The Experts below are selected from a list of 56508 Experts worldwide ranked by ideXlab platform
Marie-bernadette Villiers - One of the best experts on this subject based on the ideXlab platform.
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Design and application of a microarray for fluorescence and and Surface Plasmon Resonance imaging analysis of Peptide-Antibody interactions.
Journal of Biomedical Nanotechnology, 2006Co-Authors: Boutheina Cherif, Christian Villiers, Glaucia Paranhos-baccalà, Roberto Calemczuk, Patrice Marche, Thierry Livache, Marie-bernadette VilliersAbstract:In the past few years, protein and Peptide microarrays have shown a great potential in fundamental research, medical diagnostics and drug discovery. We have developed a new method based on covalent immobilization of Peptides on a microarray gold surface for detecting antibodies by either fluorescence or surface plasmon resonance imaging (SPRi). The fluorescence-based revelation approach allows for an indirect analysis of protein-Antibody binding via labeled molecules, whereas the SPRi-based assay is a real-time and label-free detection system suitable for the direct analysis of biological interactions. We illustrate our Peptide chip's efficiency in specifically binding serum antibodies and compare the fluorescence and SPRi approaches to detect Peptide-Antibody interactions. Moreover, we used a monoclonal Antibody against the hepatitis C virus nucleocapsid protein to provide evidence that our system is a powerful tool to identify which epitope is recognized by a given Antibody. This novel technology therefore provides a promising tool for both Antibody screening and epitope mapping.
Robert M Corn - One of the best experts on this subject based on the ideXlab platform.
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characterization and optimization of Peptide arrays for the study of epitope Antibody interactions using surface plasmon resonance imaging
Analytical Chemistry, 2002Co-Authors: Greta J Wegner, Hye Jin Lee, Robert M CornAbstract:The characterization of Peptide arrays on gold surfaces designed for the study of Peptide−Antibody interactions using surface plasmon resonance (SPR) imaging is described. A two-step process was used to prepare the Peptide arrays: (i) a set of parallel microchannels was used to deliver chemical reagents to covalently attach Peptide probes to the surface by a thiol−disulfide exchange reaction; (ii) a second microchannel with a wraparound design was used as a small-volume flow cell (5 μL) to introduce Antibody solutions to the Peptide surface. As a demonstration, the interactions of the FLAG epitope tag and monoclonal anti-FLAG M2 were monitored by SPR imaging using a Peptide array. This Peptide−Antibody pair was studied because of its importance as a means to purify fusion proteins. The surface coverage of the FLAG Peptide was precisely controlled by creating the Peptide arrays on mixed monolayers of alkanethiols containing an amine-terminated surface and an inert alkanethiol. The mole fraction of Peptide...
Katsunori Ikari - One of the best experts on this subject based on the ideXlab platform.
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effects of smoking and shared epitope on the production of anti citrullinated Peptide Antibody in a japanese adult population
Arthritis Care and Research, 2014Co-Authors: Chikashi Terao, Katsunori Ikari, Koichiro Ohmura, Takahisa Kawaguchi, Meiko Takahashi, Kazuya Setoh, Takeo Nakayama, Shinji Kosugi, Akihiro Sekine, Yasuharu TabaraAbstract:Objective Anti–citrullinated Peptide Antibody (ACPA) and rheumatoid factor (RF) are markers to rheumatoid arthritis (RA). Smoking and shared epitope (SE) in HLA–DRB1 are associated with the production of these autoantibodies in RA. Detailed distribution and characterization of ACPA and RF in the general population have remained unclear. We aimed to evaluate positivity of ACPA and RF in a general Japanese population and to detect correlates, including genetic components. Methods ACPA and RF were quantified in 9,804 Japanese volunteers ages 30–75 years. Logistic regression analyses were performed to evaluate the effects of candidates of correlates on the autoAntibody positivity. A genome-wide association study (GWAS) was performed using 394,239 single nucleotide polymorphisms for 3,170 participants, and HLA–DRB1 alleles were imputed based on the GWAS data. Results A total of 1.7% and 6.4% of subjects were positive for ACPA and RF, respectively, and the 2 markers showed a significant correlation (P = 2.0 × 10−23). Old age was associated with ACPA positivity (P = 0.00062). Sex, smoking, SE, and other candidates of correlates did not have significant effects. Interaction between smoking and SE positivity was not apparent, but smoking showed a significant association with high levels of ACPA (P = 0.0019). Conclusion ACPA and RF could be detected in 1.7% and 6.4% of the Japanese adult population without RA, respectively. ACPA and RF were suggested to share mechanisms even in healthy populations. Old age was associated with increasing ACPA positivity. While positivity of ACPA and RF was not associated with SE and smoking, an association between high ACPA and smoking was observed.
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response to peptidyl arginine deiminase type iv padi4 haplotypes interact with shared epitope regardless of anti cyclic citrullinated Peptide Antibody or erosive joint status in rheumatoid arthritis a case control study
Arthritis Research & Therapy, 2014Co-Authors: Katsunori Ikari, Koichiro Yano, Atsuo Taniguchi, Hisashi Yamanaka, Shinji Yoshida, Shigeki MomoharaAbstract:Rheumatoid arthritis (RA) is a complex polygenic disease characterized by progressive joint destruction. Anti-citrullinated Peptide Antibody (ACPA) is the most specific autoAntibody for RA. Genetic polymorphisms in the PADI4 gene, encoding citrullinating enzyme peptidylarginine deiminase 4 (PADI4), have been associated with susceptibility to RA [1,2]. They have also been reported to be associated with radiographic joint destruction in patients with RA [3,4]. We focused on ACPA-negative RA patients to investigate whether a PADI4 polymorphism is associated with joint damage in ACPA-negative patients. DNA samples from 122 Japanese ACPA-negative RA patients were used for the study; 81.1% were female, 51.6% were rheumatoid factor (RF)-positive, and the mean age was 55 years. Sharp/van der Heijde score of the hands at a 5-year disease duration, which represents joint damage, was scored and log-transformed as described elsewhere [4]. Single-nucleotide polymorphism (SNP) rs2240340 was selected and genotyped by using a TaqMan method as described elsewhere [4]. The genetic risk of joint damage associated with rs2240340 was assessed by multiple regression analysis adjusted for HLA-DRB1 shared-epitope alleles and RF that are thought to be associated with joint damage in patients with RA [4]. The PADI4 SNP was significantly associated with radiographic joint destruction in the ACPA-negative RA patients in a recessive model (P = 0.0287) (Table 1 and Figure 1). The overall genotyping success rate was 99.2% and the genotype concordance rate was 100% as assessed by duplicate samples. Although the sample size is one of the major limitations to the study of ACPA-negative patients because of the high positivity of ACPA (up to 90%) in RA populations, we were able to collect DNA samples from 122 ACPA-negative RA patients with radiographic data. Table 1 Association of PADI4 SNP (recessive model) with Sharp/van der Heijde score of hands at 5-year disease duration in ACPA-negative RA patients Figure 1 Boxplots representing the distribution of Sharp/van der Heijde score of hands at 5-year disease duration according to the number of the susceptibility allele of rs2240340 (minor allele, A) in the PADI4 locus. Each box represents the interquartile range ... PADI4 encodes citrullinating enzymes that may play an important role in ACPA formation. It has been shown that PADI4 alleles were associated with the presence of ACPA in patients with RA [1]. In the present study, we have shown that PADI4 polymorphism contributes to joint destruction in ACPA-negative RA patients. A recent study has suggested that PADI4 gene contributes to the development of RA, regardless of ACPA status [3]. We have also reported that the PADI4 risk allele has an impact on joint damage after adjustment for ACPA status [4]. The PADI4 gene is likely to play a role in the disease progression of RA in addition to its role in ACPA formation. The results of this study provide important knowledge of the risks on progressive joint damage in patients with RA.
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Response to `Peptidyl arginine deiminase type IV (PADI4) haplotypes interact with shared epitope regardless of anti-cyclic citrullinated Peptide Antibody or erosive joint status in rheumatoid arthritis: a case control study'
Arthritis Research & Therapy, 2014Co-Authors: Katsunori Ikari, Koichiro Yano, Atsuo Taniguchi, Hisashi Yamanaka, Shinji Yoshida, Shigeki MomoharaAbstract:Rheumatoid arthritis (RA) is a complex polygenic disease characterized by progressive joint destruction. Anti-citrullinated Peptide Antibody (ACPA) is the most specific autoAntibody for RA. Genetic polymorphisms in the PADI4 gene, encoding citrullinating enzyme peptidylarginine deiminase 4 (PADI4), have been associated with susceptibility to RA [1,2]. They have also been reported to be associated with radiographic joint destruction in patients with RA [3,4]. We focused on ACPA-negative RA patients to investigate whether a PADI4 polymorphism is associated with joint damage in ACPA-negative patients. DNA samples from 122 Japanese ACPA-negative RA patients were used for the study; 81.1% were female, 51.6% were rheumatoid factor (RF)-positive, and the mean age was 55 years. Sharp/van der Heijde score of the hands at a 5-year disease duration, which represents joint damage, was scored and log-transformed as described elsewhere [4]. Single-nucleotide polymorphism (SNP) rs2240340 was selected and genotyped by using a TaqMan method as described elsewhere [4]. The genetic risk of joint damage associated with rs2240340 was assessed by multiple regression analysis adjusted for HLA-DRB1 shared-epitope alleles and RF that are thought to be associated with joint damage in patients with RA [4]. The PADI4 SNP was significantly associated with radiographic joint destruction in the ACPA-negative RA patients in a recessive model (P = 0.0287) (Table 1 and Figure 1). The overall genotyping success rate was 99.2% and the genotype concordance rate was 100% as assessed by duplicate samples. Although the sample size is one of the major limitations to the study of ACPA-negative patients because of the high positivity of ACPA (up to 90%) in RA populations, we were able to collect DNA samples from 122 ACPA-negative RA patients with radiographic data. Table 1 Association of PADI4 SNP (recessive model) with Sharp/van der Heijde score of hands at 5-year disease duration in ACPA-negative RA patients Figure 1 Boxplots representing the distribution of Sharp/van der Heijde score of hands at 5-year disease duration according to the number of the susceptibility allele of rs2240340 (minor allele, A) in the PADI4 locus. Each box represents the interquartile range ... PADI4 encodes citrullinating enzymes that may play an important role in ACPA formation. It has been shown that PADI4 alleles were associated with the presence of ACPA in patients with RA [1]. In the present study, we have shown that PADI4 polymorphism contributes to joint destruction in ACPA-negative RA patients. A recent study has suggested that PADI4 gene contributes to the development of RA, regardless of ACPA status [3]. We have also reported that the PADI4 risk allele has an impact on joint damage after adjustment for ACPA status [4]. The PADI4 gene is likely to play a role in the disease progression of RA in addition to its role in ACPA formation. The results of this study provide important knowledge of the risks on progressive joint damage in patients with RA.
Boutheina Cherif - One of the best experts on this subject based on the ideXlab platform.
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Design and application of a microarray for fluorescence and and Surface Plasmon Resonance imaging analysis of Peptide-Antibody interactions.
Journal of Biomedical Nanotechnology, 2006Co-Authors: Boutheina Cherif, Christian Villiers, Glaucia Paranhos-baccalà, Roberto Calemczuk, Patrice Marche, Thierry Livache, Marie-bernadette VilliersAbstract:In the past few years, protein and Peptide microarrays have shown a great potential in fundamental research, medical diagnostics and drug discovery. We have developed a new method based on covalent immobilization of Peptides on a microarray gold surface for detecting antibodies by either fluorescence or surface plasmon resonance imaging (SPRi). The fluorescence-based revelation approach allows for an indirect analysis of protein-Antibody binding via labeled molecules, whereas the SPRi-based assay is a real-time and label-free detection system suitable for the direct analysis of biological interactions. We illustrate our Peptide chip's efficiency in specifically binding serum antibodies and compare the fluorescence and SPRi approaches to detect Peptide-Antibody interactions. Moreover, we used a monoclonal Antibody against the hepatitis C virus nucleocapsid protein to provide evidence that our system is a powerful tool to identify which epitope is recognized by a given Antibody. This novel technology therefore provides a promising tool for both Antibody screening and epitope mapping.
Shigeki Momohara - One of the best experts on this subject based on the ideXlab platform.
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response to peptidyl arginine deiminase type iv padi4 haplotypes interact with shared epitope regardless of anti cyclic citrullinated Peptide Antibody or erosive joint status in rheumatoid arthritis a case control study
Arthritis Research & Therapy, 2014Co-Authors: Katsunori Ikari, Koichiro Yano, Atsuo Taniguchi, Hisashi Yamanaka, Shinji Yoshida, Shigeki MomoharaAbstract:Rheumatoid arthritis (RA) is a complex polygenic disease characterized by progressive joint destruction. Anti-citrullinated Peptide Antibody (ACPA) is the most specific autoAntibody for RA. Genetic polymorphisms in the PADI4 gene, encoding citrullinating enzyme peptidylarginine deiminase 4 (PADI4), have been associated with susceptibility to RA [1,2]. They have also been reported to be associated with radiographic joint destruction in patients with RA [3,4]. We focused on ACPA-negative RA patients to investigate whether a PADI4 polymorphism is associated with joint damage in ACPA-negative patients. DNA samples from 122 Japanese ACPA-negative RA patients were used for the study; 81.1% were female, 51.6% were rheumatoid factor (RF)-positive, and the mean age was 55 years. Sharp/van der Heijde score of the hands at a 5-year disease duration, which represents joint damage, was scored and log-transformed as described elsewhere [4]. Single-nucleotide polymorphism (SNP) rs2240340 was selected and genotyped by using a TaqMan method as described elsewhere [4]. The genetic risk of joint damage associated with rs2240340 was assessed by multiple regression analysis adjusted for HLA-DRB1 shared-epitope alleles and RF that are thought to be associated with joint damage in patients with RA [4]. The PADI4 SNP was significantly associated with radiographic joint destruction in the ACPA-negative RA patients in a recessive model (P = 0.0287) (Table 1 and Figure 1). The overall genotyping success rate was 99.2% and the genotype concordance rate was 100% as assessed by duplicate samples. Although the sample size is one of the major limitations to the study of ACPA-negative patients because of the high positivity of ACPA (up to 90%) in RA populations, we were able to collect DNA samples from 122 ACPA-negative RA patients with radiographic data. Table 1 Association of PADI4 SNP (recessive model) with Sharp/van der Heijde score of hands at 5-year disease duration in ACPA-negative RA patients Figure 1 Boxplots representing the distribution of Sharp/van der Heijde score of hands at 5-year disease duration according to the number of the susceptibility allele of rs2240340 (minor allele, A) in the PADI4 locus. Each box represents the interquartile range ... PADI4 encodes citrullinating enzymes that may play an important role in ACPA formation. It has been shown that PADI4 alleles were associated with the presence of ACPA in patients with RA [1]. In the present study, we have shown that PADI4 polymorphism contributes to joint destruction in ACPA-negative RA patients. A recent study has suggested that PADI4 gene contributes to the development of RA, regardless of ACPA status [3]. We have also reported that the PADI4 risk allele has an impact on joint damage after adjustment for ACPA status [4]. The PADI4 gene is likely to play a role in the disease progression of RA in addition to its role in ACPA formation. The results of this study provide important knowledge of the risks on progressive joint damage in patients with RA.
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Response to `Peptidyl arginine deiminase type IV (PADI4) haplotypes interact with shared epitope regardless of anti-cyclic citrullinated Peptide Antibody or erosive joint status in rheumatoid arthritis: a case control study'
Arthritis Research & Therapy, 2014Co-Authors: Katsunori Ikari, Koichiro Yano, Atsuo Taniguchi, Hisashi Yamanaka, Shinji Yoshida, Shigeki MomoharaAbstract:Rheumatoid arthritis (RA) is a complex polygenic disease characterized by progressive joint destruction. Anti-citrullinated Peptide Antibody (ACPA) is the most specific autoAntibody for RA. Genetic polymorphisms in the PADI4 gene, encoding citrullinating enzyme peptidylarginine deiminase 4 (PADI4), have been associated with susceptibility to RA [1,2]. They have also been reported to be associated with radiographic joint destruction in patients with RA [3,4]. We focused on ACPA-negative RA patients to investigate whether a PADI4 polymorphism is associated with joint damage in ACPA-negative patients. DNA samples from 122 Japanese ACPA-negative RA patients were used for the study; 81.1% were female, 51.6% were rheumatoid factor (RF)-positive, and the mean age was 55 years. Sharp/van der Heijde score of the hands at a 5-year disease duration, which represents joint damage, was scored and log-transformed as described elsewhere [4]. Single-nucleotide polymorphism (SNP) rs2240340 was selected and genotyped by using a TaqMan method as described elsewhere [4]. The genetic risk of joint damage associated with rs2240340 was assessed by multiple regression analysis adjusted for HLA-DRB1 shared-epitope alleles and RF that are thought to be associated with joint damage in patients with RA [4]. The PADI4 SNP was significantly associated with radiographic joint destruction in the ACPA-negative RA patients in a recessive model (P = 0.0287) (Table 1 and Figure 1). The overall genotyping success rate was 99.2% and the genotype concordance rate was 100% as assessed by duplicate samples. Although the sample size is one of the major limitations to the study of ACPA-negative patients because of the high positivity of ACPA (up to 90%) in RA populations, we were able to collect DNA samples from 122 ACPA-negative RA patients with radiographic data. Table 1 Association of PADI4 SNP (recessive model) with Sharp/van der Heijde score of hands at 5-year disease duration in ACPA-negative RA patients Figure 1 Boxplots representing the distribution of Sharp/van der Heijde score of hands at 5-year disease duration according to the number of the susceptibility allele of rs2240340 (minor allele, A) in the PADI4 locus. Each box represents the interquartile range ... PADI4 encodes citrullinating enzymes that may play an important role in ACPA formation. It has been shown that PADI4 alleles were associated with the presence of ACPA in patients with RA [1]. In the present study, we have shown that PADI4 polymorphism contributes to joint destruction in ACPA-negative RA patients. A recent study has suggested that PADI4 gene contributes to the development of RA, regardless of ACPA status [3]. We have also reported that the PADI4 risk allele has an impact on joint damage after adjustment for ACPA status [4]. The PADI4 gene is likely to play a role in the disease progression of RA in addition to its role in ACPA formation. The results of this study provide important knowledge of the risks on progressive joint damage in patients with RA.