Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Human CD72 splicing isoform responsible for resistance to systemic lupus erythematosus regulates serum immunoglobulin level and is localized in endoplasmic reticulum.

BMC immunology - 26 Dec 2012

Hitomi Yuki, Adachi Takahiro, Tsuchiya Naoyuki, Honda Zen-Ichiro, Tokunaga Katsushi, Tsubata Takeshi

Abstract excerpt

BACKGROUND: CD72 is an inhibitory co-receptor expressed on B cells. We previously demonstrated significant association of the polymorphism of the CD72 gene with susceptibility to human systemic lupus erythematosus (SLE) in individuals carrying a SLE-susceptible FCGR2B genotype (FCGR2B-232Thr/Thr). The human CD72 locus generates a splicing isoform that lacks exon 8 (CD72Δex8) as well as full-length CD72 (CD72fl),...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antibody Formation
Share to Antigens, Differentiation, B-Lymphocyte

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endoplasmic Reticulum

Share to Immunoglobulins

Share to Lupus Erythematosus, Systemic

Share to Mutant Proteins

Share to Protein Splicing

Share to Transgenes

Source

Open in PubMed Open full text

Identifiers

PMID: 23268649
DOI: 10.1186/1471-2172-13-72
PMCID: PMC3565990

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Human CD72 splicing isoform responsible for resistance to systemic lupus erythematosus regulates serum immunoglobulin level and is localized in endoplasmic reticulum.PMID 23268649Read ↗

CD72 polymorphisms associated with alternative splicing modify susceptibility to human systemic lupus erythematosus through epistatic interaction with FCGR2B.Semantic proximity Read ↗

Increased mutations of CD72 transcript in B-lymphocytes from adolescent patients with systemic lupus erythematosus.Semantic proximity Read ↗

Expression profile of FcgammaRIIb on leukocytes and its dysregulation in systemic lupus erythematosus.Semantic proximity Read ↗

A bacterial artificial chromosome transgene with polymorphic Cd72 inhibits the development of glomerulonephritis and vasculitis in MRL-Faslpr lupus mice.Semantic proximity Read ↗

Decreased transcription of the human FCGR2B gene mediated by the -343 G/C promoter polymorphism and association with systemic lupus erythematosus.Semantic proximity Read ↗

Phenotypic variation in IgG receptors by nonclassical FCGR2C alleles.Semantic proximity Read ↗

CD72-semaphorin3A axis; a possible new player in immune regulationSemantic proximity Read ↗

FcgammaRIIB Ile232Thr transmembrane polymorphism associated with human systemic lupus erythematosus decreases affinity to lipid rafts and attenuates inhibitory effects on B cell receptor signaling.Semantic proximity Read ↗

Various domains of the B-cell regulatory molecule CD72 has diverged at different rates in mammals: cloning, transcription and mapping of porcine CD72.Semantic proximity Read ↗

Cd72(c) is a modifier gene that regulates Fas(lpr)-induced autoimmune disease.Semantic proximity Read ↗

A novel single-nucleotide polymorphism of the Fcgamma receptor IIIa gene is associated with genetic susceptibility to systemic lupus erythematosus in Chinese populations: a family-based association study.Semantic proximity Read ↗

Genetic polymorphism in milk fat globule-EGF factor 8 (MFG-E8) is associated with systemic lupus erythematosus in human.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.