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utr-untranslated-region

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MafB is produced in a large fraction of adult islet β-cells in βMafBTg mice...
Published: 13 November 2018
Figure 3 MafB is produced in a large fraction of adult islet β-cells in βMafBTg mice. A: The MafB transgene is driven by a mouse BAC spanning the region 1–6 control sequences required for β-cell type–specific expression in vivo ( 31 ). B: MafB is present in ∼85% of 2-month-old βMafBTg islet β-cells (insulin [INS]) and essentially only α-cells (glucagon [GCG]) in age-matched MafAfl/fl islets. C: MafB mRNA was increased by 2.5-fold, whereas MafA mRNA levels were unchanged in βMafBTg islets. qPCR signals were normalized to Gapdh expression (n = 5). *P < 0.05. UTR, untranslated region. Figure 3. MafB is produced in a large fraction of adult islet β-cells in βMafBTg mice. A: The MafB transgene is driven by a mouse BAC spanning the region 1–6 control sequences required for β-cell type–specific expression in vivo (31). B: MafB is present in ∼85% of 2-month-old βMafBTg islet β-cells (insulin [INS]) and essentially only α-cells (glucagon [GCG]) in age-matched MafAfl/fl islets. C: MafB mRNA was increased by 2.5-fold, whereas MafA mRNA levels were unchanged in βMafBTg islets. qPCR signals were normalized to Gapdh expression (n = 5). *P < 0.05. UTR, untranslated region. More
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pCpGL-<em>Dpp4</em> luciferase reporter assays. <em>A</em>:...
Published: 10 October 2016
Figure 6 pCpGL-Dpp4 luciferase reporter assays. A: Intragenic region of murine Dpp4 gene spanning from 500 to 1,500 bp. Recognition sites for methyltransferases HpaII, HhaI, and M.SssI, and CpG877, CpG1204, CpG1253, and CpG1255 are depicted in bold. UTR, untranslated region. B: Luciferase activity upon selective in vitro methylation of pCpGL-Dpp4. C: Luciferase activity at increasing glucose concentrations. pCpGL-cytomegalovirus (CMV) served as a control plasmid. D: Influence of DNA methylation on glucose-dependent induction of pCpGL-Dpp4. Data are represented as mean ± SEM of three to four independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 compared with the appropriate control group. TSS, transcription start site. Figure 6. pCpGL-Dpp4 luciferase reporter assays. A: Intragenic region of murine Dpp4 gene spanning from 500 to 1,500 bp. Recognition sites for methyltransferases HpaII, HhaI, and M.SssI, and CpG877, CpG1204, CpG1253, and CpG1255 are depicted in bold. UTR, untranslated region. B: Luciferase activity upon selective in vitro methylation of pCpGL-Dpp4. C: Luciferase activity at increasing glucose concentrations. pCpGL-cytomegalovirus (CMV) served as a control plasmid. D: Influence of DNA methylation on glucose-dependent induction of pCpGL-Dpp4. Data are represented as mean ± SEM of three to four independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 compared with the appropriate control group. TSS, transcription start site. More
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Methylation profile of the <em>Dpp4</em> gene in liver tissue. <ita
Published: 10 October 2016
Figure 5 Methylation profile of the Dpp4 gene in liver tissue. A: Genomic organization of the murine Dpp4 gene 2,000 bp upstream and downstream of the transcription start site (TSS) (GRCm38/mm10 NM010074.3 Chr2: 62,410,231 to 624,14,231). CpG sites are indicated as lines. UTR, untranslated region. B: Methylation profile of hepatic Dpp4 in LG and HG mice, analyzed by dBSP sequencing. CF: Single CpG methylation discovered by dBSP sequencing was validated by pyrosequencing. Correlation of Dpp4 expression with absolute methylation at CpG877 (G), CpG1204 (H), CpG1253 (I), and CpG1255 (J). Statistical evaluation of correlations is indicated in each graph (n = 16 animals). Data are represented as mean ± SEM of seven to eight animals per group. *P < 0.05; ** P < 0.01; ***P < 0.001 compared with LG group. Figure 5. Methylation profile of the Dpp4 gene in liver tissue. A: Genomic organization of the murine Dpp4 gene 2,000 bp upstream and downstream of the transcription start site (TSS) (GRCm38/mm10 NM010074.3 Chr2: 62,410,231 to 624,14,231). CpG sites are indicated as lines. UTR, untranslated region. B: Methylation profile of hepatic Dpp4 in LG and HG mice, analyzed by dBSP sequencing. C–F: Single CpG methylation discovered by dBSP sequencing was validated by pyrosequencing. Correlation of Dpp4 expression with absolute methylation at CpG877 (G), CpG1204 (H), CpG1253 (I), and CpG1255 (J). Statistical evaluation of correlations is indicated in each graph (n = 16 animals). Data are represented as mean ± SEM of seven to eight animals per group. *P < 0.05; ** P < 0.01; ***P < 0.001 compared with LG group. More
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DOT1L-mediated H3K79 methylation is associated with BAT-selective gene and ...
Published: 01 April 2021
Figure 5 DOT1L-mediated H3K79 methylation is associated with BAT-selective gene and metabolic regulatory gene program. Flox refers to Dot1Lflox/flox mice, and KO refers to Dot1Lucp1 knockout mice. ChIP-seq was performed using BAT samples from Flox and KO mice, respectively. A: Genome-wide distribution of H3K79me2 mark within genomic regions from BAT of Flox mice. B: Average plots of the H3K79me2 mark across ±5 kb around the transcription start site. C: Heat map of average signal values of the H3K79me2 mark on differential regions of abundant BAT-selective genes and common fat genes Fabp4 and Pparg in BAT. D: H3K79me2 signal tracks for representative BAT-selective genes, including key BAT transcriptional regulators Prdm16, Pparα, and Pgc-1α and common fat genes Fabp4 and Pparg. The black arrow marks the first exon and transcript orientation. Numbers on the left of each graph represent the number of reads. E: KEGG pathway analysis of differential genes with significantly H3K79me2 reduction in BAT of Dot1Lucp1 knockout mice identified by ChIP-seq. DIST, distant; DOWNSTR, downstream; PROM, promoter; PROX, proximal; UTR, untranslated region. Figure 5. DOT1L-mediated H3K79 methylation is associated with BAT-selective gene and metabolic regulatory gene program. Flox refers to Dot1Lflox/flox mice, and KO refers to Dot1Lucp1 knockout mice. ChIP-seq was performed using BAT samples from Flox and KO mice, respectively. A: Genome-wide distribution of H3K79me2 mark within genomic regions from BAT of Flox mice. B: Average plots of the H3K79me2 mark across ±5 kb around the transcription start site. C: Heat map of average signal values of the H3K79me2 mark on differential regions of abundant BAT-selective genes and common fat genes Fabp4 and Pparg in BAT. D: H3K79me2 signal tracks for representative BAT-selective genes, including key BAT transcriptional regulators Prdm16, Pparα, and Pgc-1α and common fat genes Fabp4 and Pparg. The black arrow marks the first exon and transcript orientation. Numbers on the left of each graph represent the number of reads. E: KEGG pathway analysis of differential genes with significantly H3K79me2 reduction in BAT of Dot1Lucp1 knockout mice identified by ChIP-seq. DIST, distant; DOWNSTR, downstream; PROM, promoter; PROX, proximal; UTR, untranslated region. More
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Characterization of LRNA9884 in kidney. <em>A</em>: Real-time PCR s...
Published: 02 May 2019
Figure 1 Characterization of LRNA9884 in kidney. A: Real-time PCR shows expression of 21 common lncRNAs in db/db and db/m mice (n = 8 in each group). B: Real-time PCR detects the upregulation of na_9884 in the kidney during progression of db/db mice from the age of 8 weeks. C: A full length of na_9884 (508 base pairs [bp], named as LRNA9884) amplified by PCR is detected by electrophoresis in 1% agarose gel. D: Gene location of LRNA9884 in chromosome 5 of the mouse genome. E: Scores calculated by using the CPC and CPAT analysis. UTR, untranslated region. F: ISH detects LRNA9884 expression (nuclear pattern, presumably by glomerular [g] and tubular cells) at the age of 8 weeks and 20 weeks in the kidneys of db/db and db/m mice (original magnification ×400). Each bar represents the mean ± SEM for groups of eight mice. *P < 0.05, **P < 0.01, ***P < 0.001 vs. db/m mice. Figure 1. Characterization of LRNA9884 in kidney. A: Real-time PCR shows expression of 21 common lncRNAs in db/db and db/m mice (n = 8 in each group). B: Real-time PCR detects the upregulation of na_9884 in the kidney during progression of db/db mice from the age of 8 weeks. C: A full length of na_9884 (508 base pairs [bp], named as LRNA9884) amplified by PCR is detected by electrophoresis in 1% agarose gel. D: Gene location of LRNA9884 in chromosome 5 of the mouse genome. E: Scores calculated by using the CPC and CPAT analysis. UTR, untranslated region. F: ISH detects LRNA9884 expression (nuclear pattern, presumably by glomerular [g] and tubular cells) at the age of 8 weeks and 20 weeks in the kidneys of db/db and db/m mice (original magnification ×400). Each bar represents the mean ± SEM for groups of eight mice. *P < 0.05, **P < 0.01, ***P < 0.001 vs. db/m mice. More
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Hypoxia induces TrkA and may lead to kidney damage in vivo. <em>A</em>...
Published: 17 August 2012
FIG. 4. Hypoxia induces TrkA and may lead to kidney damage in vivo. A: Bioinformatics analysis of the promoter of TrkA was performed and four HRE sites were found and are diagrammatically presented. kb, kilobases; bp, base pairs. B: Vista Genome browser analysis was performed to find homology between the human and the mouse promoter sequence for TrkA. C: Western blot analysis for TrkA and β-actin was performed in HK2 cells treated with DFO or DMOG. Representative blot is shown (n = 4). D: Densitometry of TrkA protein expression was performed (n = 4). E: A mouse model of ischemia–reperfusion was used to study the expression of TrkA in vivo. H&E and PAS were performed to assess renal damage after ischemic injury. TrkA was detected, immunohistochemically, in ischemic kidneys but was absent in the contralateral control kidneys (right side, brown stain; n = 5). UTR, untranslated regions. The error bars show the SD. (A high-quality digital representation of this figure is available in the online issue.) FIG. 4. Hypoxia induces TrkA and may lead to kidney damage in vivo. A: Bioinformatics analysis of the promoter of TrkA was performed and four HRE sites were found and are diagrammatically presented. kb, kilobases; bp, base pairs. B: Vista Genome browser analysis was performed to find homology between the human and the mouse promoter sequence for TrkA. C: Western blot analysis for TrkA and β-actin was performed in HK2 cells treated with DFO or DMOG. Representative blot is shown (n = 4). D: Densitometry of TrkA protein expression was performed (n = 4). E: A mouse model of ischemia–reperfusion was used to study the expression of TrkA in vivo. H&E and PAS were performed to assess renal damage after ischemic injury. TrkA was detected, immunohistochemically, in ischemic kidneys but was absent in the contralateral control kidneys (right side, brown stain; n = 5). UTR, untranslated regions. The error bars show the SD. (A high-quality digital representation of this figure is available in the online issue.) More
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Knockdown of miR-182 or miR-203 causes reduction of BAT markers in primary ...
Published: 13 November 2014
Figure 6 Knockdown of miR-182 or miR-203 causes reduction of BAT markers in primary brown adipocytes. A: LNA miRNA inhibitors for miR-182 (i-miR 182), miR-203 (i-miR 203), and miR-708 (i-miR 708) were transfected into brown preadipocytes before differentiation. Real-time PCR was performed 4 days after differentiation to examine the expression of the indicated markers. B: Brown preadipocytes were transfected with miRNA inhibitors before differentiation, and ORO staining was performed 4 days after differentiation. C: Real-time PCR was performed to examine indicated marker gene expression at 4 days after differentiation (n = 3). D: Profiles from GSEA. Respiratory electron transport (upper panel) and oxidative phosphorylation pathway (lower panel). Genes were ranked based on the expression fold change of miRNA-inhibited cells vs. control. The black lines represent genes “hits” with the specified annotation. Shown on each is the normalized enrichment score (NES) and nominal P value. Real-time PCR of miR-182 targets Insig-1 and Pdgfra (E) and miR-203 target Pdgfra (F); UTR, untranslated region. *P < 0.05, Student t test. Data are shown as means ± SEM. Figure 6. Knockdown of miR-182 or miR-203 causes reduction of BAT markers in primary brown adipocytes. A: LNA miRNA inhibitors for miR-182 (i-miR 182), miR-203 (i-miR 203), and miR-708 (i-miR 708) were transfected into brown preadipocytes before differentiation. Real-time PCR was performed 4 days after differentiation to examine the expression of the indicated markers. B: Brown preadipocytes were transfected with miRNA inhibitors before differentiation, and ORO staining was performed 4 days after differentiation. C: Real-time PCR was performed to examine indicated marker gene expression at 4 days after differentiation (n = 3). D: Profiles from GSEA. Respiratory electron transport (upper panel) and oxidative phosphorylation pathway (lower panel). Genes were ranked based on the expression fold change of miRNA-inhibited cells vs. control. The black lines represent genes “hits” with the specified annotation. Shown on each is the normalized enrichment score (NES) and nominal P value. Real-time PCR of miR-182 targets Insig-1 and Pdgfra (E) and miR-203 target Pdgfra (F); UTR, untranslated region. *P < 0.05, Student t test. Data are shown as means ± SEM. More
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Islet CAGE TC identification. <em>A</em>: Genome browser view of th...
Published: 13 April 2021
Figure 1 Islet CAGE TC identification. A: Genome browser view of the intronic region of the ST18 gene as an example locus where an islet TC overlaps an islet ATAC-seq peak and active TSS chromatin state. This TC also overlaps an enhancer element, which was validated by the VISTA Enhancer Browser ( 35 ). Also shown is the human-mouse-rat conserved TF binding site (TFBS) track from the TRANSFAC matrix database ( 51 ). B: Cumulative fraction of islet TC segments overlapping with TCs identified in X number of FANTOM tissues. C: Distribution of the log10(distance to the nearest known protein-coding gene TSS + 1 bp) with classification of islet TC segments by the number of FANTOM tissues where TCs overlap. Number of TC segments in each category is shown in parentheses. D: Genome browser view of an example locus near the AP1G2 gene that highlights an islet TC (blue box) that is also identified in FANTOM tissues (FANTOM TCs track is a dense depiction of TCs called across 118 human tissues), occurs in a ATAC-seq peak region in both islets and GM12878 (ATAC-seq track), and overlaps active TSS chromatin states across numerous tissues. Another islet TC (orange box) ∼34 kb distal to the AP1G2 gene is not identified as a TC in other FANTOM tissues and occurs in an islet ATAC-seq peak and a more islet-specific active enhancer chromatin state region. E: Enrichment of islet TCs to overlap islet chromatin state and other common annotations. Error bars represent the 95% CIs. Bonferroni correction accounted for 40 total annotations. HSMM, human skeletal muscle myoblasts; Huvec, Human umbilical vein endothelial cells; mRNA-seq, mRNA sequencing; NHEK, normal human epidermal keratinocytes; UTR, untranslated region. Figure 1. Islet CAGE TC identification. A: Genome browser view of the intronic region of the ST18 gene as an example locus where an islet TC overlaps an islet ATAC-seq peak and active TSS chromatin state. This TC also overlaps an enhancer element, which was validated by the VISTA Enhancer Browser (35). Also shown is the human-mouse-rat conserved TF binding site (TFBS) track from the TRANSFAC matrix database (51). B: Cumulative fraction of islet TC segments overlapping with TCs identified in X number of FANTOM tissues. C: Distribution of the log10(distance to the nearest known protein-coding gene TSS + 1 bp) with classification of islet TC segments by the number of FANTOM tissues where TCs overlap. Number of TC segments in each category is shown in parentheses. D: Genome browser view of an example locus near the AP1G2 gene that highlights an islet TC (blue box) that is also identified in FANTOM tissues (FANTOM TCs track is a dense depiction of TCs called across 118 human tissues), occurs in a ATAC-seq peak region in both islets and GM12878 (ATAC-seq track), and overlaps active TSS chromatin states across numerous tissues. Another islet TC (orange box) ∼34 kb distal to the AP1G2 gene is not identified as a TC in other FANTOM tissues and occurs in an islet ATAC-seq peak and a more islet-specific active enhancer chromatin state region. E: Enrichment of islet TCs to overlap islet chromatin state and other common annotations. Error bars represent the 95% CIs. Bonferroni correction accounted for 40 total annotations. HSMM, human skeletal muscle myoblasts; Huvec, Human umbilical vein endothelial cells; mRNA-seq, mRNA sequencing; NHEK, normal human epidermal keratinocytes; UTR, untranslated region. More
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Beneficial and harmful effects of PERK activation. Normal PERK function is ...
Published: 22 October 2021
Figure 2 Beneficial and harmful effects of PERK activation. Normal PERK function is required for proinsulin folding, ER calcium balance, translation regulation, and cell survival, but PERK activation can also lead to cell death and loss of maturation markers. Activated by ER stress, low glucose, and low ER calcium, PERK phosphorylates eIF2α to simultaneously suppress global translation but selectively activate translation of some transcripts such as Atf4 and Aatf. Beneficial effects of PERK activation include suppression of translation when the ER is overloaded with peptide inputs, promotion of cell survival through activation of ATF4 and AATF, improved SERCA pump function by dephosphorylation of CLNX to derepress calcium transport, and proliferation. Harmful effects of PERK activation include suppression of translation of required genes including maturation factors and insulin itself (although PERK deletion also caused loss of MAFA and PDX1), as well as increased cell death through CHOP and inflammatory pathways. Green arrows indicate transcriptional regulation. AATF, apoptosis antagonizing transcription factor; AKT1, protein kinase B; ATF4, activating transcription factor 4; CALN, calcineurin; CHOP, C/EBP homologous protein; CLNX, calnexin; eIF2α, eukaryotic translation initiation factor 2 subunit 1; GRP78, glucose-regulated protein 78; Iapp, islet amyloid polypeptide precursor; IFNAR1, interferon α and β subunit 1; Ins1/2, insulin 1/2; MAFA, Maf bZIP transcription factor A; circled P indicates phosphorylation; PDX1, pancreatic and duodenal homeobox 1; PERK, protein kinase R-like ER kinase; UTR, untranslated region. Figure 2. Beneficial and harmful effects of PERK activation. Normal PERK function is required for proinsulin folding, ER calcium balance, translation regulation, and cell survival, but PERK activation can also lead to cell death and loss of maturation markers. Activated by ER stress, low glucose, and low ER calcium, PERK phosphorylates eIF2α to simultaneously suppress global translation but selectively activate translation of some transcripts such as Atf4 and Aatf. Beneficial effects of PERK activation include suppression of translation when the ER is overloaded with peptide inputs, promotion of cell survival through activation of ATF4 and AATF, improved SERCA pump function by dephosphorylation of CLNX to derepress calcium transport, and proliferation. Harmful effects of PERK activation include suppression of translation of required genes including maturation factors and insulin itself (although PERK deletion also caused loss of MAFA and PDX1), as well as increased cell death through CHOP and inflammatory pathways. Green arrows indicate transcriptional regulation. AATF, apoptosis antagonizing transcription factor; AKT1, protein kinase B; ATF4, activating transcription factor 4; CALN, calcineurin; CHOP, C/EBP homologous protein; CLNX, calnexin; eIF2α, eukaryotic translation initiation factor 2 subunit 1; GRP78, glucose-regulated protein 78; Iapp, islet amyloid polypeptide precursor; IFNAR1, interferon α and β subunit 1; Ins1/2, insulin 1/2; MAFA, Maf bZIP transcription factor A; circled P indicates phosphorylation; PDX1, pancreatic and duodenal homeobox 1; PERK, protein kinase R-like ER kinase; UTR, untranslated region. More
Images
NF-Y–regulated insulin secretion in β-cells is mediated by GLUT2. <em>A</em>...
Published: 12 May 2021
Figure 7 NF-Y–regulated insulin secretion in β-cells is mediated by GLUT2. A: Representative immunostaining (left) and quantification of relative immunofluorescence of GLUT2 (right) in pancreatic islets of Nf-ya βKO and Nf-yafl/fl mice at the age of 12 weeks (n = 4 mice/group). B: Glucose uptake ability in islets was measured using 2-NBDG and fluorescent images measured at 488 nm 1 h after loading 60 μmol/L 2-NBDG on isolated islets (10–20 islets each from 5–6 individual mice from each group). C and D: The effect of Nf-y overexpression on GLUT2 expression and glucose uptake in NIT-1 cells, which were the same as described in the legend of Fig. 5D and E . The protein levels of the GLUT2 were determined by Western blotting (C), and cellular glucose uptake ability was measured using 2-NBDG (D) from 4–6 independent experiments. E: Effects of Nf-y expression on the Glut2 promoter activity. 293T cells were transiently transfected with the Glut2 luciferase (Luc) construct together with expression vector for Nf-ya, Nf-yb, and Nf-yc. E, top: Positions of the promoter fragments and the putative Nf-y–binding elements CCAAT relative to the transcription start site (+1) are indicated, with blue text showing the mutations generated using PCR site-directed mutagenesis at the sequence CCAAT. E, middle: The expression of the firefly luciferase was measured in cells transfected with the constructs comprised of serially deleted portions of the upstream region of Glut2. E, bottom: Firefly luciferase activities were measured in cells transfected with three mutant constructs (M1–M3). Relative luciferase activity of each construct (i.e., compared with that of the control, pGL3-Basic vector) were shown (n = 3 independent experiments). *P < 0.05, **P < 0.01, ***P < 0.001. UTR, untranslated region. Figure 7. NF-Y–regulated insulin secretion in β-cells is mediated by GLUT2. A: Representative immunostaining (left) and quantification of relative immunofluorescence of GLUT2 (right) in pancreatic islets of Nf-ya βKO and Nf-yafl/fl mice at the age of 12 weeks (n = 4 mice/group). B: Glucose uptake ability in islets was measured using 2-NBDG and fluorescent images measured at 488 nm 1 h after loading 60 μmol/L 2-NBDG on isolated islets (10–20 islets each from 5–6 individual mice from each group). C and D: The effect of Nf-y overexpression on GLUT2 expression and glucose uptake in NIT-1 cells, which were the same as described in the legend of Fig. 5D and E. The protein levels of the GLUT2 were determined by Western blotting (C), and cellular glucose uptake ability was measured using 2-NBDG (D) from 4–6 independent experiments. E: Effects of Nf-y expression on the Glut2 promoter activity. 293T cells were transiently transfected with the Glut2 luciferase (Luc) construct together with expression vector for Nf-ya, Nf-yb, and Nf-yc. E, top: Positions of the promoter fragments and the putative Nf-y–binding elements CCAAT relative to the transcription start site (+1) are indicated, with blue text showing the mutations generated using PCR site-directed mutagenesis at the sequence CCAAT. E, middle: The expression of the firefly luciferase was measured in cells transfected with the constructs comprised of serially deleted portions of the upstream region of Glut2. E, bottom: Firefly luciferase activities were measured in cells transfected with three mutant constructs (M1–M3). Relative luciferase activity of each construct (i.e., compared with that of the control, pGL3-Basic vector) were shown (n = 3 independent experiments). *P < 0.05, **P < 0.01, ***P < 0.001. UTR, untranslated region. More
Journal Articles
Journal: Diabetes
Diabetes 2002;51(3):860–862
Published: 01 March 2002
... resistance. Thus, the resistin gene represents a potential candidate for the etiology of insulin resistance and type 2 diabetes. In this study, we analyzed the coding sequence of the three exons of the resistin gene, together with its 5′ regulatory region and 3′ untranslated region (UTR...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(11):1955–1957
Published: 01 November 2000
...'-untranslated region (UTR) (-477G/A, -436delA, -324delT, -107insTTTT, and -104T/C [cDNA sequences]) and two in the 3'-UTR (1027C/T and 1076C/A). A missense mutation, K68T (203A/C), was found in a heterozygous state in one MODY subject and two nondiabetic subjects. The results of our study suggest that genetic...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(5):1635–1639
Published: 01 May 2002
... of diabetic retinopathy. In the present study, we examined the genetic variations of the VEGF gene to assess its possible relation to diabetic retinopathy in type 2 diabetic patients. Among seven common polymorphisms in the promoter region, 5′-untranslated region (UTR) and 3′UTR of the VEGF gene, genotype...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(3):847–851
Published: 01 March 2004
... identified in PPAR-δ: four in the intron, one in the 5′ untranslated region (UTR), and four in the 3′ UTR. Among identified polymorphisms, five common sites, including c.−13454G>T, c.−87T>C, c.2022+12G>A, c.2629T>C, and c.2806C>G, were genotyped in subjects with type 2 diabetes and normal...
Includes: Supplementary data
Journal Articles
Journal: Diabetes
Diabetes 2002;51(9):2866–2870
Published: 01 September 2002
... small clinical sample sizes. Consequently, no definite conclusions can be drawn from their negative results. We have therefore systematically searched all exons, the 3′ untranslated region (UTR), the 5′ UTR, and the 5′ upstream region of GAD2, for polymorphisms in 32 white European individuals...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(9):1877–1880
Published: 01 September 1999
...) of 4,014 bp and 5'- and 3'-untranslated regions (UTRs) of 516 and 2,466 bp (5). Although the IRS-2 gene has previously been thought to lack introns within the coding region (6,7), the amino acid sequence predicted from our cDNA sequence differed at its very COOH-terminal end from an IRS-2 protein sequence...
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(7):1469–1472
Published: 01 July 1999
...H Maegawa; K Shi; H Hidaka; N Iwai; Y Nishio; K Egawa; H Kojima; M Haneda; H Yasuda; Y Nakamura; M Kinoshita; R Kikkawa; A Kashiwagi A newly identified 3'-untranslated region (UTR) polymorphism of the gene for skeletal muscle-specific glycogen-targeting subunit of protein phosphatase 1 (PPP1R3...
Meeting Abstracts
Journal: Diabetes
Diabetes 1998;47(9):1519–1524
Published: 01 September 1998
... variant of an "ATTTA" element in the 3'-untranslated region (UTR) of the corresponding gene (PPP1R3). The 3'-UTR variant resembled the mRNA-destabilizing AT(AU)-rich elements (AREs) and resulted in a 10-fold difference in reporter mRNA half-life, was correlated with PPP1R3 transcript and protein...
Journal Articles
Journal: Diabetes
Diabetes 2002;51(5):1649–1650
Published: 01 May 2002
...-Traverso, Via E. Ramarini 32, Monterotondo 00016, Rome, Italy. E-mail: lnistico@ibc.rm.cnr.it . Received for publication 9 January 2002 and accepted in revised form 11 February 2002. AFBAC, affected family-based control subject; LD, linkage disequilibrium; UTR, untranslated region. DIABETES 2002...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(12):3089–3094
Published: 01 December 2007
... to functionally evaluate a variant in the 3′ untranslated region (UTR). RESULTS— A novel G/A variant in the 3′-UTR was associated with young-onset type 2 diabetes (odds ratio 2.09 per copy of the G-allele [95% CI 1.31–3.33], adjusted P = 0.001) and had an effect on the evidence for linkage...
Includes: Supplementary data