ArticleGenes and immunity2003
Aberrant HS1 molecule in a patient with systemic lupus erythematosus.
Article in Genes and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- The Arp2/3 complex binding protein HS1 is required for efficient dendritic cell random migration and force generation.Integrative biology : quantitative biosciences from nano to macro · 2017Article
- The actin regulatory protein HS1 is required for antigen uptake and presentation by dendritic cells.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Regulation of cytoskeletal dynamics at the immune synapse: new stars join the actin troupe.Traffic (Copenhagen, Denmark) · 2006Review
- Comparative genome analysis of cortactin and HS1: the significance of the F-actin binding repeat domain.BMC genomics · 2005Article
- Current advances in the human lupus genetics.Current rheumatology reports · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the activation of autoreactive B lymphocytes, which are supposed to carry aberrant signal transduction after the stimulation of B-cell receptor (BCR). To investigate abnormalities in BCR-mediated signaling pathway in lupus B lymphocytes, we analyzed HS1, a molecule downstream of BCR, in 80 Japanese SLE patients. We identified 37 amino acid deletion of HS1 in a 25-year-old female patient, and the aberrant HS1 lacked a part of a functional motif. Analysis of genomic DNA revealed that the aberrant HS1 was caused by exon skipping. Family study showed that the patient as well as her father and sister are heterozygous for the abnormality. WEHI-231 cell, a mouse B cell line, transfected with the aberrant HS1 displayed a significantly increased cell death upon cross-linking of BCR. Additionally, peripheral B lymphocytes from the patient exerted increased apoptosis after BCR stimulation compared to those from control SLE patients. These data suggest that the aberrant HS1 molecule may transmit an accelerated signal after BCR stimulation and may play a role in the activation of autoreactive B lymphocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.