Predicting and diagnosing patients with autoimmune disease

Chemistry: molecular biology and microbiology – Measuring or testing process involving enzymes or... – Involving nucleic acid

Reexamination Certificate

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C435S091100, C436S063000

Reexamination Certificate

active

08008013

ABSTRACT:
The present invention provides methods for the prediction and diagnosis of autoimmune diseases, including Systemic Lupus Erythematosus, using single nucleotide polymorphism in TNFAIP3 (A20).

REFERENCES:
patent: 7259179 (2007-08-01), Burns et al.
patent: 7262199 (2007-08-01), Fraley et al.
patent: 7265134 (2007-09-01), Hartman et al.
patent: 7276581 (2007-10-01), Yeatman et al.
patent: 7279469 (2007-10-01), Pierce et al.
patent: 7282504 (2007-10-01), Armistead et al.
patent: 2003/0171253 (2003-09-01), Ma et al.
patent: WO 2008/041953 (2008-04-01), None
Dieguez-Gonzalez et al. (Arthritis Research and Therapy 2009 vol. 11 p. 42).
Halushka (Nature Genetics, 1999; 22:239-247).
Langdahl (Journal of Bone and Mineral Research 2000 vol. 15 p. 402).
Wall (Nature Reviews Genetics 2003 vol. 4, pp. 587-597).
Musone et al. (Nature 2008 vol. 40 p. 1062).
Baechler et al., “Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus,”PNAS, 100:2610-2615, 2003.
Beyaert et al., “A20 and A20-binding proteins as cellular inhibitors of nuclear factor-kappa B-dependent gene expression and apoptosis,”Biochem. Pharmacol., 60:1143-1151, 2000.
Boone et al., “The ubiquitin-modifying enzyme A20 is required for termination of Toll-like receptor responses,”Nat. Immunol. 5:1052-1060,2004.
Durkop et al., “Differential expression and function of A20 and TRAF1 in Hodgkin lymphoma and anaplastic large cell lymphoma and their induction by CD30 stimulation,”J. Path., 200:229-239, 2003.
Ferretti et al., “PReMod: a database of genome-wide mammalian cis-regulatory module predictions,”Nucleic Acids Res., 35:D122-D126, 2007.
Fung et al., “Analysis of 17 autoimmune disease-associated variants in type 1 diabetes identifies 6q23/TNFAIP3 as a susceptibility locus,”Genes and Immunity, 1-4, 2008.
Gaffney et al., “Fine-mapping chromosome 20 in 230 systemic lupus erythematosus sib pair and multiplex families: evidence for genetic epistasis with chromosome 16q12,”Am. J. Hum. Genet., 78:747-758, 2006.
Gaffney et al., “A genome-wide search for susceptibility genes in human systemic lupus erythematosus sib-pair families,”PNAS, 95:14875-14879, 1998.
Gaffney, “Genome screening in human systemic lupus erythematosus: results from a second Minnesota cohort and combined analyses of 187 sib-pair families,”Am. J. Hum. Genet., 66:547-556, 2000.
Graham et al., “Genetic variants near TNFAIP3 on 6q23 are associated with systemic lupus erythematosus,”Nature Genetics, 40:1059-1061, 2008.
Grey et al., “Adenovirus-mediated gene transfer of A20 in murine islets inhibits Fas-induced apoptosis,”Transplant Proc., 33:577-578, 2001.
Grey et al., “Genetic engineering of a suboptimal islet graft with A20 preserves beta cell mass and function,”J. Immunol., 170:6250-6256,2003.
Harley et al., “The genetics of human systemic lupus erythematosus,”Current Opinions in Immunology, 10:690-696, 1998.
He and Ting, “A20 inhibits tumor necrosis factor (TNF) alpha-induced apoptosis by disrupting recruitment of TRADD and RIP to the TNF receptor 1 complex in Jurkat T cells,”Mol. Cell Biol., 22:3034-3045, 2002.
Heyninck and Beyaert, “The cytokine-inducible zinc finger protein A20 inhibits IL-1-induced NF-kappaB activation at the level of TRAF6,”FEBS Lett., 442:147-150, 1999.
Heyninck and Beyaert, “A20 inhibits NF-kappaB activation by dual ubiquitin-editing functions,”Trends Biochem. Sci., 30:1-4, 2005.
Heyninck, “The zinc finger protein A20 inhibits TNF-induced NF-kappaB-dependent gene expression by interfering with an RIP- or TRAF2-mediated transactivation signal and directly binds to a novel NF-kappaB-inhibiting protein ABIN,”J. Cell Biol., 145:1471-1482, 1999.
Jarvis et al., “Human cytomegalovirus attenuates interleukin-1 beta and tumor necrosis factor alpha proinflammatory signaling by inhibition of NF-kappaB activation,”J. Virol., 80:5588-5598, 2006.
Liuwantara et al., “Nuclear factor-kappaB regulates beta-cell death: a critical role for A20 in beta-cell protection,”Diabetes, 55:2491-2501, 2006.
Moser et al., “Genome scan of human systemic lupus erythematosus: evidence for linkage on chromosome 1q in African-American pedigrees,”PNAS, 95:14869-14874, 1998.
Musone et al., “Multiple polymorphisms in the TNFAIP3 region are independently associated with systemic lupus erythematosus,”Nat. Genet., 40:1062-1064, 2008.
NCBI Accession No. NM—006290.2,Homo sapienstumor necrosis factor, alpha-induced protein 3 (TNFAIP3), mRNA, 1990.
NCBI Accession No. NP—006281.1, Tumor necrosis factor, alpha-induced protein 3 [Homo Sapiens], 1990.
Plenge et al., “Two independent alleles at 6q23 associated with risk of rheumatoid arthritis,”Nature Genetics, 39:1477-1482, 2007.
Ramensky et al., “Human non-synonymous SNPs: server and survey,”Nucleic Acid Res., 30:3894-3900, 2002.
Song et al., “The tumor necrosis factor-inducible zinc finger protein A20 interacts with TRAF1/TRAF2 and inhibits NF-kappaB activation,”PNAS, 93:6721-6725, 1996.
Thomson et al., “Rheumatoid arthritis association at 6q23,”Nature Genetics, 39:1431-1433, 2007.
Wellcome Trust Case Control Consortium, “Genome-wide association study of 14,000 cases of seven common disease and 3,000 shared controls,”Nature, 447:661-678, 2007.
Wertz et al., “De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-kappaB signalling,”Nature, 430:694-699, 2004.
Idel et al., “A20, a regulator of NFκB, maps to an atherosclerosis locus and differs between parental sensitive C577BL/6J and resistant FVB/N strains,”PNAS, 100:14235-14240, 2003.
Boonyasrisawat et al., “Tag polymorphisms at the A20 (TNFAIP3) locus are associated with lower gene expression and increased risk of coronary artery disease in type 2 diabetes,”Diabetes, 56:499-505, 2007.
Gaffney et al., “Recent advances in the genetics of systemic lupus erythematosus,”Rheumatic Disease Clinics of North America, 28:111-126, 2002.
Graham et al., “A genome-wide association scan identifies tumor necrosis factor alpha inducible protein 3 (TNFAIP3/A20) as a susceptibility locus for systemic lupus erythematosus,”Arthritis&Rheumatism, 58 (Suppl. S.):S621-S622, Abstract # 1218, 2008.
Idel et al., “A20, a regulator of NFκB, maps to an atherosclerosis locus and differs between parental sensitive C577BL/6J and resistant FVB/N strains,”PNAS, 100:14235-14240, 2003.
Kyogoku et al., “Genetic association if the R620W polymorphism of protein tyrosine phosphate PTPN22 with human SLE,”Am. J. Hum. Genet., 75:504-507, 2004.
Lessard et al., “Imputation and meta-analysis define a similar to 100 kb risk haplotype spanning TNFAIP3 associated with SLE,”Arthritis&Rheumatism, 58 (Suppl. S): S219, Abstract # 140, 2008.
Luettich et al., “Global gene expression analysis identifies a novel apoptotic pathway in cutaneous lupus erythematosus,”J. Invest. Dermat., vol. 121, Abstract # 0113, 2003.
Musone et al., “Multiple polymorphisms in the TNFAIP3 region are independently associated with systemic lupus erythematosus,”Arthritis&Rheumatism, 58 (Suppl. S):S622, Abstract # 1219, 2008.

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