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Items 1 to 10 of about 325650
1. Ayuso T, Aznar P, Soriano L, Olaskoaga A, Roldán M, Otano M, Ajuria I, Soriano G, Lacruz F, Mendioroz M: Vitamin D receptor gene is epigenetically altered and transcriptionally up-regulated in multiple sclerosis. PLoS One; 2017;12(3):e0174726
MedlinePlus Health Information. consumer health - Multiple Sclerosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vitamin D receptor gene is epigenetically altered and transcriptionally up-regulated in multiple sclerosis.
  • OBJECTIVE: Vitamin D deficiency has been linked to increased risk of multiple sclerosis (MS) and poor outcome.
  • However, the specific role that vitamin D plays in MS still remains unknown.
  • In order to identify potential mechanisms underlying vitamin D effects in MS, we profiled epigenetic changes in vitamin D receptor (VDR) gene to identify genomic regulatory elements relevant to MS pathogenesis.
  • METHODS: Human T cells derived from whole blood by negative selection were isolated in a set of 23 relapsing-remitting MS (RRMS) patients and 12 controls matched by age and gender.
  • CONCLUSIONS: An alternative promoter of the VDR gene shows altered DNA methylation levels in patients with multiple sclerosis, and it is associated with VDR mRNA upregulation.
  • This locus may represent a candidate regulatory element in the genome relevant to MS pathogenesis.
  • [MeSH-major] Epigenesis, Genetic. Multiple Sclerosis / genetics. Receptors, Calcitriol / genetics. Transcriptional Activation. Up-Regulation
  • [MeSH-minor] Adult. CpG Islands / genetics. DNA Methylation. Female. Humans. Male. Middle Aged. Multiple Sclerosis, Relapsing-Remitting / blood. Multiple Sclerosis, Relapsing-Remitting / genetics. Promoter Regions, Genetic / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Vitamin D / blood. Young Adult

  • Genetic Alliance. consumer health - Multiple Sclerosis.
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  • [Cites] J Immunol. 2009 Feb 15;182(4):2063-73 [19201859.001]
  • [Cites] Bioinformatics. 2002 Nov;18(11):1427-31 [12424112.001]
  • [Cites] Clin Epigenetics. 2015 Nov 05;7:118 [26550040.001]
  • [Cites] J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):352-6 [17240138.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Ann Neurol. 2011 Feb;69(2):292-302 [21387374.001]
  • [Cites] J Neurol Sci. 2010 Mar 15;290(1-2):16-21 [20064646.001]
  • [Cites] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216.001]
  • [Cites] Autoimmun Rev. 2011 Oct;10(12):733-43 [21621002.001]
  • [Cites] Mol Cell Biol. 2011 Sep;31(17):3653-69 [21746882.001]
  • [Cites] J Neuropathol Exp Neurol. 2013 Feb;72 (2):91-105 [23334593.001]
  • [Cites] PLoS Med. 2015 Aug 25;12(8):e1001866 [26305103.001]
  • [Cites] Gene. 2015 May 1;561(2):171-80 [25682935.001]
  • [Cites] Mult Scler. 2008 Nov;14(9):1220-4 [18653736.001]
  • [Cites] Neurology. 2014 Jul 15;83(3):278-86 [24871874.001]
  • [Cites] Nat Rev Genet. 2008 Jun;9(6):465-76 [18463664.001]
  • [Cites] Neuromolecular Med. 2015 Jun;17(2):83-96 [24652042.001]
  • [Cites] J Neurosci Res. 2007 Jul;85(9):2006-16 [17469138.001]
  • [Cites] Nat Rev Neurol. 2013 Jan;9(1):35-43 [23165337.001]
  • [Cites] J Clin Endocrinol Metab. 2011 Jan;96(1):53-8 [21118827.001]
  • [Cites] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W170-5 [18487274.001]
  • [Cites] JAMA Neurol. 2014 Mar;71(3):306-14 [24445558.001]
  • [Cites] Brain. 2009 May;132(Pt 5):1146-60 [19321461.001]
  • [Cites] Am J Physiol Renal Physiol. 2014 Dec 15;307(12):F1412-26 [25339699.001]
  • [Cites] Front Physiol. 2014 Apr 29;5:164 [24808866.001]
  • [Cites] Nat Rev Genet. 2013 Dec;14(12):880-93 [24217315.001]
  • [Cites] Ann Neurol. 2012 Aug;72(2):234-40 [22926855.001]
  • [Cites] J Immunol. 2011 Jan 1;186(1):92-102 [21131423.001]
  • [Cites] Neurologia. 2015 May 11;:null [25976949.001]
  • (PMID = 28355272.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, Calcitriol; 0 / VDR protein, human; 1406-16-2 / Vitamin D
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2. Ehya F, Abdul Tehrani H, Garshasbi M, Nabavi SM: Identification of miR-24 and miR-137 as novel candidate multiple sclerosis miRNA biomarkers using multi-staged data analysis protocol. Mol Biol Res Commun; 2017 Sep;6(3):127-140

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Identification of miR-24 and miR-137 as novel candidate multiple sclerosis miRNA biomarkers using multi-staged data analysis protocol.
  • Many studies have investigated misregulation of miRNAs relevant to multiple sclerosis (MS) pathogenesis.
  • Abnormal miRNAs can be used both as candidate biomarker for MS diagnosis and understanding the disease miRNA-mRNA regulatory network.
  • In this comprehensive study, misregulated miRNAs related to MS were collected from existing literature, databases and via in silico prediction.
  • A multi-staged data integration strategy (including the construction of miRNA-mRNA regulatory network and systematic data analysis) was conducted in order to investigate MS related miRNAs and their regulatory networks.
  • The final outcome was a bi-layer MS related regulatory network constructed with 27 miRNAs (seven of them were novel) and 59 mRNA targets.
  • The expression of themiR-24 and miR-137(as novel MS candidate biomarker) and miR-16, and miR-181 (as previously reported MS candidate biomarker) showed significant deregulation in 33 MS patients compared to the control.
  • The optimized data integration strategy conducted in this study found two miRNAs (miR-24and miR-16)that can be considered as candidate biomarkers for MS and also has the potential to generate a regulatory network to aid in further understanding the mechanisms underlying this disease.

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  • [Cites] J Immunol. 2013 May 15;190(10 ):5102-9 [23589616.001]
  • [Cites] Exp Neurol. 2015 Feb;264:1-7 [25433215.001]
  • [Cites] J Proteome Res. 2009 Jan;8(1):113-7 [19072545.001]
  • [Cites] Front Cell Neurosci. 2014 Mar 14;8:78 [24672429.001]
  • [Cites] Nat Methods. 2011 Sep 04;8(10):841-3 [21892151.001]
  • [Cites] Bone Marrow Transplant. 2015 Mar;50(3):380-9 [25486582.001]
  • [Cites] Neurol Neuroimmunol Neuroinflamm. 2016 Apr 20;3(3):e219 [27144214.001]
  • [Cites] PLoS One. 2011;6(9):e24604 [21949733.001]
  • [Cites] Ann Neurol. 2001 Jul;50(1):121-7 [11456302.001]
  • [Cites] Cell Physiol Biochem. 2015;35(1):281-91 [25591770.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Epigenetics. 2006 Apr-Jun;1(2):67-75 [17998807.001]
  • [Cites] Mol Psychiatry. 2017 Jan;22(1):44-55 [27620842.001]
  • [Cites] Int J Mol Sci. 2011;12(12):8695-712 [22272099.001]
  • [Cites] Autoimmun Rev. 2012 Jan;11(3):174-9 [21621006.001]
  • [Cites] Cytokine. 2009 Feb;45(2):58-69 [19121586.001]
  • [Cites] Hum Immunol. 2014 Jul;75(7):677-85 [24704866.001]
  • [Cites] J Neurosci. 2013 Dec 4;33(49):19112-9 [24305808.001]
  • [Cites] Ann Neurol. 2013 Jun;73(6):729-40 [23494648.001]
  • [Cites] J Neuroimmunol. 2014 Jan 15;266(1-2):56-63 [24332164.001]
  • [Cites] Biochim Biophys Acta. 2009 Jun;1792(6):497-505 [19268705.001]
  • [Cites] J Cell Mol Med. 2011 Jan;15(1):14-23 [21091634.001]
  • [Cites] Nat Immunol. 2009 Dec;10(12):1252-9 [19838199.001]
  • [Cites] Immune Netw. 2011 Oct;11(5):227-44 [22194706.001]
  • [Cites] PLoS One. 2009 Oct 13;4(10):e7440 [19823682.001]
  • [Cites] Nat Rev Genet. 2015 Feb;16(2):85-97 [25582081.001]
  • [Cites] Brain. 2001 Jun;124(Pt 6):1114-24 [11353727.001]
  • [Cites] Ann Neurol. 2013 Nov;74(5):709-20 [23818336.001]
  • [Cites] J Neuroimmunol. 2012 May 15;246(1-2):27-33 [22445295.001]
  • [Cites] J Transl Med. 2014 Mar 11;12:66 [24618011.001]
  • [Cites] Brain. 2009 Dec;132(Pt 12):3342-52 [19952055.001]
  • [Cites] Nucleic Acids Res. 1999 Jan 1;27(1):29-34 [9847135.001]
  • (PMID = 29071282.001).
  • [ISSN] 2322-181X
  • [Journal-full-title] Molecular biology research communications
  • [ISO-abbreviation] Mol Biol Res Commun
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Iran
  • [Keywords] NOTNLM ; Data integration / miR-137 / miR-24 / miRNA-mRNA regulatory network
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3. Dixit A, Tanaka A, Greer JM, Donnelly S: Novel Therapeutics for Multiple Sclerosis Designed by Parasitic Worms. Int J Mol Sci; 2017 Oct 13;18(10)

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel Therapeutics for Multiple Sclerosis Designed by Parasitic Worms.
  • According to the old friend's hypothesis, the diminished exposure to these parasites in the developed world has resulted in a dysregulated immune response that contributes to the increased incidence of immune mediated diseases such as Multiple Sclerosis (MS).
  • Indeed, the global distribution of MS shows an inverse correlation to the prevalence of helminth infection.
  • On this basis, the possibility of treating MS with helminth infection has been explored in animal models and phase 1 and 2 human clinical trials.

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  • [Cites] PLoS Pathog. 2011 May;7(5):e1002042 [21589904.001]
  • [Cites] Science. 2016 Mar 18;351(6279):1329-33 [26847546.001]
  • [Cites] Genome Biol. 2015 Apr 03;16:71 [25887684.001]
  • [Cites] J Interferon Cytokine Res. 2011 Dec;31(12):907-16 [21936633.001]
  • [Cites] J Immunol. 2009 Aug 1;183(3):1577-86 [19587018.001]
  • [Cites] Expert Rev Clin Immunol. 2009 Sep;5(5):487-9 [20477636.001]
  • [Cites] Immunol Rev. 2004 Oct;201:139-55 [15361238.001]
  • [Cites] Nat Immunol. 2016 Jun 21;17 (7):765-74 [27328006.001]
  • [Cites] Int J Parasitol. 2010 Apr;40(5):617-28 [19917288.001]
  • [Cites] J Biol Chem. 2014 Jan 17;289(3):1441-56 [24280214.001]
  • [Cites] Immunol Res. 2015 Mar;61(3):312-25 [25616617.001]
  • [Cites] Infect Immun. 2005 Jan;73(1):166-73 [15618151.001]
  • [Cites] Int Immunol. 2003 Jan;15(1):59-69 [12502726.001]
  • [Cites] J Exp Med. 2006 Apr 17;203(4):1105-16 [16606668.001]
  • [Cites] Mediators Inflamm. 2017;2017:8494572 [28744067.001]
  • [Cites] PLoS Negl Trop Dis. 2016 Sep 15;10 (9):e0004944 [27632204.001]
  • [Cites] Int J Parasitol. 2013 Mar;43(3-4):301-10 [23291463.001]
  • [Cites] Parasite Immunol. 2006 Oct;28(10):515-23 [16965287.001]
  • [Cites] Parasite Immunol. 2010 Jun;32(6):450-9 [20500676.001]
  • [Cites] Mult Scler. 2010 Apr;16(4):398-405 [20167594.001]
  • [Cites] Acta Parasitol. 2017 Mar 1;62(1):22-28 [28030334.001]
  • [Cites] Trials. 2013 Apr 25;14:112 [23782752.001]
  • [Cites] Parasitology. 2009 Feb;136(2):125-47 [19079844.001]
  • [Cites] Curr Top Behav Neurosci. 2015;26:195-220 [25472634.001]
  • [Cites] Clin Microbiol Rev. 2002 Oct;15(4):595-612 [12364371.001]
  • [Cites] Med Hypotheses. 2011 Oct;77(4):494-504 [21741180.001]
  • [Cites] Nat Rev Immunol. 2010 Apr;10(4):278-84 [20224568.001]
  • [Cites] Exp Parasitol. 2008 Apr;118(4):641-7 [18226814.001]
  • [Cites] Ann Neurol. 2007 Jun;61(6):504-13 [17492755.001]
  • [Cites] Immunol Rev. 2012 Jul;248(1):87-103 [22725956.001]
  • [Cites] Parasite Immunol. 2015 Jun;37(6):277-92 [25600983.001]
  • [Cites] Ann Neurol. 2007 Feb;61(2):97-108 [17230481.001]
  • [Cites] J Biol. 2009;8(7):62 [19664200.001]
  • [Cites] Parasite Immunol. 2011 May;33(5):303-8 [21477142.001]
  • [Cites] PLoS Pathog. 2012 Feb;8(2):e1002520 [22346753.001]
  • [Cites] Curr Opin Infect Dis. 2007 Oct;20(5):489-94 [17762782.001]
  • [Cites] J Exp Med. 2009 Jun 8;206(6):1395-408 [19468064.001]
  • [Cites] Parasitology. 1997 Jul;115 ( Pt 1):101-4 [9226957.001]
  • [Cites] Curr Med Chem. 2016;23 (11):1152-70 [26947777.001]
  • [Cites] Clin Dev Immunol. 2008;2008:567314 [18509490.001]
  • [Cites] Mol Cell Proteomics. 2009 Aug;8(8):1891-907 [19443417.001]
  • [Cites] J Biol Chem. 2010 Jan 29;285(5):3383-92 [19923225.001]
  • [Cites] Exp Parasitol. 2012 Oct;132(2):243-8 [22898371.001]
  • [Cites] J Allergy Clin Immunol. 2012 Jul;130(1):3-10; quiz 11-2 [22742834.001]
  • [Cites] Clin Exp Immunol. 2010 Apr;160(1):1-9 [20415844.001]
  • [Cites] N Engl J Med. 2002 Sep 19;347(12):911-20 [12239261.001]
  • [Cites] Gut. 2005 Jan;54(1):87-90 [15591509.001]
  • [Cites] Mol Biochem Parasitol. 2009 Sep;167(1):1-11 [19406170.001]
  • [Cites] Nat Rev Neurol. 2017 Jan;13(1):25-36 [27934854.001]
  • [Cites] Acta Neurol Scand. 2015;132(199):46-55 [26046559.001]
  • [Cites] J Immunol. 2016 Jan 15;196(2):703-14 [26673140.001]
  • [Cites] J Helminthol. 2012 Sep;86(3):339-47 [21838960.001]
  • [Cites] Mult Scler. 2011 Jun;17(6):743-54 [21372112.001]
  • [Cites] Chem Immunol Allergy. 2008;94:112-23 [18802342.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2010 Jan;81(1):31-6 [19710047.001]
  • [Cites] Mult Scler. 2011 Oct;17(10):1174-5 [21980151.001]
  • [Cites] Curr Opin Infect Dis. 2012 Aug;25(4):458-63 [22691685.001]
  • [Cites] N Engl J Med. 1986 Dec 25;315(26):1638-42 [3785335.001]
  • [Cites] J Neurol. 2012 Apr;259(4):684-93 [21947224.001]
  • [Cites] Sci Transl Med. 2010 Dec 1;2(60):60ra88 [21123809.001]
  • [Cites] Sci Rep. 2016 Nov 24;6:37789 [27883079.001]
  • [Cites] Infect Immun. 2003 Sep;71(9):4996-5004 [12933842.001]
  • [Cites] Nat Rev Immunol. 2013 Aug;13(8):607-14 [23827958.001]
  • [Cites] J Neuroimmunol. 2008 Feb;194(1-2):107-14 [18207251.001]
  • [Cites] Brain. 2005 Dec;128(Pt 12):2899-910 [16183661.001]
  • [Cites] Mult Scler. 2011 Oct;17(10):1171-3 [21980150.001]
  • [Cites] Neurology. 2006 Dec 12;67(11):2085-6 [17159130.001]
  • [Cites] Int J Parasitol. 2005 Oct;35(11-12):1255-78 [16150452.001]
  • [Cites] Nat Rev Immunol. 2011 Jun;11(6):375-88 [21610741.001]
  • [Cites] Biomed Res Int. 2014;2014:964350 [25133189.001]
  • [Cites] Immunology. 2009 Jan;126(1):18-27 [19120495.001]
  • [Cites] Cell Immunol. 2011;267(2):77-87 [21185554.001]
  • [Cites] J Neuroimmunol. 2011 Apr;233(1-2):6-11 [21277637.001]
  • [Cites] EBioMedicine. 2016 Nov;13:46-54 [27863931.001]
  • [Cites] Int J Parasitol. 2013 Mar;43(3-4):259-74 [23298637.001]
  • [Cites] Lancet Infect Dis. 2014 Nov;14 (11):1150-1162 [24981042.001]
  • [Cites] Adv Parasitol. 2009;69:41-146 [19622408.001]
  • [Cites] In Vivo. 2007 Jul-Aug;21(4):599-602 [17708352.001]
  • [Cites] Nat Rev Immunol. 2008 Dec;8(12):958-69 [19029990.001]
  • [Cites] J Clin Invest. 2008 Apr;118(4):1311-21 [18382743.001]
  • [Cites] Int J Parasitol. 2013 Mar;43(3-4):293-9 [23291459.001]
  • [Cites] Mult Scler J Exp Transl Clin. 2017 Jun 13;3(2):2055217317715049 [28638627.001]
  • [Cites] PLoS Pathog. 2011 May;7(5):e1002003 [21589896.001]
  • [Cites] FASEB J. 2008 Nov;22(11):4022-32 [18708590.001]
  • [Cites] Blood Cells Mol Dis. 2009 Mar-Apr;42(2):105-7 [19027331.001]
  • [Cites] Mult Scler. 2015 Nov;21(13):1723-9 [25698173.001]
  • [Cites] Parasite Immunol. 2013 Mar-Apr;35(3-4):103-8 [23227936.001]
  • [Cites] Mol Immunol. 2012 Jun;51(2):210-8 [22482518.001]
  • [Cites] Ann Neurol. 2007 Apr;61(4):288-99 [17444504.001]
  • [Cites] FASEB J. 2012 Nov;26(11):4614-27 [22872675.001]
  • [Cites] J Biomed Biotechnol. 2010;2010:262609 [20145705.001]
  • [Cites] Nat Rev Immunol. 2007 Dec;7(12):975-87 [18007680.001]
  • [Cites] Parasitol Res. 2010 Oct;107(5):1173-88 [20661746.001]
  • (PMID = 29027962.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Switzerland
  • [Keywords] NOTNLM ; environmental factors / helminth parasites / immune modulation / innate immunity / multiple sclerosis / old friend’s hypothesis
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4. Semnani M, Mashayekhi F, Azarnia M, Salehi Z: Effects of green tea epigallocatechin-3-gallate on the proteolipid protein and oligodendrocyte transcription factor 1 messenger RNA gene expression in a mouse model of multiple sclerosis. Folia Neuropathol; 2017;55(3):199-205
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of green tea epigallocatechin-3-gallate on the proteolipid protein and oligodendrocyte transcription factor 1 messenger RNA gene expression in a mouse model of multiple sclerosis.
  • The cuprizone multiple sclerosis (MS) animal model is characteristic for toxic demyelination and represents a reversible demyelination and remyelination system.
  • It is concluded that EGCG increases PLP and Olig1 expression in the cerebral cortex of a mouse model of MS induced by cuprizone.

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  • (PMID = 28984112.001).
  • [ISSN] 1509-572X
  • [Journal-full-title] Folia neuropathologica
  • [ISO-abbreviation] Folia Neuropathol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Keywords] NOTNLM ; EAE / EGCG / Olig1 / Plp / cuprizone
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5. Matute-Blanch C, Río J, Villar LM, Midaglia L, Malhotra S, Álvarez-Cermeño JC, Vidal-Jordana A, Montalban X, Comabella M: Chitinase 3-like 1 is associated with the response to interferon-beta treatment in multiple sclerosis. J Neuroimmunol; 2017 Feb 15;303:62-65
Genetic Alliance. consumer health - Multiple Sclerosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chitinase 3-like 1 is associated with the response to interferon-beta treatment in multiple sclerosis.
  • Chitinase 3-like 1 (CHI3L1) plays a prognostic role in patients with multiple sclerosis (MS).
  • Serum CHI3L1 levels were measured by ELISA in 117 relapsing-remitting MS (RRMS) patients, 76 IFNβ-treated and 41 GA-treated patients.
  • [MeSH-major] Chitinase-3-Like Protein 1 / blood. Interferon-beta / therapeutic use. Multiple Sclerosis, Relapsing-Remitting / blood. Multiple Sclerosis, Relapsing-Remitting / drug therapy

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  • [Copyright] Copyright © 2016 Elsevier B.V. All rights reserved.
  • (PMID = 28063616.001).
  • [ISSN] 1872-8421
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers; 0 / CHI3L1 protein, human; 0 / Chitinase-3-Like Protein 1; 5M691HL4BO / Glatiramer Acetate; 77238-31-4 / Interferon-beta
  • [Keywords] NOTNLM ; Biomarkers / Chitinase 3-like 1 / Glatiramer acetate / Interferon-beta / Multiple sclerosis
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6. Shahbazi M, Abadi JSA, Roshandel D, Koochaki M, Amiri H, Kohansal R, Baghbanian SM, Zamani M: Combination of interleukin-10 gene promoter polymorphisms with HLA-DRB1*15 allele is associated with multiple sclerosis. Indian J Med Res; 2017 Jun;145(6):746-752

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination of interleukin-10 gene promoter polymorphisms with HLA-DRB1*15 allele is associated with multiple sclerosis.
  • BACKGROUND & OBJECTIVES: Multiple sclerosis (MS) is common in some ethnic groups.
  • Interleukin-10 (IL-10) is a potent anti-inflammatory and immunosuppressive cytokine that may be an important regulator in MS disease pathogenesis.
  • Furthermore, loci within the histocompatibility regions are responsible for susceptibility to MS.
  • The aim of this study was to investigate the association of IL-10 gene promoter polymorphisms and HLA-DRB1*15 allele frequencies with MS susceptibility in an Iranian population.
  • METHODS: In this study 336 MS patients and 454 healthy controls were included.
  • RESULTS: IL-10 -1082 G/G and IL-10 -819 C/C genotypes were more frequent in MS patients than healthy individuals.
  • DRB1*15 allele showed a higher frequency among MS patients compared to controls.
  • INTERPRETATION & CONCLUSIONS: The IL-10 and HLA-DRB1*15 polymorphisms were associated with the susceptibility to MS in Iranian patients.
  • Our results suggest that gene-gene interaction of IL-10 polymorphisms and HLA-DRB1*15 alleles may be important factors in the development of MS.

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  • (PMID = 29067976.001).
  • [ISSN] 0971-5916
  • [Journal-full-title] The Indian journal of medical research
  • [ISO-abbreviation] Indian J. Med. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] India
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7. Cardamone G, Paraboschi EM, Rimoldi V, Duga S, Soldà G, Asselta R: The Characterization of GSDMB Splicing and Backsplicing Profiles Identifies Novel Isoforms and a Circular RNA That Are Dysregulated in Multiple Sclerosis. Int J Mol Sci; 2017 Mar 07;18(3)
MedlinePlus Health Information. consumer health - Multiple Sclerosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Characterization of GSDMB Splicing and Backsplicing Profiles Identifies Novel Isoforms and a Circular RNA That Are Dysregulated in Multiple Sclerosis.
  • In particular, a growing body of evidence suggests the existence of a pathogenic association between a generalized defect in splicing regulatory genes and multiple sclerosis (MS).
  • Moreover, several studies have documented an unbalance in alternatively-spliced isoforms in MS patients possibly contributing to the disease etiology.
  • In this work, using a combination of PCR-based techniques (reverse-transcription (RT)-PCR, fluorescent-competitive, real-time, and digital RT-PCR assays), we investigated the alternatively-spliced gene encoding Gasdermin B, <i>GSDMB</i>, which was repeatedly associated with susceptibility to asthma and AIDs.
  • Importantly, both AS isoforms and the identified ecircRNA were significantly dysregulated in peripheral blood mononuclear cells of relapsing-remitting MS patients compared to controls, further supporting the notion that aberrant RNA metabolism is a characteristic feature of the disease.
  • [MeSH-major] Gene Expression Regulation. Multiple Sclerosis / genetics. Neoplasm Proteins / genetics. RNA. RNA Splicing
  • [MeSH-minor] Alternative Splicing. Case-Control Studies. Exons. Female. Gene Order. Humans. Male. Multiple Sclerosis, Relapsing-Remitting / blood. Multiple Sclerosis, Relapsing-Remitting / genetics. Nonsense Mediated mRNA Decay

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  • [Cites] J Clin Cell Immunol. 2016 Apr;7(2):402 [27375925.001]
  • [Cites] Biomed Rep. 2015 Mar;3(2):152-158 [25798239.001]
  • [Cites] Eur J Endocrinol. 2016 May;174(5):R225-38 [26628584.001]
  • [Cites] Genomics. 2007 May;89(5):618-29 [17350798.001]
  • [Cites] N Engl J Med. 2009 Jun 11;360(24):2544-55 [19458352.001]
  • [Cites] Genome Biol. 2015 Mar 25;16:58 [25885816.001]
  • [Cites] Int J Mol Sci. 2015 Dec 22;17 (1):null [26703587.001]
  • [Cites] Nucleic Acids Res. 2006 May 08;34(8):e63 [16682442.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] RNA Biol. 2010 Jul-Aug;7(4):462-73 [20639696.001]
  • [Cites] Cell. 2014 Sep 25;159(1):134-47 [25242744.001]
  • [Cites] Nat Commun. 2016 Nov 16;7:13426 [27848966.001]
  • [Cites] Int J Mol Sci. 2015 Sep 30;16(10):23463-81 [26437396.001]
  • [Cites] Nat Immunol. 2001 Sep;2(9):759-61 [11526377.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] Cell Rep. 2015 Jan 6;10(1):103-11 [25543144.001]
  • [Cites] EMBO J. 2013 Apr 3;32(7):923-5 [23463100.001]
  • [Cites] Genes Dev. 2014 Oct 15;28(20):2233-47 [25281217.001]
  • [Cites] Autoimmun Rev. 2014 Apr-May;13(4-5):518-24 [24424194.001]
  • [Cites] Nature. 2015 Oct 29;526(7575):666-71 [26375259.001]
  • [Cites] Transl Oncol. 2008 Jul;1(2):73-83 [18633457.001]
  • [Cites] Am J Cancer Res. 2016 Jun 01;6(6):1167-76 [27429839.001]
  • [Cites] BMC Genomics. 2013 Sep 17;14:627 [24044605.001]
  • [Cites] PLoS One. 2015 Oct 20;10(10):e0141214 [26485708.001]
  • [Cites] Cell Mol Neurobiol. 2016 Aug;36(6):865-72 [26768647.001]
  • [Cites] PLoS One. 2014 Mar 27;9(3):e90099 [24675552.001]
  • [Cites] Mol Immunol. 2015 Feb;63(2):521-9 [25458313.001]
  • [Cites] J Neuroimmunol. 2010 May;222(1-2):82-6 [20226540.001]
  • [Cites] Lancet Neurol. 2008 Dec;7(12):1078-9 [19007729.001]
  • [Cites] Genes Genet Syst. 2010 Feb;85(1):75-83 [20410667.001]
  • [Cites] PLoS Genet. 2013;9(9):e1003777 [24039610.001]
  • [Cites] RNA. 2014 Dec;20(12):1829-42 [25404635.001]
  • [Cites] J Immunol. 2000 May 15;164(10):5015-8 [10799854.001]
  • [Cites] Nat Genet. 2009 Jun;41(6):703-7 [19430480.001]
  • [Cites] Front Genet. 2016 Apr 06;7:53 [27092176.001]
  • [Cites] Nat Rev Microbiol. 2009 Feb;7(2):99-109 [19148178.001]
  • [Cites] Oncogene. 2016 May 12;35(19):2413-27 [26300000.001]
  • [Cites] RNA. 2013 Feb;19(2):141-57 [23249747.001]
  • [Cites] Nat Rev Immunol. 2004 Dec;4(12):931-40 [15573128.001]
  • [Cites] PLoS One. 2009 Oct 13;4(10):e7440 [19823682.001]
  • [Cites] Annu Rev Biochem. 2003;72:291-336 [12626338.001]
  • [Cites] F1000Res. 2014 Jun 20;3:132 [25254102.002]
  • [Cites] J Pathol. 2010 Jan;220(2):152-63 [19918805.001]
  • [Cites] Genome Res. 2016 Sep;26(9):1277-87 [27365365.001]
  • [Cites] Cell Mol Life Sci. 2015 Dec;72(23):4523-44 [26283621.001]
  • [Cites] J Allergy Clin Immunol. 2004 Dec;114(6):1463-70 [15577853.001]
  • [Cites] Nature. 2013 Mar 21;495(7441):384-8 [23446346.001]
  • [Cites] Proc Natl Acad Sci U S A. 2016 Nov 15;113(46):13132-13137 [27799535.001]
  • [Cites] Mol Cell. 2014 Oct 2;56(1):55-66 [25242144.001]
  • [Cites] Clin Exp Immunol. 1998 Jul;113(1):96-9 [9697990.001]
  • [Cites] Genes Chromosomes Cancer. 2009 Mar;48(3):261-71 [19051310.001]
  • [Cites] Cytokine. 2013 Mar;61(3):720-3 [23375120.001]
  • [Cites] Ann Allergy Asthma Immunol. 2012 Jun;108(6):402-411.e9 [22626592.001]
  • [Cites] Nature. 2016 Jul 7;535(7610):111-6 [27281216.001]
  • [Cites] EMBO Rep. 2008 Nov;9(11):1087-93 [18846105.001]
  • [Cites] Nature. 2015 Oct 29;526(7575):660-5 [26375003.001]
  • [Cites] Nat Genet. 2008 Dec;40(12):1413-5 [18978789.001]
  • [Cites] FASEB J. 1993 Jan;7(1):155-60 [7678559.001]
  • [Cites] Pathology. 2008 Jan;40(1):13-24 [18038310.001]
  • [Cites] Immunol Rev. 2011 Sep;243(1):163-73 [21884175.001]
  • [Cites] RNA. 2014 Nov;20(11):1666-70 [25234927.001]
  • [Cites] Mult Scler. 2004 Oct;10(5):482-7 [15471361.001]
  • [Cites] Clin Diagn Lab Immunol. 1999 Sep;6(5):660-4 [10473513.001]
  • [Cites] Mult Scler. 2006 Jun;12(3):294-301 [16764342.001]
  • [Cites] Genome Biol. 2014 Jul 29;15(7):409 [25070500.001]
  • [Cites] Int J Mol Sci. 2013 Aug 05;14(8):16087-110 [23921681.001]
  • [Cites] Hum Mol Genet. 2014 Dec 20;23(25):6746-61 [25080502.001]
  • (PMID = 28272342.001).
  • [ISSN] 1422-0067
  • [Journal-full-title] International journal of molecular sciences
  • [ISO-abbreviation] Int J Mol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / GSDMB protein, human; 0 / Neoplasm Proteins; 0 / RNA, circular; 63231-63-0 / RNA
  • [Keywords] NOTNLM ; GSDMB / alternative splicing / circRNA / multiple sclerosis / nonsense-mediated mRNA decay
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8. Liu H, Huang J, Dou M, Liu Y, Xiao B, Liu X, Huang Z: Variants in the IL7RA gene confer susceptibility to multiple sclerosis in Caucasians: evidence based on 9734 cases and 10436 controls. Sci Rep; 2017 Apr 26;7(1):1207

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Variants in the IL7RA gene confer susceptibility to multiple sclerosis in Caucasians: evidence based on 9734 cases and 10436 controls.
  • Recently, numerous genome wide association studies (GWAS) and other case-control association studies examining the relationship between interleukin-7 receptor α chain (IL7RA) gene rs3194051, rs987107, rs11567686, and rs11567685 variants and multiple sclerosis (MS) risk have been conducted, but the conclusions have been inconsistent.
  • The main objective of this meta-analysis was to more precisely explore the association of these four IL7RA variants with MS development.
  • Power calculation, publication bias, sensitivity analysis and cumulative meta-analysis were performed to derive a reliable conclusion.
  • Our study indicated three IL7RA loci were significantly associated with increasing MS risk (rs3194051: recessive model: OR = 1.22, 95% CI 1.08-1.38; rs987107: recessive model: OR = 1.44, 95% CI 1.22-1.69; and rs11567686: dominant model: OR = 1.18, 95% CI 1.01-1.37).
  • Additionally, IL7RA rs11567685 variants might not be related to MS development.
  • In all, IL7RA locus polymorphisms could play an important role in the predisposition to MS, which could contribute to a better understanding the pathogenesis of multiple sclerosis.

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  • [Cites] Brain. 2013 Jun;136(Pt 6):1778-82 [23739915.001]
  • [Cites] J Neurol. 2014 Sep;261(9):1677-83 [24923244.001]
  • [Cites] Hum Mol Genet. 2009 May 1;18(9):1670-83 [19221116.001]
  • [Cites] Expert Opin Ther Targets. 2014 May;18(5):581-94 [24641111.001]
  • [Cites] Nature. 2011 Aug 10;476(7359):214-9 [21833088.001]
  • [Cites] Nat Genet. 2007 Sep;39(9):1108-13 [17660816.001]
  • [Cites] Stat Med. 2005 May 15;24(9):1291-306 [15568190.001]
  • [Cites] Lancet. 2008 Oct 25;372(9648):1502-17 [18970977.001]
  • [Cites] Am Fam Physician. 2004 Nov 15;70(10):1935-44 [15571060.001]
  • [Cites] J Interferon Cytokine Res. 2010 May;30(5):291-8 [20187771.001]
  • [Cites] J Mol Med (Berl). 2005 Oct;83(10):822-30 [16075257.001]
  • [Cites] Control Clin Trials. 1998 Dec;19(6):589-601 [9875838.001]
  • [Cites] Neurol Sci. 2001 Apr;22(2):117-39 [11603614.001]
  • [Cites] J Mol Neurosci. 2014 Apr;52(4):467-72 [24166352.001]
  • [Cites] Nat Genet. 2009 Jul;41(7):824-8 [19525955.001]
  • [Cites] J Autoimmun. 2009 Mar;32(2):110-5 [19231135.001]
  • [Cites] Int J Cancer. 2013 Aug 15;133(4):944-51 [23382012.001]
  • [Cites] Iran J Basic Med Sci. 2015 Jun;18(6):593-8 [26221483.001]
  • [Cites] Immunol Invest. 2011;40(3):279-89 [21190413.001]
  • [Cites] Immunity. 2001 Nov;15(5):813-23 [11728342.001]
  • [Cites] Genes Immun. 2013 Oct;14(7):453-61 [23985573.001]
  • [Cites] Curr Opin Neurol. 2009 Jun;22(3):219-25 [19387341.001]
  • [Cites] Eur J Hum Genet. 2003 Jul;11(7):509-15 [12825072.001]
  • [Cites] Scand J Immunol. 2000 Apr;51(4):361-71 [10736108.001]
  • [Cites] Ann Neurol. 2013 Sep;74(3):317-27 [23955638.001]
  • [Cites] J Exp Med. 2000 Mar 20;191(6):1045-50 [10727465.001]
  • [Cites] Nat Genet. 2005 Oct;37(10):1108-12 [16186814.001]
  • [Cites] Arch Neurol. 2005 Apr;62(4):688; author reply 688-9 [15824275.001]
  • [Cites] Neuron. 2006 Oct 5;52(1):61-76 [17015227.001]
  • [Cites] Ann Neurol. 2007 Mar;61(3):228-36 [17252545.001]
  • [Cites] Genes Immun. 2005 Mar;6(2):145-52 [15674389.001]
  • [Cites] Autoimmun Rev. 2010 Apr;9(6):407-13 [19896562.001]
  • [Cites] Hum Mol Genet. 2006 Sep 15;15(18):2813-24 [16905561.001]
  • [Cites] J Autoimmun. 2008 Aug;31(1):52-8 [18406576.001]
  • [Cites] Nat Genet. 2013 Nov;45(11):1353-60 [24076602.001]
  • [Cites] Genes Immun. 2010 Jun;11(4):326-33 [20072142.001]
  • [Cites] Sci Rep. 2015 Dec 11;5:18083 [26656273.001]
  • [Cites] J Neuroimmunol. 2015 May 15;282:80-4 [25903732.001]
  • [Cites] N Engl J Med. 2008 Feb 14;358(7):753-4 [18272905.001]
  • [Cites] Nat Genet. 2007 Sep;39(9):1083-91 [17660817.001]
  • [Cites] N Engl J Med. 2007 Aug 30;357(9):851-62 [17660530.001]
  • [Cites] J Neurol. 2015 Dec;262(12):2713-21 [26429571.001]
  • [Cites] Am J Manag Care. 2013 Feb;19(2 Suppl):S15-20 [23544716.001]
  • [Cites] Nat Immunol. 2007 Sep;8(9):913-9 [17712344.001]
  • [Cites] J Manag Care Pharm. 2013 Jan-Feb;19(1 Suppl A):S41-53 [23383732.001]
  • [Cites] Immunol Rev. 2005 Feb;203:110-26 [15661025.001]
  • (PMID = 28446795.001).
  • [ISSN] 2045-2322
  • [Journal-full-title] Scientific reports
  • [ISO-abbreviation] Sci Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
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9. Algahtani H, Marzouk Y, Algahtani R, Salman S, Shirah B: Autosomal Recessive Cerebellar Ataxia type 1 mimicking multiple sclerosis: A report of two siblings with a novel mutation in SYNE1 gene in a Saudi family. J Neurol Sci; 2017 Jan 15;372:97-100
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autosomal Recessive Cerebellar Ataxia type 1 mimicking multiple sclerosis: A report of two siblings with a novel mutation in SYNE1 gene in a Saudi family.
  • A mutation in the synaptic nuclear envelope protein 1 (SYNE1) gene that is located on chromosome 6p25 results in premature termination of the protein.
  • It was first reported in 2007 as the first identified gene responsible for a recessively inherited pure cerebellar ataxia.
  • In this article, we are presenting two brothers with ARCA1 who were misdiagnosed and treated as multiple sclerosis for more than a decade.
  • We are not only presenting a rare mutation in a Saudi family, but we are also expanding on the heterogeneity of the clinical presentation of this disorder and elaborating on the pathophysiology of neurological involvement.
  • The clinical and radiological spectrum of ARCA1 indicate that this disease is more than a pure cerebellar degeneration.
  • ARCA1 should be considered in the differential diagnosis of patients diagnosed with MS especially in the presence of strong family history.
  • The disease is gradually progressive, and clinical features are atypical for MS.
  • Applying diagnostic criteria for MS is extremely important for confirming or excluding the diagnosis.
  • Detailed history and physical examination are of paramount importance to score the final diagnosis.
  • [MeSH-minor] Brain / diagnostic imaging. DNA Mutational Analysis. Humans. Magnetic Resonance Imaging. Male. Saudi Arabia. Spinal Cord / diagnostic imaging. Young Adult

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  • [Copyright] Copyright © 2016 Elsevier B.V. All rights reserved.
  • (PMID = 28017257.001).
  • [ISSN] 1878-5883
  • [Journal-full-title] Journal of the neurological sciences
  • [ISO-abbreviation] J. Neurol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Nerve Tissue Proteins; 0 / Nuclear Proteins; 0 / SYNE1 protein, human; Autosomal Recessive Cerebellar Ataxia Type 1
  • [Keywords] NOTNLM ; Autosomal Recessive Cerebellar Ataxia type 1 (major topic) / Genetic mutation (major topic) / Multiple sclerosis (major topic) / SYNE1 (major topic) / White matter disease (major topic)
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10. Vavougios GD, Zarogiannis SG, Krogfelt KA, Gourgoulianis K, Mitsikostas DD, Hadjigeorgiou G: Novel candidate genes of the PARK7 interactome as mediators of apoptosis and acetylation in multiple sclerosis: An in silico analysis. Mult Scler Relat Disord; 2017 Oct 24;19:8-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel candidate genes of the PARK7 interactome as mediators of apoptosis and acetylation in multiple sclerosis: An in silico analysis.
  • BACKGROUND: currently only 4 studies have explored the potential role of PARK7's dysregulation in MS pathophysiology Currently, no study has evaluated the potential role of the PARK7 interactome in MS.
  • OBJECTIVE: The aim of our study was to assess the differential expression of PARK7 mRNA in peripheral blood mononuclears (PBMCs) donated from MS versus healthy patients using data mining techniques.
  • METHODS: The PARK7 interactome data from the GDS3920 profile were scrutinized for differentially expressed genes (DEGs); Gene Enrichment Analysis (GEA) was used to detect significantly enriched biological functions.
  • RESULTS: 27 differentially expressed genes in the MS dataset were detected; 12 of these (NDUFA4, UBA2, TDP2, NPM1, NDUFS3, SUMO1, PIAS2, KIAA0101, RBBP4, NONO, RBBP7 AND HSPA4) are reported for the first time in MS.
  • Gene Enrichment Analysis revealed that induction and regulation of programmed / intrinsic cell death represented the most salient Gene Ontology annotations.
  • Cross-validation on systemic lupus erythematosus and ischemic stroke datasets revealed that these functions are unique to the MS dataset.
  • CONCLUSIONS: Based on our results, novel potential target genes are revealed; these differentially expressed genes regulate epigenetic and apoptotic pathways that may further elucidate underlying mechanisms of autorreactivity in MS.

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  • [Copyright] Copyright © 2017 Elsevier B.V. All rights reserved.
  • (PMID = 29100048.001).
  • [ISSN] 2211-0356
  • [Journal-full-title] Multiple sclerosis and related disorders
  • [ISO-abbreviation] Mult Scler Relat Disord
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
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