Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy
Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kamiyama, Masumi [verfasserIn] Kobayashi, Masaaki [verfasserIn] Araki, Shin-ichi [verfasserIn] Iida, Aritoshi [verfasserIn] Tsunoda, Tatsuhiko [verfasserIn] Kawai, Koichi [verfasserIn] Imanishi, Masahito [verfasserIn] Nomura, Makoto [verfasserIn] Babazono, Tetsuya [verfasserIn] Iwamoto, Yasuhiko [verfasserIn] Kashiwagi, Atsunori [verfasserIn] Kaku, Kohei [verfasserIn] Kawamori, Ryuzou [verfasserIn] Ng, Daniel P. K. [verfasserIn] Hansen, Torben [verfasserIn] Gaede, Peter [verfasserIn] Pedersen, Oluf [verfasserIn] Nakamura, Yusuke [verfasserIn] Maeda, Shiro [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Human genetics |
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| Übergeordnetes Werk: |
volume:122 ; year:2007 ; number:3-4 ; day:02 ; month:08 ; pages:397-407 |
| Links: |
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| DOI / URN: |
10.1007/s00439-007-0414-3 |
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| Katalog-ID: |
SPR00629460X |
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| 100 | 1 | |a Kamiyama, Masumi |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
| 264 | 1 | |c 2007 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a Computermedien |b c |2 rdamedia | ||
| 338 | |a Online-Ressource |b cr |2 rdacarrier | ||
| 520 | |a Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. | ||
| 650 | 4 | |a Diabetic Nephropathy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Major Haplotype |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Overt Nephropathy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Normal Kidney Tissue |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Entire Human Genome |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Kobayashi, Masaaki |e verfasserin |4 aut | |
| 700 | 1 | |a Araki, Shin-ichi |e verfasserin |4 aut | |
| 700 | 1 | |a Iida, Aritoshi |e verfasserin |4 aut | |
| 700 | 1 | |a Tsunoda, Tatsuhiko |e verfasserin |4 aut | |
| 700 | 1 | |a Kawai, Koichi |e verfasserin |4 aut | |
| 700 | 1 | |a Imanishi, Masahito |e verfasserin |4 aut | |
| 700 | 1 | |a Nomura, Makoto |e verfasserin |4 aut | |
| 700 | 1 | |a Babazono, Tetsuya |e verfasserin |4 aut | |
| 700 | 1 | |a Iwamoto, Yasuhiko |e verfasserin |4 aut | |
| 700 | 1 | |a Kashiwagi, Atsunori |e verfasserin |4 aut | |
| 700 | 1 | |a Kaku, Kohei |e verfasserin |4 aut | |
| 700 | 1 | |a Kawamori, Ryuzou |e verfasserin |4 aut | |
| 700 | 1 | |a Ng, Daniel P. K. |e verfasserin |4 aut | |
| 700 | 1 | |a Hansen, Torben |e verfasserin |4 aut | |
| 700 | 1 | |a Gaede, Peter |e verfasserin |4 aut | |
| 700 | 1 | |a Pedersen, Oluf |e verfasserin |4 aut | |
| 700 | 1 | |a Nakamura, Yusuke |e verfasserin |4 aut | |
| 700 | 1 | |a Maeda, Shiro |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Human genetics <Berlin> |d Berlin : Springer, 1964 |g 122(2007), 3-4 vom: 02. Aug., Seite 397-407 |w (DE-627)253723973 |w (DE-600)1459188-1 |x 1432-1203 |7 nnns |
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10.1007/s00439-007-0414-3 doi (DE-627)SPR00629460X (SPR)s00439-007-0414-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Kamiyama, Masumi verfasserin aut Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 Kobayashi, Masaaki verfasserin aut Araki, Shin-ichi verfasserin aut Iida, Aritoshi verfasserin aut Tsunoda, Tatsuhiko verfasserin aut Kawai, Koichi verfasserin aut Imanishi, Masahito verfasserin aut Nomura, Makoto verfasserin aut Babazono, Tetsuya verfasserin aut Iwamoto, Yasuhiko verfasserin aut Kashiwagi, Atsunori verfasserin aut Kaku, Kohei verfasserin aut Kawamori, Ryuzou verfasserin aut Ng, Daniel P. K. verfasserin aut Hansen, Torben verfasserin aut Gaede, Peter verfasserin aut Pedersen, Oluf verfasserin aut Nakamura, Yusuke verfasserin aut Maeda, Shiro verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 122(2007), 3-4 vom: 02. Aug., Seite 397-407 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 https://dx.doi.org/10.1007/s00439-007-0414-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.48 ASE AR 122 2007 3-4 02 08 397-407 |
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10.1007/s00439-007-0414-3 doi (DE-627)SPR00629460X (SPR)s00439-007-0414-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Kamiyama, Masumi verfasserin aut Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 Kobayashi, Masaaki verfasserin aut Araki, Shin-ichi verfasserin aut Iida, Aritoshi verfasserin aut Tsunoda, Tatsuhiko verfasserin aut Kawai, Koichi verfasserin aut Imanishi, Masahito verfasserin aut Nomura, Makoto verfasserin aut Babazono, Tetsuya verfasserin aut Iwamoto, Yasuhiko verfasserin aut Kashiwagi, Atsunori verfasserin aut Kaku, Kohei verfasserin aut Kawamori, Ryuzou verfasserin aut Ng, Daniel P. K. verfasserin aut Hansen, Torben verfasserin aut Gaede, Peter verfasserin aut Pedersen, Oluf verfasserin aut Nakamura, Yusuke verfasserin aut Maeda, Shiro verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 122(2007), 3-4 vom: 02. Aug., Seite 397-407 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 https://dx.doi.org/10.1007/s00439-007-0414-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.48 ASE AR 122 2007 3-4 02 08 397-407 |
| allfields_unstemmed |
10.1007/s00439-007-0414-3 doi (DE-627)SPR00629460X (SPR)s00439-007-0414-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Kamiyama, Masumi verfasserin aut Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 Kobayashi, Masaaki verfasserin aut Araki, Shin-ichi verfasserin aut Iida, Aritoshi verfasserin aut Tsunoda, Tatsuhiko verfasserin aut Kawai, Koichi verfasserin aut Imanishi, Masahito verfasserin aut Nomura, Makoto verfasserin aut Babazono, Tetsuya verfasserin aut Iwamoto, Yasuhiko verfasserin aut Kashiwagi, Atsunori verfasserin aut Kaku, Kohei verfasserin aut Kawamori, Ryuzou verfasserin aut Ng, Daniel P. K. verfasserin aut Hansen, Torben verfasserin aut Gaede, Peter verfasserin aut Pedersen, Oluf verfasserin aut Nakamura, Yusuke verfasserin aut Maeda, Shiro verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 122(2007), 3-4 vom: 02. Aug., Seite 397-407 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 https://dx.doi.org/10.1007/s00439-007-0414-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.48 ASE AR 122 2007 3-4 02 08 397-407 |
| allfieldsGer |
10.1007/s00439-007-0414-3 doi (DE-627)SPR00629460X (SPR)s00439-007-0414-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Kamiyama, Masumi verfasserin aut Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 Kobayashi, Masaaki verfasserin aut Araki, Shin-ichi verfasserin aut Iida, Aritoshi verfasserin aut Tsunoda, Tatsuhiko verfasserin aut Kawai, Koichi verfasserin aut Imanishi, Masahito verfasserin aut Nomura, Makoto verfasserin aut Babazono, Tetsuya verfasserin aut Iwamoto, Yasuhiko verfasserin aut Kashiwagi, Atsunori verfasserin aut Kaku, Kohei verfasserin aut Kawamori, Ryuzou verfasserin aut Ng, Daniel P. K. verfasserin aut Hansen, Torben verfasserin aut Gaede, Peter verfasserin aut Pedersen, Oluf verfasserin aut Nakamura, Yusuke verfasserin aut Maeda, Shiro verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 122(2007), 3-4 vom: 02. Aug., Seite 397-407 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 https://dx.doi.org/10.1007/s00439-007-0414-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.48 ASE AR 122 2007 3-4 02 08 397-407 |
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10.1007/s00439-007-0414-3 doi (DE-627)SPR00629460X (SPR)s00439-007-0414-3-e DE-627 ger DE-627 rakwb eng 610 ASE 44.48 bkl Kamiyama, Masumi verfasserin aut Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 Kobayashi, Masaaki verfasserin aut Araki, Shin-ichi verfasserin aut Iida, Aritoshi verfasserin aut Tsunoda, Tatsuhiko verfasserin aut Kawai, Koichi verfasserin aut Imanishi, Masahito verfasserin aut Nomura, Makoto verfasserin aut Babazono, Tetsuya verfasserin aut Iwamoto, Yasuhiko verfasserin aut Kashiwagi, Atsunori verfasserin aut Kaku, Kohei verfasserin aut Kawamori, Ryuzou verfasserin aut Ng, Daniel P. K. verfasserin aut Hansen, Torben verfasserin aut Gaede, Peter verfasserin aut Pedersen, Oluf verfasserin aut Nakamura, Yusuke verfasserin aut Maeda, Shiro verfasserin aut Enthalten in Human genetics <Berlin> Berlin : Springer, 1964 122(2007), 3-4 vom: 02. Aug., Seite 397-407 (DE-627)253723973 (DE-600)1459188-1 1432-1203 nnns volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 https://dx.doi.org/10.1007/s00439-007-0414-3 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.48 ASE AR 122 2007 3-4 02 08 397-407 |
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Enthalten in Human genetics <Berlin> 122(2007), 3-4 vom: 02. Aug., Seite 397-407 volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 |
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Enthalten in Human genetics <Berlin> 122(2007), 3-4 vom: 02. Aug., Seite 397-407 volume:122 year:2007 number:3-4 day:02 month:08 pages:397-407 |
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Diabetic Nephropathy Major Haplotype Overt Nephropathy Normal Kidney Tissue Entire Human Genome |
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Kamiyama, Masumi @@aut@@ Kobayashi, Masaaki @@aut@@ Araki, Shin-ichi @@aut@@ Iida, Aritoshi @@aut@@ Tsunoda, Tatsuhiko @@aut@@ Kawai, Koichi @@aut@@ Imanishi, Masahito @@aut@@ Nomura, Makoto @@aut@@ Babazono, Tetsuya @@aut@@ Iwamoto, Yasuhiko @@aut@@ Kashiwagi, Atsunori @@aut@@ Kaku, Kohei @@aut@@ Kawamori, Ryuzou @@aut@@ Ng, Daniel P. K. @@aut@@ Hansen, Torben @@aut@@ Gaede, Peter @@aut@@ Pedersen, Oluf @@aut@@ Nakamura, Yusuke @@aut@@ Maeda, Shiro @@aut@@ |
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Kamiyama, Masumi |
| spellingShingle |
Kamiyama, Masumi ddc 610 bkl 44.48 misc Diabetic Nephropathy misc Major Haplotype misc Overt Nephropathy misc Normal Kidney Tissue misc Entire Human Genome Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
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610 ASE 44.48 bkl Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy Diabetic Nephropathy (dpeaa)DE-He213 Major Haplotype (dpeaa)DE-He213 Overt Nephropathy (dpeaa)DE-He213 Normal Kidney Tissue (dpeaa)DE-He213 Entire Human Genome (dpeaa)DE-He213 |
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Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
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(DE-627)SPR00629460X (SPR)s00439-007-0414-3-e |
| title_full |
Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
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Kamiyama, Masumi |
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Human genetics <Berlin> |
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Kamiyama, Masumi Kobayashi, Masaaki Araki, Shin-ichi Iida, Aritoshi Tsunoda, Tatsuhiko Kawai, Koichi Imanishi, Masahito Nomura, Makoto Babazono, Tetsuya Iwamoto, Yasuhiko Kashiwagi, Atsunori Kaku, Kohei Kawamori, Ryuzou Ng, Daniel P. K. Hansen, Torben Gaede, Peter Pedersen, Oluf Nakamura, Yusuke Maeda, Shiro |
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Kamiyama, Masumi |
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610 |
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verfasserin |
| title_sort |
polymorphisms in the 3′ utr in the neurocalcin δ gene affect mrna stability, and confer susceptibility to diabetic nephropathy |
| title_auth |
Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
| abstract |
Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. |
| abstractGer |
Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. |
| abstract_unstemmed |
Abstract Using a large-scale genotyping analysis of gene-based single nucleotide polymorphisms (SNPs) in Japanese type 2 diabetic patients, we have identified a gene encoding neurocalcin δ (NCALD) as a candidate for a susceptibility gene to diabetic nephropathy; the landmark SNP was found in the 3′ UTR of NCALD (rs1131863: exon 4 +1340 A vs. G, P = 0.00004, odds ratio = 1.59, 95% CI 1.27–1.98). We also discovered two other SNPs in exon 4 of this gene (+999 T/A, +1307 A/G) that showed absolute linkage disequilibrium to the landmark SNP. Subsequent in vitro functional analysis revealed that synthetic mRNA corresponding to the disease susceptible haplotype (exon 4 +1340 G, +1307 G, +999 A) was degraded faster than mRNA corresponding to the major haplotype (exon 4 +1340 A, +1307 A, +999 T), and allelic mRNA expression of the disease susceptibility allele was significantly lower than that of the major allele in normal kidney tissues. In an experiment using a short interfering RNA targeting NCALD, we found that silencing of the NCALD led to a considerable enhancement of cell migration, accompanied by a significant reduction in E-cadherin expression, and by an elevation of α smooth muscle actin expression in cultured renal proximal tubular epithelial cells. We also identified the association of the landmark SNP with the progression of diabetic nephropathy in a 8-year prospective study (A vs. G, P = 0.03, odds ratio = 1.91, 95% CI 1.07–3.42). These results suggest that the NCALD gene is a likely candidate for conferring susceptibility to diabetic nephropathy. |
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3-4 |
| title_short |
Polymorphisms in the 3′ UTR in the neurocalcin δ gene affect mRNA stability, and confer susceptibility to diabetic nephropathy |
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https://dx.doi.org/10.1007/s00439-007-0414-3 |
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Kobayashi, Masaaki Araki, Shin-ichi Iida, Aritoshi Tsunoda, Tatsuhiko Kawai, Koichi Imanishi, Masahito Nomura, Makoto Babazono, Tetsuya Iwamoto, Yasuhiko Kashiwagi, Atsunori Kaku, Kohei Kawamori, Ryuzou Ng, Daniel P. K. Hansen, Torben Gaede, Peter Pedersen, Oluf Nakamura, Yusuke Maeda, Shiro |
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Kobayashi, Masaaki Araki, Shin-ichi Iida, Aritoshi Tsunoda, Tatsuhiko Kawai, Koichi Imanishi, Masahito Nomura, Makoto Babazono, Tetsuya Iwamoto, Yasuhiko Kashiwagi, Atsunori Kaku, Kohei Kawamori, Ryuzou Ng, Daniel P. K. Hansen, Torben Gaede, Peter Pedersen, Oluf Nakamura, Yusuke Maeda, Shiro |
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| doi_str |
10.1007/s00439-007-0414-3 |
| up_date |
2024-07-03T22:05:55.228Z |
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| score |
7.400199 |