:10.2174/138620710790980522. PMC 3427726. PMID 20015017.
^ “Large-scale mapping of branchpoints in human pre-mRNA transcripts in vivo”. Nature Structural & Molecular Biology 19 (7): 719–21. (June 2012). doi:10.1038/nsmb.2327. PMC 3465671. PMID 22705790.

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