We began analyzing https://www.nature.com/articles/jhg2006114, but it redirected us to https://www.nature.com/articles/jhg2006114. The analysis below is for the second page.

Title[redir]:
Role of B cell inhibitory receptor polymorphisms in systemic lupus erythematosus: a negative times a negative makes a positive | Journal of Human Genetics
Description:
B lymphocytes play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). Here, we will review our studies on the role of polymorphisms of two genes coding for B cell inhibitory receptors, FCGR2B and CD72. In FCGR2B, a single nucleotide polymorphism leading to a nonsynonymous substitution, Ile232Thr, within the transmembrane domain was identified, and a significant association of the 232Thr/Thr genotype with SLE was observed in Japanese, Thai and Chinese populations, while this allele was found to be rare in Caucasians. On the other hand, the association of FCGR2B promoter polymorphism with SLE in Caucasians has been reported by two independent groups, but this allele was not found to be present in Japanese. These observations demonstrate that the association of FCGR2B polymorphisms with SLE is common to multiple populations, but the alleles associated with SLE depend upon the genetic background of each population. Functional analyses using a human B cell line lacking endogenous FcγRIIb revealed that SLE-associated 232Thr allele product was partially excluded from membrane lipid rafts under resting conditions and after coligation with B cell receptor, and was significantly less potent at inhibiting B cell activation. Two haplotypes were identified in CD72, one of which was associated with increased production of an alternative splicing isoform that substantially alters the extracellular region of CD72. Interestingly, the presence of the haplotype significantly decreased the risk of SLE conferred by FCGR2B-232Thr in an epistatic manner. These observations emphasize the need to understand human immune system diversity if we are to improve our understanding of the pathogenesis of autoimmune diseases.

Matching Content Categories {📚}

Education
Science
Non-Profit & Charity

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month

Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

check SE Ranking
check Ahrefs
check Similarweb
check Ubersuggest
check Semrush

How Does Link.springer.com Make Money? {💸}

We see no obvious way the site makes money.

While profit motivates many websites, others exist to inspire, entertain, or provide valuable resources. Websites have a variety of goals. And this might be one of them. Link.springer.com could have a money-making trick up its sleeve, but it's undetectable for now.

Keywords {🔍}

pubmed, google, scholar, cas, fcgrb, human, receptor, association, sle, fcγriib, lupus, systemic, erythematosus, cells, genes, lipid, cell, polymorphisms, polymorphism, rafts, allele, susceptibility, populations, immunol, gene, fcγ, nature, tsuchiya, signaling, inhibitory, isoform, found, kyogoku, role, thr, splicing, bcr, ravetch, studies, reported, kono, tokunaga, genetic, immune, arthritis, honda, receptors, transmembrane, genotype, japanese,

Topics {✒️}

nature portfolio permissions reprints privacy policy advertising nature 439 nature 368 nature 387 nature social media strain-specific epistasis author information authors + anti-dna plasma cells author correspondence 13-amino-acid motif receptor-proximal events fcγ receptor-mediated phagocytosis c-terminal src kinase n-terminal palmitoylation site regulated pre-mrna splicing fcγ riiia-f158 allele full size image c-type lectin domain anti-dna antibody cd19-induced ca2+ mobilization detergent-insoluble membrane domains yin-yang1 transcription factors determined ligand-binding parameters fcγriib-deficient mice results fcγ receptor iib wild-type fcgr2b gene attenuates inhibitory effects systemic lupus erythematosus permissions lipid raft components lipid raft structure inhibitory receptor pd-1 akt tyrosine phosphorylation mrl/lpr lupus mice inhibitory coreceptors activated cell regulatory molecules function inhibitory receptor fcγ receptor iia amino acid substitution family-based association study correlated receptor expression spontaneously develop lupus spontaneously develop lupus fcγ receptor iiib case-control association study altered subcellular distribution

Questions {❓}

Does the altered subcellular distribution of 232Thr, the partial exclusion from lipid rafts, provide a mechanistic basis for its phenotype?

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Role of B cell inhibitory receptor polymorphisms in systemic lupus erythematosus: a negative times a negative makes a positive
         description:B lymphocytes play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). Here, we will review our studies on the role of polymorphisms of two genes coding for B cell inhibitory receptors, FCGR2B and CD72. In FCGR2B, a single nucleotide polymorphism leading to a nonsynonymous substitution, Ile232Thr, within the transmembrane domain was identified, and a significant association of the 232Thr/Thr genotype with SLE was observed in Japanese, Thai and Chinese populations, while this allele was found to be rare in Caucasians. On the other hand, the association of FCGR2B promoter polymorphism with SLE in Caucasians has been reported by two independent groups, but this allele was not found to be present in Japanese. These observations demonstrate that the association of FCGR2B polymorphisms with SLE is common to multiple populations, but the alleles associated with SLE depend upon the genetic background of each population. Functional analyses using a human B cell line lacking endogenous FcÎ³RIIb revealed that SLE-associated 232Thr allele product was partially excluded from membrane lipid rafts under resting conditions and after coligation with B cell receptor, and was significantly less potent at inhibiting B cell activation. Two haplotypes were identified in CD72, one of which was associated with increased production of an alternative splicing isoform that substantially alters the extracellular region of CD72. Interestingly, the presence of the haplotype significantly decreased the risk of SLE conferred by FCGR2B-232Thr in an epistatic manner. These observations emphasize the need to understand human immune system diversity if we are to improve our understanding of the pathogenesis of autoimmune diseases.
         datePublished:2006-09-01T00:00:00Z
         dateModified:2006-09-01T00:00:00Z
         pageStart:741
         pageEnd:750
         sameAs:https://doi.org/10.1007/s10038-006-0030-4
         keywords:
            Systemic lupus erythematosus
            Polymorphism
             FCGR2B
             CD72
            Lipid raft
            Alternative splicing
            Epistasis
            Inhibitory receptor
            Human Genetics
            Molecular Medicine
            Gene Function
            Gene Expression
            Gene Therapy
         image:
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10038-006-0030-4/MediaObjects/10038_2006_30_Fig1_HTML.gif
            https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10038-006-0030-4/MediaObjects/10038_2006_30_Fig2_HTML.gif
         isPartOf:
            name:Journal of Human Genetics
            issn:
               1435-232X
               1434-5161
            volumeNumber:51
            type:
               Periodical
               PublicationVolume
         publisher:
            name:Springer Japan
            logo:
               url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
               type:ImageObject
            type:Organization
         author:
               name:Naoyuki Tsuchiya
               affiliation:
                     name:The University of Tokyo
                     address:
                        name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                        type:PostalAddress
                     type:Organization
               email:[email protected]
               type:Person
               name:Zen-ichiro Honda
               affiliation:
                     name:The University of Tokyo
                     address:
                        name:Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
               name:Katsushi Tokunaga
               affiliation:
                     name:The University of Tokyo
                     address:
                        name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                        type:PostalAddress
                     type:Organization
               type:Person
         isAccessibleForFree:1
         type:ScholarlyArticle
      context:https://schema.org
ScholarlyArticle:
      headline:Role of B cell inhibitory receptor polymorphisms in systemic lupus erythematosus: a negative times a negative makes a positive
      description:B lymphocytes play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). Here, we will review our studies on the role of polymorphisms of two genes coding for B cell inhibitory receptors, FCGR2B and CD72. In FCGR2B, a single nucleotide polymorphism leading to a nonsynonymous substitution, Ile232Thr, within the transmembrane domain was identified, and a significant association of the 232Thr/Thr genotype with SLE was observed in Japanese, Thai and Chinese populations, while this allele was found to be rare in Caucasians. On the other hand, the association of FCGR2B promoter polymorphism with SLE in Caucasians has been reported by two independent groups, but this allele was not found to be present in Japanese. These observations demonstrate that the association of FCGR2B polymorphisms with SLE is common to multiple populations, but the alleles associated with SLE depend upon the genetic background of each population. Functional analyses using a human B cell line lacking endogenous FcÎ³RIIb revealed that SLE-associated 232Thr allele product was partially excluded from membrane lipid rafts under resting conditions and after coligation with B cell receptor, and was significantly less potent at inhibiting B cell activation. Two haplotypes were identified in CD72, one of which was associated with increased production of an alternative splicing isoform that substantially alters the extracellular region of CD72. Interestingly, the presence of the haplotype significantly decreased the risk of SLE conferred by FCGR2B-232Thr in an epistatic manner. These observations emphasize the need to understand human immune system diversity if we are to improve our understanding of the pathogenesis of autoimmune diseases.
      datePublished:2006-09-01T00:00:00Z
      dateModified:2006-09-01T00:00:00Z
      pageStart:741
      pageEnd:750
      sameAs:https://doi.org/10.1007/s10038-006-0030-4
      keywords:
         Systemic lupus erythematosus
         Polymorphism
          FCGR2B
          CD72
         Lipid raft
         Alternative splicing
         Epistasis
         Inhibitory receptor
         Human Genetics
         Molecular Medicine
         Gene Function
         Gene Expression
         Gene Therapy
      image:
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10038-006-0030-4/MediaObjects/10038_2006_30_Fig1_HTML.gif
         https://media.springernature.com/lw1200/springer-static/image/art%3A10.1007%2Fs10038-006-0030-4/MediaObjects/10038_2006_30_Fig2_HTML.gif
      isPartOf:
         name:Journal of Human Genetics
         issn:
            1435-232X
            1434-5161
         volumeNumber:51
         type:
            Periodical
            PublicationVolume
      publisher:
         name:Springer Japan
         logo:
            url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
            type:ImageObject
         type:Organization
      author:
            name:Naoyuki Tsuchiya
            affiliation:
                  name:The University of Tokyo
                  address:
                     name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                     type:PostalAddress
                  type:Organization
            email:[email protected]
            type:Person
            name:Zen-ichiro Honda
            affiliation:
                  name:The University of Tokyo
                  address:
                     name:Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Katsushi Tokunaga
            affiliation:
                  name:The University of Tokyo
                  address:
                     name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
                     type:PostalAddress
                  type:Organization
            type:Person
      isAccessibleForFree:1
["Periodical","PublicationVolume"]:
      name:Journal of Human Genetics
      issn:
         1435-232X
         1434-5161
      volumeNumber:51
Organization:
      name:Springer Japan
      logo:
         url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
         type:ImageObject
      name:The University of Tokyo
      address:
         name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
         type:PostalAddress
      name:The University of Tokyo
      address:
         name:Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
         type:PostalAddress
      name:The University of Tokyo
      address:
         name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
         type:PostalAddress
ImageObject:
      url:https://www.springernature.com/app-sn/public/images/logo-springernature.png
Person:
      name:Naoyuki Tsuchiya
      affiliation:
            name:The University of Tokyo
            address:
               name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
      email:[email protected]
      name:Zen-ichiro Honda
      affiliation:
            name:The University of Tokyo
            address:
               name:Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
      name:Katsushi Tokunaga
      affiliation:
            name:The University of Tokyo
            address:
               name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
               type:PostalAddress
            type:Organization
PostalAddress:
      name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
      name:Department of Allergy and Rheumatology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan
      name:Department of Human Genetics, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

External Links {🔗}(349)

Analytics and Tracking {📊}

Google Tag Manager

Libraries {📚}

Prism.js
Zoom.js

CDN Services {📦}

Crossref

5.49s.

LINK . SPRINGER . COM {}