All Phenotypes Cd59a<tm1Bpm> MGI Mouse

Phenotypes associated with this allele

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cd59a^tm1Bpm/Cd59a^tm1Bpm	B6.129-Cd59a^tm1Bpm	MGI:5298853
hm2	Cd59a^tm1Bpm/Cd59a^tm1Bpm	involves: 129	MGI:5298852
hm3	Cd59a^tm1Bpm/Cd59a^tm1Bpm	involves: 129 * BALB/c	MGI:5298858
hm4	Cd59a^tm1Bpm/Cd59a^tm1Bpm	involves: 129 * C57BL/6	MGI:5298851
hm5	Cd59a^tm1Bpm/Cd59a^tm1Bpm	involves: 129/Sv * C57BL/6	MGI:2662104
cx6	Cd55^tm1Song/Cd55^tm1Song Cd59a^tm1Bpm/Cd59a^tm1Bpm	B6.129-Cd55^tm1Song Cd59a^tm1Bpm	MGI:5298856
cx7	C3^tm1Crr/C3^tm1Crr Cd59a^tm1Bpm/Cd59a^tm1Bpm	B6.129-Cd59a^tm1Bpm C3^tm1Crr	MGI:5298854
cx8	Apoe^tm1Bres/Apoe^tm1Bres Cd59a^tm1Bpm/Cd59a^tm1Bpm	involves: 129 * 129P2/OlaHsd	MGI:5298859

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

renal/urinary system

increased renal tubule apoptosis ( J:92414 )

• following ischemic reperfusion injury

increased susceptibility to kidney reperfusion injury ( J:92414 )

• following ischemic reperfusion injury, mice exhibit more severe tubular damage, greater lymphocyte infiltration, increased tubular apoptosis, increased deposition of C9, and fail to recover compared with wild-type mice

immune system

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

increased double-positive T cell number ( J:123582 )

• in the lungs of influenza-infected mice originating from the thymus

increased neutrophil cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased plasma cell number ( J:119703 )

• following stimulation with sheep red blood cells

increased CD4-positive, alpha-beta T cell number ( J:123582 )

• in the lungs of influenza-infected mice

abnormal CD4-positive, alpha-beta T cell physiology ( J:119703 , J:123582 )

• CD4+ T cells exhibit decreased ability to activate B cells compared with wild-type T cells (J:119703)

• CD4+ T cells from influenza-infected mice exhibit increased influenza-specific activation (J:123582)

abnormal humoral immune response ( J:119703 )

• reduced in response to stimulation with sheep red blood cells

decreased IgG level ( J:119703 )

• all sub-classes of anti-sheep red blood cell IgG following second immunization

abnormal complement pathway ( J:92414 )

• following ischemic reperfusion injury, mice exhibit a greater accumulation of C9 in the kidneys compared with wild-type mice

increased susceptibility to experimental autoimmune myasthenia gravis ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis, mice exhibit a mild decreased grip strength and worse clinical scores compared with wild-type mice

myositis ( J:113567 )

• some following induction of experimental autoimmune myasthenia gravis

lung inflammation ( J:123582 )

• following infection with influenza

decreased susceptibility to Poxviridae infection ( J:122201 )

• mice infected with recombinant vaccinia virus exhibit lower viral titers 3 days post-infection compared with wild-type mice

increased susceptibility to Orthomyxoviridae infection ( J:123582 )

• mice infected with influenza exhibit increased lung pathology (the degree of haemorrhage, interstitial leukocyte infiltration (neutrophil, CD4+ T cell, and CD4+CD8+ T cells), and perivascular lymphoid aggregation), mild fibrosis, and increased complement-independent deposition of membrane attack complex in the respiratory airways compared with wild-type mice

cellular

increased renal tubule apoptosis ( J:92414 )

• following ischemic reperfusion injury

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

homeostasis/metabolism

increased susceptibility to kidney reperfusion injury ( J:92414 )

hematopoietic system

decreased B cell proliferation ( J:119703 )

• following stimulation with LPS or anti-CD40 antibodies

increased T cell proliferation ( J:122201 )

• in CD4+ T cells stimulated in vitro or in vivo with recombinant vaccinia virus glycoprotein 13 (p13)

• in CD4+ T cells stimulated with anti CD3 antibodies and antigen presenting cells

• however, proliferation in response to anti-CD3 and anti-CD28 antibodies is normal

increased double-positive T cell number ( J:123582 )

• in the lungs of influenza-infected mice originating from the thymus

increased neutrophil cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased plasma cell number ( J:119703 )

• following stimulation with sheep red blood cells

increased CD4-positive, alpha-beta T cell number ( J:123582 )

• in the lungs of influenza-infected mice

decreased IgG level ( J:119703 )

• all sub-classes of anti-sheep red blood cell IgG following second immunization

abnormal CD4-positive, alpha-beta T cell physiology ( J:119703 , J:123582 )

• CD4+ T cells exhibit decreased ability to activate B cells compared with wild-type T cells (J:119703)

• CD4+ T cells from influenza-infected mice exhibit increased influenza-specific activation (J:123582)

behavior/neurological

decreased grip strength ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

muscle

myositis ( J:113567 )

• some following induction of experimental autoimmune myasthenia gravis

cardiovascular system

choroidal neovascularization ( J:143638 )

• in response to laser treatment, mice exhibit severe choroid neovasculatization with deposition of membrane attack complex compared with wild-type mice

vision/eye

choroidal neovascularization ( J:143638 )

• in response to laser treatment, mice exhibit severe choroid neovasculatization with deposition of membrane attack complex compared with wild-type mice

respiratory system

lung inflammation ( J:123582 )

• following infection with influenza

pulmonary fibrosis ( J:123582 )

• mild following infection with influenza

Allelic Composition	Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	involves: 129

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased macrophage cell number ( J:148367 )

• 1 day post-injury the number of endoneurial macrophages is increased compared to in wild-type mice

abnormal complement pathway ( J:148367 )

• following nerve crush injury, mice exhibit increased C9/membrane attack complex accumulation compared with wild-type mice

increased susceptibility to induced arthritis ( J:146711 )

nervous system

abnormal Wallerian degeneration ( J:148367 )

• exacerbated following nerve crush injury

skeleton

increased susceptibility to induced arthritis ( J:146711 )

hematopoietic system

increased macrophage cell number ( J:148367 )

• 1 day post-injury the number of endoneurial macrophages is increased compared to in wild-type mice

homeostasis/metabolism

abnormal Wallerian degeneration ( J:148367 )

• exacerbated following nerve crush injury

increased susceptibility to injury ( J:148367 )

• following nerve crush injury, mice exhibit increased C9/membrane attack complex accumulation, exacerbated Wallerian degeneration, and increased macrophage accumulation compared with wild-type mice

Allelic Composition	Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	involves: 129 * BALB/c

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased susceptibility to Orthomyxoviridae infection ( J:123582 )

• mice infected with influenza exhibit greater weight loss than wild-type mice

growth/size/body

increased susceptibility to weight loss ( J:123582 )

• following infection with influenza

Allelic Composition	Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	involves: 129 * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:89014 )

• mice treated with MOG33-35 exhibit earlier onset and more severe experimental autoimmune encephalomyelitis with increased demyelination and axon injury compared with wild-type mice

nervous system

demyelination ( J:89014 )

• in MOG33-35 treated mice

Allelic Composition	Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	involves: 129/Sv * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

hematopoietic system

reticulocytosis ( J:70419 )

• homozygotes exhibit a significant increase in reticulocyte count relative to wild-type mice

• however, homozygotes are not anemic, and hemoglobin concentration, red cell number, white cell number, and platelet number are within normal range at both ages tested

• at 10 weeks of age, male homozygotes display higher reticulocyte counts than female homozygotes (mean of 5.63% vs 4.23%) and shorter calculated t^1/2 (7.9 days vs 10.7 days)

increased erythrocyte osmotic fragility ( J:70419 )

• in vitro, mutant erythrocytes are much more susceptible in a classical pathway assay to lysis by homologous or heterologous serum than heterozygous or wild-type erythrocytes

• mutant erythrocytes bearing human or rat C5b-7 sites are extremely susceptible to lysis when either rat or mouse serum is provided as a source of terminal C components, whereas similarly treated wild-type cells are resistant

• furthermore, mutant erythrocytes are positive in the acidified serum lysis assay (Ham test), whereas wild-type erythrocytes are negative (i.e. they do not lyse)

homeostasis/metabolism

hemoglobinemia ( J:70419 )

• at 10 weeks of age, homozygotes display spontaneous intravascular hemolysis with a significant rise in mean plasma hemoglobin concentration relative to wild-type mice (12.6 g/L vs 4.8 g/L, respectively), as measured by spectrophotometry at multiple wavelengths

• notably, plasma hemoglobin concentration is significantly higher in male homozygotes than in female homozygotes (14.6 g/L vs 10.6 g/L, respectively), although erythrocytes tested in vitro are equally susceptible to complement lysis

• administration of cobra venom factor (CVF) to male homozygotes causes a further increase in intravascular hemolysis, as shown by a significant rise in plasma hemoglobin concentration at 1 hr after CVF treatment; by contrast, only a modest increase in hemoglobin concentration is observed in CVF-treated female homozygotes

• analysis of plasma hemolytic activities indicate that male homozygotes have significantly higher hemolytic complement activities, providing a putative explanation for the observed sex differences

hemoglobinuria ( J:70419 )

• at 8 weeks of age, homozygotes exhibit significant hemoglobinuria, as determined by measuring absorbance at 412 nm

renal/urinary system

hemoglobinuria ( J:70419 )

• at 8 weeks of age, homozygotes exhibit significant hemoglobinuria, as determined by measuring absorbance at 412 nm

growth/size/body

decreased body weight ( J:70419 )

• male, but not female, homozygotes are consistently 10% (2 to 3 g in adults) lighter than their wild-type counterparts

• however, both sexes are fully viable, fertile, and otherwise normal up to 30 weeks of age

Allelic Composition	Cd55^tm1Song/Cd55^tm1Song Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	B6.129-Cd55^tm1Song Cd59a^tm1Bpm

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd55^tm1Song mutation (2 available); any Cd55 mutation (39 available)
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

immune system

abnormal complement pathway ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis, mice accumulate C3 in endplates unlike wild-type mice

increased susceptibility to experimental autoimmune myasthenia gravis ( J:113567 )

• 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

myositis ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

behavior/neurological

decreased grip strength ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

muscle

myositis ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis

abnormal muscle morphology ( J:113567 )

• 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

growth/size/body

weight loss ( J:113567 )

• following induction of experimental autoimmune myasthenia gravis that necessitated euthanasia

Allelic Composition	C3^tm1Crr/C3^tm1Crr Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	B6.129-Cd59a^tm1Bpm C3^tm1Crr

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
C3^tm1Crr mutation (3 available); any C3 mutation (102 available)
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

immune system

increased T cell proliferation ( J:122201 )

• n CD4+ T cells stimulated with recombinant vaccinia virus glycoprotein 13 (p13) to the same extent as in Cd59a^tm1Bpm homozygotes

hematopoietic system

increased T cell proliferation ( J:122201 )

• n CD4+ T cells stimulated with recombinant vaccinia virus glycoprotein 13 (p13) to the same extent as in Cd59a^tm1Bpm homozygotes

cellular

increased T cell proliferation ( J:122201 )

• n CD4+ T cells stimulated with recombinant vaccinia virus glycoprotein 13 (p13) to the same extent as in Cd59a^tm1Bpm homozygotes

Allelic Composition	Apoe^tm1Bres/Apoe^tm1Bres Cd59a^tm1Bpm/Cd59a^tm1Bpm
Genetic Background	involves: 129 * 129P2/OlaHsd

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apoe^tm1Bres mutation (11 available); any Apoe mutation (145 available)
Cd59a^tm1Bpm mutation (0 available); any Cd59a mutation (18 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cardiovascular system

increased susceptibility to atherosclerosis ( J:158457 )

• mice fed a high-fat diet exhibit increased atherosclerotic plaque formation, decreased deposition of membrane attack complex, increased smooth muscle cells in early plaques, and decreased smooth muscle cells in advanced plaques compared with Apoe^tm1Bres homozygotes

vascular smooth muscle hyperplasia ( J:158457 )

• in advanced plaques of mice fed a high-fat diet

vascular smooth muscle hypoplasia ( J:158457 )

• in early plaques of mice fed a high-fat diet

muscle

vascular smooth muscle hyperplasia ( J:158457 )

• in advanced plaques of mice fed a high-fat diet

vascular smooth muscle hypoplasia ( J:158457 )

• in early plaques of mice fed a high-fat diet

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