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Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease
The alpha-synuclein–caveolin 1 axis is suggested to be of role in the pathogenesis of Parkinson’s disease in cell line models. The objective of this study was to analyze the homozygous haplotype compartment of the human caveolin 1 gene upstream purine complex in patients afflicted with Parkinson’s d...
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| Published in: | Journal of molecular neuroscience 2013-10, Vol.51 (2), p.389-393 |
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| creator | Darvish, Hossein Heidari, Abolfazl Hosseinkhani, Saman Movafagh, Abolfazl Khaligh, Ali Jamshidi, Javad Noorollahi-Moghaddam, Hamid Heidari-Rostami, Hamid Reza Karkheiran, Siamak Shahidi, Gholam-Ali Togha, Mansoureh Paknejad, Seyed Mohammad Hassan Ashrafian, Hossein Abdi, Siamak Firouzabadi, Saghar Ghasemi Jamaldini, Seyed Hamid Ohadi, Mina |
| description | The alpha-synuclein–caveolin 1 axis is suggested to be of role in the pathogenesis of Parkinson’s disease in cell line models. The objective of this study was to analyze the homozygous haplotype compartment of the human caveolin 1 gene upstream purine complex in patients afflicted with Parkinson’s disease. This complex was screened in patients with Parkinson’s disease (
n
= 141) and compared with a group of controls (
n
= 760) using polymerase chain reaction and sequencing. The expression activity of the homozygous haplotypes was then examined using luciferase Dual-Glo system in human neuronal cell line, LAN-5. Six haplotypes were found to be homozygous in the patients, and not in the control pool (Fisher exact
p
|
| doi_str_mv | 10.1007/s12031-013-0021-9 |
| format | article |
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n
= 141) and compared with a group of controls (
n
= 760) using polymerase chain reaction and sequencing. The expression activity of the homozygous haplotypes was then examined using luciferase Dual-Glo system in human neuronal cell line, LAN-5. Six haplotypes were found to be homozygous in the patients, and not in the control pool (Fisher exact
p
< 1 × 10
−6
). Three of those haplotypes were specific to Parkinson’s disease (Fisher exact
p
< 0.002), and the remaining three overlapped with homozygous haplotypes in Alzheimer’s disease and multiple sclerosis (Fisher exact
p
< 0.002). The disease haplotypes contained motif lengths that were nonexistent in the control homozygous haplotype pool and significantly increased gene expression (
p
< 9 × 10
—6
). We conclude that skew in the caveolin 1 purine complex homozygous haplotype compartment and an additive effect of those haplotypes may be linked with Parkinson’s disease.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-013-0021-9</identifier><identifier>PMID: 23640536</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adult ; Aged ; Alzheimer's disease ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Case-Control Studies ; Caveolin 1 - genetics ; Cell Biology ; Cell Line ; Dopamine ; Female ; Gene expression ; Haplotypes ; Homozygote ; Hospitals ; Humans ; Male ; Middle Aged ; Neurochemistry ; Neurology ; Neurosciences ; Parkinson Disease - genetics ; Parkinson's disease ; Proteomics ; Purines - chemistry ; Regulatory Sequences, Nucleic Acid - genetics ; Signal transduction</subject><ispartof>Journal of molecular neuroscience, 2013-10, Vol.51 (2), p.389-393</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-b4f47a5f45573c2d7f524d5460916c977235dd9727a28db4267da2d22c50d1b23</citedby><cites>FETCH-LOGICAL-c372t-b4f47a5f45573c2d7f524d5460916c977235dd9727a28db4267da2d22c50d1b23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23640536$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Darvish, Hossein</creatorcontrib><creatorcontrib>Heidari, Abolfazl</creatorcontrib><creatorcontrib>Hosseinkhani, Saman</creatorcontrib><creatorcontrib>Movafagh, Abolfazl</creatorcontrib><creatorcontrib>Khaligh, Ali</creatorcontrib><creatorcontrib>Jamshidi, Javad</creatorcontrib><creatorcontrib>Noorollahi-Moghaddam, Hamid</creatorcontrib><creatorcontrib>Heidari-Rostami, Hamid Reza</creatorcontrib><creatorcontrib>Karkheiran, Siamak</creatorcontrib><creatorcontrib>Shahidi, Gholam-Ali</creatorcontrib><creatorcontrib>Togha, Mansoureh</creatorcontrib><creatorcontrib>Paknejad, Seyed Mohammad Hassan</creatorcontrib><creatorcontrib>Ashrafian, Hossein</creatorcontrib><creatorcontrib>Abdi, Siamak</creatorcontrib><creatorcontrib>Firouzabadi, Saghar Ghasemi</creatorcontrib><creatorcontrib>Jamaldini, Seyed Hamid</creatorcontrib><creatorcontrib>Ohadi, Mina</creatorcontrib><title>Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>The alpha-synuclein–caveolin 1 axis is suggested to be of role in the pathogenesis of Parkinson’s disease in cell line models. The objective of this study was to analyze the homozygous haplotype compartment of the human caveolin 1 gene upstream purine complex in patients afflicted with Parkinson’s disease. This complex was screened in patients with Parkinson’s disease (
n
= 141) and compared with a group of controls (
n
= 760) using polymerase chain reaction and sequencing. The expression activity of the homozygous haplotypes was then examined using luciferase Dual-Glo system in human neuronal cell line, LAN-5. Six haplotypes were found to be homozygous in the patients, and not in the control pool (Fisher exact
p
< 1 × 10
−6
). Three of those haplotypes were specific to Parkinson’s disease (Fisher exact
p
< 0.002), and the remaining three overlapped with homozygous haplotypes in Alzheimer’s disease and multiple sclerosis (Fisher exact
p
< 0.002). The disease haplotypes contained motif lengths that were nonexistent in the control homozygous haplotype pool and significantly increased gene expression (
p
< 9 × 10
—6
). We conclude that skew in the caveolin 1 purine complex homozygous haplotype compartment and an additive effect of those haplotypes may be linked with Parkinson’s disease.</description><subject>Adult</subject><subject>Aged</subject><subject>Alzheimer's disease</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Case-Control Studies</subject><subject>Caveolin 1 - genetics</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Dopamine</subject><subject>Female</subject><subject>Gene expression</subject><subject>Haplotypes</subject><subject>Homozygote</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Parkinson Disease - genetics</subject><subject>Parkinson's disease</subject><subject>Proteomics</subject><subject>Purines - chemistry</subject><subject>Regulatory Sequences, Nucleic Acid - genetics</subject><subject>Signal transduction</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1kctOwzAQRS0EgvL4ADbIEhs2Ab-dLEt5FAmJLmBtubFTAkkc7ARRVvwGv8eX4NKCEBKrWcyZOzP3ArCP0TFGSJ4ETBDFCcI0QYjgJFsDA8x5lmAsxDoYoDTjSSoysQW2Q3hYMAynm2CLUMEQp2IAytNSB2vg2NXudT5zfYBj3Vaum7c2wGHuXQiwu7dw3Ne6gSP9bF1VNhDDuzZ03uoaTnpfNhaOXN1W9gXG5kT7x7IJrvl4ew_wrAw27tgFG4Wugt1b1R1wd3F-Oxon1zeXV6PhdZJTSbpkygomNS8Y55LmxMiCE2Y4EyjDIs-kJJQbk0kiNUnNlBEhjSaGkJwjg6eE7oCjpW7r3VNvQ6fqMuS2qnRj43sKM8pTJgVlET38gz643jfxugXFuCAsFZHCS-rLDG8L1fqy1n6uMFKLHNQyBxVzUAuPVRZnDlbK_bS25mfi2_gIkCUQYquZWf9r9b-qn-AFknM</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Darvish, Hossein</creator><creator>Heidari, Abolfazl</creator><creator>Hosseinkhani, Saman</creator><creator>Movafagh, Abolfazl</creator><creator>Khaligh, Ali</creator><creator>Jamshidi, Javad</creator><creator>Noorollahi-Moghaddam, Hamid</creator><creator>Heidari-Rostami, Hamid Reza</creator><creator>Karkheiran, Siamak</creator><creator>Shahidi, Gholam-Ali</creator><creator>Togha, Mansoureh</creator><creator>Paknejad, Seyed Mohammad Hassan</creator><creator>Ashrafian, Hossein</creator><creator>Abdi, Siamak</creator><creator>Firouzabadi, Saghar Ghasemi</creator><creator>Jamaldini, Seyed Hamid</creator><creator>Ohadi, Mina</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20131001</creationdate><title>Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease</title><author>Darvish, Hossein ; Heidari, Abolfazl ; Hosseinkhani, Saman ; Movafagh, Abolfazl ; Khaligh, Ali ; Jamshidi, Javad ; Noorollahi-Moghaddam, Hamid ; Heidari-Rostami, Hamid Reza ; Karkheiran, Siamak ; Shahidi, Gholam-Ali ; Togha, Mansoureh ; Paknejad, Seyed Mohammad Hassan ; Ashrafian, Hossein ; Abdi, Siamak ; Firouzabadi, Saghar Ghasemi ; Jamaldini, Seyed Hamid ; Ohadi, Mina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-b4f47a5f45573c2d7f524d5460916c977235dd9727a28db4267da2d22c50d1b23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Alzheimer's disease</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Case-Control Studies</topic><topic>Caveolin 1 - genetics</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Dopamine</topic><topic>Female</topic><topic>Gene expression</topic><topic>Haplotypes</topic><topic>Homozygote</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Parkinson Disease - genetics</topic><topic>Parkinson's disease</topic><topic>Proteomics</topic><topic>Purines - chemistry</topic><topic>Regulatory Sequences, Nucleic Acid - genetics</topic><topic>Signal transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Darvish, Hossein</creatorcontrib><creatorcontrib>Heidari, Abolfazl</creatorcontrib><creatorcontrib>Hosseinkhani, Saman</creatorcontrib><creatorcontrib>Movafagh, Abolfazl</creatorcontrib><creatorcontrib>Khaligh, Ali</creatorcontrib><creatorcontrib>Jamshidi, Javad</creatorcontrib><creatorcontrib>Noorollahi-Moghaddam, Hamid</creatorcontrib><creatorcontrib>Heidari-Rostami, Hamid Reza</creatorcontrib><creatorcontrib>Karkheiran, Siamak</creatorcontrib><creatorcontrib>Shahidi, Gholam-Ali</creatorcontrib><creatorcontrib>Togha, Mansoureh</creatorcontrib><creatorcontrib>Paknejad, Seyed Mohammad Hassan</creatorcontrib><creatorcontrib>Ashrafian, Hossein</creatorcontrib><creatorcontrib>Abdi, Siamak</creatorcontrib><creatorcontrib>Firouzabadi, Saghar Ghasemi</creatorcontrib><creatorcontrib>Jamaldini, Seyed Hamid</creatorcontrib><creatorcontrib>Ohadi, Mina</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Database (ProQuest)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Darvish, Hossein</au><au>Heidari, Abolfazl</au><au>Hosseinkhani, Saman</au><au>Movafagh, Abolfazl</au><au>Khaligh, Ali</au><au>Jamshidi, Javad</au><au>Noorollahi-Moghaddam, Hamid</au><au>Heidari-Rostami, Hamid Reza</au><au>Karkheiran, Siamak</au><au>Shahidi, Gholam-Ali</au><au>Togha, Mansoureh</au><au>Paknejad, Seyed Mohammad Hassan</au><au>Ashrafian, Hossein</au><au>Abdi, Siamak</au><au>Firouzabadi, Saghar Ghasemi</au><au>Jamaldini, Seyed Hamid</au><au>Ohadi, Mina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>51</volume><issue>2</issue><spage>389</spage><epage>393</epage><pages>389-393</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>The alpha-synuclein–caveolin 1 axis is suggested to be of role in the pathogenesis of Parkinson’s disease in cell line models. The objective of this study was to analyze the homozygous haplotype compartment of the human caveolin 1 gene upstream purine complex in patients afflicted with Parkinson’s disease. This complex was screened in patients with Parkinson’s disease (
n
= 141) and compared with a group of controls (
n
= 760) using polymerase chain reaction and sequencing. The expression activity of the homozygous haplotypes was then examined using luciferase Dual-Glo system in human neuronal cell line, LAN-5. Six haplotypes were found to be homozygous in the patients, and not in the control pool (Fisher exact
p
< 1 × 10
−6
). Three of those haplotypes were specific to Parkinson’s disease (Fisher exact
p
< 0.002), and the remaining three overlapped with homozygous haplotypes in Alzheimer’s disease and multiple sclerosis (Fisher exact
p
< 0.002). The disease haplotypes contained motif lengths that were nonexistent in the control homozygous haplotype pool and significantly increased gene expression (
p
< 9 × 10
—6
). We conclude that skew in the caveolin 1 purine complex homozygous haplotype compartment and an additive effect of those haplotypes may be linked with Parkinson’s disease.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23640536</pmid><doi>10.1007/s12031-013-0021-9</doi><tpages>5</tpages></addata></record> |
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| ispartof | Journal of molecular neuroscience, 2013-10, Vol.51 (2), p.389-393 |
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| language | eng |
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| subjects | Adult Aged Alzheimer's disease Biochemistry Biomedical and Life Sciences Biomedicine Case-Control Studies Caveolin 1 - genetics Cell Biology Cell Line Dopamine Female Gene expression Haplotypes Homozygote Hospitals Humans Male Middle Aged Neurochemistry Neurology Neurosciences Parkinson Disease - genetics Parkinson's disease Proteomics Purines - chemistry Regulatory Sequences, Nucleic Acid - genetics Signal transduction |
| title | Biased Homozygous Haplotypes Across the Human Caveolin 1 Upstream Purine Complex in Parkinson’s Disease |
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