Analysis Tools|
Allele Symbol Allele Name Allele ID |
Cd55tm1Song targeted mutation 1, Wen-Chao Song MGI:2387405 |
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| Summary |
7 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following induction of experimental autoimmune myasthenia gravis, mice exhibit a mild decreased grip strength and worse clinical scores compared with wild-type mice
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• following induction of experimental autoimmune myasthenia gravis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• erythrocytes show increased susceptibility to antibody-induced lysis by rat, and to a lesser extent, human complement compared to wild-type
• antibody-sensitized erythrocytes exhibit increased C3 deposition compared to wild-type cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• in vivo, mutant erythrocytes display no increase in spontaneous (autologous) C3 deposition relative to wild-type erythrocytes
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• notably, mutant erythrocytes show increased susceptibility to heterologous complement hemolysis when tested with human or guinea pig sera
• increased susceptibility to heterologous complement lysis also correlates with increased complement activation at the C3 level
• when antibody-sensitized mouse erythrocytes are incubated with factor B-depleted human serum, mutant erythrocytes show a significant increase in hemolysis, indicating inhibition of human classical pathway complement activation
• in vitro, mutant erythrocytes show increased autologous C3 deposition from bystander and antibody-initiated complement activation relative to wild-type erythrocytes
• no homologous hemolysis is observed despite a significantly high level of C3 fixation on mutant erythrocytes
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• in vitro, mutant erythrocytes show impaired regulation of bystander complement fixation initiated by the alternative pathway complement activator zymosan, resulting in increased autologous C3 deposition
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• in vitro, mutant erythrocytes show impaired regulation of antibody-triggered classical pathway complement activation, resulting in increased autologous C3 deposition
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| N |
• homozygotes are viable, fertile and display neither overt abnormalities nor signs of hemolytic anemia
• in addition, total erythrocyte and leukocyte counts remain normal relative to wild-type counts
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following induction of experimental autoimmune myasthenia gravis
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• following induction of experimental autoimmune myasthenia gravis, mice accumulate C3 in endplates unlike wild-type mice
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• following induction of experimental autoimmune myasthenia gravis, mice exhibit increased weight loss, decreased grip strength, loss of endplate structures, C3 deposits in endplates, increased muscle inflammation, and worse clinical scores requiring euthanasia compared with wild-type mice
• however, treatment with anti-C5 antibodies improves resistance and reduces endplate loss and muscle inflammation
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• following induction of experimental autoimmune myasthenia gravis
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• following induction of experimental autoimmune myasthenia gravis, mice exhibit loss of endplate structures compared with wild-type mice
• however, treatment with anti-C5 antibodies reduces endplate structures loss
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• following induction of experimental autoimmune myasthenia gravis that necessitated euthanasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• transplanted platelets exhibit a decreased half-life compared to wild-type platelets that is complement and macrophage dependent
• however, transgenic expression of Cd55 rescues platelet half-life following transplantation
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• transplanted platelets exhibit a decreased half-life compared to wild-type platelets that is complement and macrophage dependent
• however, transgenic expression of Cd55 rescues platelet half-life following transplantation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• unlike in C3tm1Hrc Cd55tm1Song Cr1ltm1Hmo homozygotes, platelet half-life is normal
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• unlike in C3tm1Hrc Cd55tm1Song Cr1ltm1Hmo homozygotes, platelet half-life is normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in vitro, double-mutant erythrocytes display a significantly increased sensitivity to antibody-induced autologous and heterologous complement lysis by membrane attack complex (MAC) relative to wild-type or single mutant erythrocytes
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| N |
• despite enhanced sensitivity to antibody-induced complement lysis in vitro, double mutants develop no signs of hemolytic anemia and are resistant to spontaneous complement attack in vivo
• total peripheral erythrocyte counts, blood hemoglobin concentrations, and the average reticulocyte count remain unaffected; transfusion experiments confirm normal erythrocyte lifespans in vivo
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/12/2024 MGI 6.24 |
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