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http://purl.uniprot.org/citations/31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31081901http://www.w3.org/2000/01/rdf-schema#comment"Innate-like B-1a cells are an important cell population for production of natural IgM and interleukin-10 (IL-10), and act as the first line against pathogens. We determined that CMTM7 is essential for B-1a cell development. Following Cmtm7 (CKLF-like MARVEL transmembrane domain-containing 7) knockout, B-1a cell numbers decreased markedly in all investigated tissues. Using a bone marrow and fetal liver adoptive transfer model and conditional knockout mice, we showed that the reduction of B-1a cells resulted from B-cell-intrinsic defects. Because of B-1a cell loss, Cmtm7-deficient mice produced less IgM and IL-10, and were more susceptible to microbial sepsis. Self-renewal and homeostasis of mature B-1a cells in Cmtm7-/-mice were not impaired, suggesting the effect of Cmtm7 on B-1a cell development. Further investigations demonstrated that the function of Cmtm7 in B-1a cell development occurred at the specific transitional B-1a (TrB-1a) stage. Cmtm7 deficiency resulted in a slow proliferation and high cell death rate of TrB-1a cells. Thus, Cmtm7 controls B-1a cell development at the transitional stage."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.org/dc/terms/identifier"doi:10.1093/intimm/dxz041"xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Han W."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Li T."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Liu Z."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Ma D."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Wang P."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Mo X."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Ge Q."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/author"Lv P."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/name"Int Immunol"xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/pages"715-728"xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/title"Cmtm7 knockout inhibits B-1a cell development at the transitional (TrB-1a) stage."xsd:string
http://purl.uniprot.org/citations/31081901http://purl.uniprot.org/core/volume"31"xsd:string
http://purl.uniprot.org/citations/31081901http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31081901
http://purl.uniprot.org/citations/31081901http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31081901
http://purl.uniprot.org/uniprot/#_A0A1L1SRR1-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901
http://purl.uniprot.org/uniprot/#_Q3THH0-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901
http://purl.uniprot.org/uniprot/#_Q3TI37-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901
http://purl.uniprot.org/uniprot/#_Q3U9H9-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901
http://purl.uniprot.org/uniprot/#_Q3TIE7-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901
http://purl.uniprot.org/uniprot/#_Q9ESD6-mappedCitation-31081901http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31081901