The gene encoding the mouse analogue of the human complement regulator CD59 was cloned using a combination of long range PCR and genomic library screening. Sequence obtained showed that its genomic structure closely resembled that of the human CD59 gene, comprising 4 exons, each separated by a long intron region. The sizes of introns and exons were comparable to those of the human gene with the exception of the third intron which is 2.5 kb in the mouse compared to 7 kb in the human gene. All exon/intron boundaries conformed to the GT-AG rules for splicing. Radiation hybrid mapping localised mouse Cd59 between D2Mit333 and D2Mit127 on chromosome 2, a region homologous with human chromosome 11p13 where the human CD59 gene is localised. These data have permitted the construction of a gene targeting vector for the generation of transgenic mice deficient in CD59.
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http://dx.doi.org/10.1159/000015630 | DOI Listing |
Front Immunol
January 2025
Division for Biochemistry of Joint and Connective Tissue Diseases, Department of Orthopedics, Ulm University Medical Center, Ulm, Germany.
Background: The complement system is locally activated after joint injuries and leads to the deposition of the terminal complement complex (TCC). Sublytic TCC deposition is associated with phenotypical alterations of human articular chondrocytes (hAC) and enhanced release of inflammatory cytokines. Chronic inflammation is a known driver of chondrosenescence in osteoarthritis (OA).
View Article and Find Full Text PDFJ Cell Mol Med
December 2024
Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
PIGA mutation cannot fully explain the proliferative advantage of abnormal clones and thrombosis tendency in paroxysmal nocturnal haemoglobinuria (PNH), and additional genes may play a role, justifying further investigation. CD59+ and CD59- peripheral blood mononuclear cells from six PNH patients were sorted and subjected to whole-exon sequencing (WES) and whole-transcriptome sequencing respectively. Six age- and sex-matched healthy volunteers were enrolled as controls.
View Article and Find Full Text PDFSchizophr Res
January 2025
Department of Neuroscience & Physiology, Upstate Medical University, Syracuse, NY 13210, USA; Neuroscience Research Australia, Randwick, NSW, Australia; Discipline of Psychiatry and Mental Health, Faculty of Medicine and Health, University of New South Wales, Sydney, NSW, Australia. Electronic address:
Deficits in neurogenesis markers in the subependymal zone (SEZ) are associated with elevated inflammation in schizophrenia and bipolar disorder. However, the extent to which complement factors are also changed in the SEZ of these major psychiatric disorders and their impact on neurogenesis remains poorly understood. We extracted RNA from the SEZ of 93 brains, including controls (n = 32), schizophrenia (n = 32), and bipolar disorder (n = 29) cases.
View Article and Find Full Text PDFJ Gastrointest Oncol
October 2024
Department of Breast and Thyroid Surgery, Cancer Hospital Affiliated to Xinjiang Medical University, Xinjiang Medical University, Urumqi, China.
Background: The tumor microenvironment (TME) could be critical in carcinogenesis, immune evasion, and treatment response. TME-related genes are limited in their ability to predict gastric cancer (GC) outcomes. We utilized data from The Cancer Genome Atlas (TCGA) to investigate the functional roles of TME-related genes in GC.
View Article and Find Full Text PDFFASEB J
November 2024
Section for Medical Protein Chemistry, Department of Translational Medicine, Lund university, Malmö, Sweden.
CD59 is a cell-surface inhibitor of the terminal step in the complement cascade. However, in addition to its complement inhibitory function, a non-canonical role of CD59 in pancreatic beta cells has been identified. Two recently discovered intracellular alternative splice forms of CD59, IRIS-1 and IRIS-2, are involved in insulin exocytosis through interactions with SNARE-complex components.
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