We are analyzing https://link.springer.com/article/10.1007/s10048-007-0106-0.

Title:
Identification and characterization of a new alpha-synuclein isoform and its role in Lewy body diseases | Neurogenetics
Description:
Alternative splicing is an important mechanism to generate a large number of mRNAs, thus increasing proteome diversity and tissue specificity. Three transcript variants of alpha-synuclein, a neuronal protein mainly involved in synapses, have been described so far. Whereas alpha-synuclein 140 is the whole and main transcript, alpha-synuclein 112 and 126 are short proteins that result from in-frame deletions of exons 3 and 5, respectively. Because the aforesaid alpha-synuclein isoforms show differential expression changes in Lewy body diseases (LBDs), in the present work, we searched for a fourth alpha-synuclein isoform and studied its expression levels in LBD brains. By using isoform-specific primers, isoform co-amplification and direct sequencing, we identified alpha-synuclein 98, which lacks exons 3 and 5. mRNA expression analyses in non-neuronal tissue revealed that alpha-synuclein 98 is a brain-specific splice variant with varying expression levels in different areas of fetal and adult brain. Additionally, we studied alpha-synuclein 98 expression levels by real-time semi-quantitative RT-PCR in the frontal cortices of LBD patients and compared them with those of Alzheimer disease (AD) patients and control subjects. Overexpression of alpha-synuclein 98 in LBD and AD brains would indicate its specific involvement in the pathogenesis of these neurodegenerative disorders.
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article, google, scholar, cas, pubmed, alphasynuclein, disease, lewy, splicing, expression, beyer, ferrer, bodies, alternative, body, alzheimer, barcelona, isoform, ariza, access, dementia, res, sci, lao, carrato, structure, biol, alzheimers, lee, privacy, cookies, content, role, diseases, katrin, tissue, protein, mrna, brain, parkinsons, neuropathol, exon, proc, natl, acad, domain, spain, analysis, publish, search,

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real-time semi-quantitative rt-pcr month download article/chapter membrane-bound alpha-synuclein studied tissue-dependent alternative splicing mice lacking alpha-synuclein isidro ferrer & aurelio ariza membrane-bound alpha-synuclein brain-specific splice variant protein-membrane interacting domain fourth alpha-synuclein isoform abnormal alpha-synuclein interactions site-directed spin labeling protein-protein interacting domain mrna expression analyses tissue-specific alternative splicing differential expression alpha-synuclein secondary structure full article pdf disease neurodegeneration parkinson' neuronal tissue revealed synphilin-1 isoform expression article neurogenetics aims varying expression levels alpha-synuclein isoform privacy choices/manage cookies isoform-specific primers human alpha-synuclein alpha-synuclein regulates mrna transcripts encoded lewy body diseases article beyer author information authors de silva ha de jong pj α-synuclein alpha-synuclein isoforms katrin beyer related subjects identified alpha-synuclein 98 alpha-synuclein crosslinks lewy body disease unorganized c-terminal lewy bodies imply check access instant access alpha-synuclein structure attenuated synaptic responses schizophrenia brain cortex secondary structure propensities electronic supplementary material

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         description:Alternative splicing is an important mechanism to generate a large number of mRNAs, thus increasing proteome diversity and tissue specificity. Three transcript variants of alpha-synuclein, a neuronal protein mainly involved in synapses, have been described so far. Whereas alpha-synuclein 140 is the whole and main transcript, alpha-synuclein 112 and 126 are short proteins that result from in-frame deletions of exons 3 and 5, respectively. Because the aforesaid alpha-synuclein isoforms show differential expression changes in Lewy body diseases (LBDs), in the present work, we searched for a fourth alpha-synuclein isoform and studied its expression levels in LBD brains. By using isoform-specific primers, isoform co-amplification and direct sequencing, we identified alpha-synuclein 98, which lacks exons 3 and 5. mRNA expression analyses in non-neuronal tissue revealed that alpha-synuclein 98 is a brain-specific splice variant with varying expression levels in different areas of fetal and adult brain. Additionally, we studied alpha-synuclein 98 expression levels by real-time semi-quantitative RT-PCR in the frontal cortices of LBD patients and compared them with those of Alzheimer disease (AD) patients and control subjects. Overexpression of alpha-synuclein 98 in LBD and AD brains would indicate its specific involvement in the pathogenesis of these neurodegenerative disorders.
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