The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
Xiaoying Meng - One of the best experts on this subject based on the ideXlab platform.
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comparison of petunia inflata s locus f box protein pi slf with pi slf like proteins reveals its Unique Function in s rnase based self incompatibility
The Plant Cell, 2007Co-Authors: Xiaoying MengAbstract:Petunia inflata possesses S-RNase–based self-incompatibility (SI), which prevents inbreeding and promotes outcrossing. Two polymorphic genes at the S-locus, S-RNase and P. inflata S-locus F-box (Pi SLF), determine the pistil and pollen specificity, respectively. To understand how the interactions between Pi SLF and S-RNase result in SI responses, we identified four Pi SLF–like (Pi SLFL) genes and used them, along with two previously identified Pi SLFLs, for comparative studies with Pi SLF2. We examined the in vivo Functions of three of these Pi SLFLs and found that none Functions in SI. These three Pi SLFLs and two other Pi SLFs either failed to interact with S3-RNase (a non-self S-RNase for all of them) or interacted much more weakly than did Pi SLF2 in vitro. We divided Pi SLF2 into FD1 (for Functional Domain1), FD2, and FD3, each containing one of the Pi SLF–specific regions, and used truncated Pi SLF2, chimeric proteins between Pi SLF2 and one of the Pi SLFLs that did not interact with S3-RNase, and chimeric proteins between Pi SLF1 and Pi SLF2 to address the biochemical roles of these three domains. The results suggest that FD2, conserved among three allelic variants of Pi SLF, plays a major role in the strong interaction with S-RNase; additionally, FD1 and FD3 (each containing one of the two variable regions of Pi SLF) together negatively modulate this interaction, with a greater effect on interactions with self S-RNase than with non-self S-RNases. A model for how an allelic product of Pi SLF determines the fate of its self and non-self S-RNases in the pollen tube is presented.
Maki Fukami - One of the best experts on this subject based on the ideXlab platform.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
Clinical epigenetics, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
BMC, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Abstract Background Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. Methods We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. Results We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. Conclusions We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases
Keiko Matsubara - One of the best experts on this subject based on the ideXlab platform.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
Clinical epigenetics, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
BMC, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Abstract Background Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. Methods We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. Results We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. Conclusions We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases
Silvio Danese - One of the best experts on this subject based on the ideXlab platform.
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Unique Function of Protein C in Controlling Epithelial Tight Junction Expression and in Regulating Mucosal Healing in Experimental Colitis
Gastroenterology, 2011Co-Authors: Stefania Vetrano, Emanuela Sala, Carmen Correale, Antonino Spinelli, Vincenzo Arena, Alberto Malesci, Silvio DaneseAbstract:of NHE3 to the development of colitis, immune activation and mucosal homeostasis in IL10-/mice. Methods: We back-crossed NHE3-/mice to 129/SvEv genetic background for more than ten generations with no apparent changes to their survival or phenotype as compared to the original mixed background. We then crossed them with IL-10-deficient mice on the same genetic background. This double knockout (DK) model allows for the development of an unrestrained activation of the Th-1/Th-17-mediated immune response to further study the consequence of NHE3 loss on the inflammatory process and epithelial integrity. It also represents a conjunction of several key factors implicated in the pathogenesis of IBD: genetic predisposition and loss of immune tolerance to colonic commensal bacteria as well as defective barrier Function. Mice at 10 weeks of age were used in the study. Results: Histological examination of H&E stained proximal and distal colon and immunohistochemistry with a Ly-6B.2-specific antibody established important architectural alterations including a massive neutrophil infiltration in IL-10-/xNHE3-/as compared to IL-10-/xNHE3+/+ or IL-10+/+xNHE3-/-. Consistently, we observed increased colonic expression of neutrophil collagenase MMP-8 as well as of the potent mouse neutrophil chemoattractant MIP-2 in DK mice. Colonic IFNγ and IL-17 mRNA expression as well as protein secretion were increased in the distal colon of IL-10-/-xNHE3-/mice compared to NHE3 or IL-10 single KO. Interestingly, IL-10-/-xNHE3-/colonic epithelium had increased hallmarks of apoptosis, including significantly increased number of cleaved caspase-3 positive surface epithelial cells in the proximal and distal colon (>2.5 fold and >3.5 fold increase as compared to NHE-3+/+xIL10-/or NHE3-/-xIL-10+/+, respectively). Conclusions: These results highlight the importance of NHE3 in the maintenance of intestinal integrity and in modulating the inflammatory process in IL-10-deficient mice. These novel observations may be of great importance to the pathogenesis of IBD, where NHE3 inhibition, associated with genetic predisposition such as IL-10R deficiency, may influence the extent of the epithelial barrier defect and contribute to the ultimate degree of inflammation.
Kenichiro Hata - One of the best experts on this subject based on the ideXlab platform.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
Clinical epigenetics, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases.
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Exploring the Unique Function of imprinting control centers in the PWS/AS-responsible region: finding from array-based methylation analysis in cases with variously sized microdeletions
BMC, 2019Co-Authors: Keiko Matsubara, Masatsune Itoh, Kenji Shimizu, Shinji Saito, Keisuke Enomoto, Kazuhiko Nakabayashi, Kenichiro Hata, Kenji Kurosawa, Tsutomu Ogata, Maki FukamiAbstract:Abstract Background Human 15q11–13 is responsible for Prader-Willi syndrome (PWS) and Angelman syndrome (AS) and includes several imprinted genes together with bipartite elements named AS-IC (imprinting center) and PWS-IC. These concertedly confer allele specificity on 15q11–13. Here, we report DNA methylation status of 15q11–13 and other autosomal imprinted differentially methylated regions (iDMRs) in cases with various deletions within the PWS/AS-responsible region. Methods We performed array-based methylation analysis and examined the methylation status of CpG sites in 15q11–13 and in 71 iDMRs in six cases with various microdeletions, eight cases with conventional deletions within 15q11–13, and healthy controls. Results We detected 89 CpGs in 15q11–13 showing significant methylation changes in our cases. Of them, 14 CpGs in the SNORD116s cluster presented slight hypomethylation in the PWS cases and hypermethylation in the AS cases. No iDMRs at regions other than 15q11–13 showed abnormal methylation. Conclusions We identified CpG sites and regions in which methylation status is regulated by AS-IC and PWS-IC. This result indicated that each IC had Unique Functions and coordinately regulated the DNA methylation of respective alleles. In addition, only aberrant methylation at iDMRs in 15q11–13 leads to the development of the phenotypes in our cases
