Analysis Tools|
Allele Symbol Allele Name Allele ID |
Vav2tm1Kdf targeted mutation 1, Klaus-Dieter Fischer MGI:2387822 |
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| Summary |
8 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Progressive iridocorneal angle closures in Vav2tm1Kdf/Vav2tm1Kdf Vav3tm1Swat/Vav3tm1Swat and Vav2tm1Kdf/Vav2tm1Kdf mice
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• between 4 and 16 weeks, some mice exhibit closed iridocorneal angles unlike wild-type mice
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• between 4 and 16 weeks, some mice exhibit peripheral anterior synechiae unlike wild-type mice
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• at 7 weeks and increasing through 12 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• however, proliferation in response to stimulation with a stronger antigen (polyclonal anti-IgM antibody) is similar to controls
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• slight decrease in the number of B220hiIgMlo B cells in the bone marrow
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• following TNP-Ficoll stimulation
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• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• however, proliferation in response to stimulation with a stronger antigen (polyclonal anti-IgM antibody) is similar to controls
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• slight decrease in the number of B220hiIgMlo B cells in the bone marrow
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• following TNP-Ficoll stimulation
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• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• however, proliferation in response to stimulation with a stronger antigen (polyclonal anti-IgM antibody) is similar to controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Vav2tm1Kdf/Vav2tm1Kdf Vav3tm1Swat/Vav3tm1Swat mice develop buphthalmos
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• some eyes are atrophic and phthisical unlike in wild-type mice
• at 6 months, 75% of mice exhibit enlarged eyes compared with wild-type mice
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• at 15 and 30 weeks
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• at 10, 15, and 30 weeks
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• as early as 18 days, some mice exhibit closed iridocorneal angles unlike wild-type mice
• at 7 weeks, 50% of mice exhibit closed iridocorneal angles unlike wild-type mice
• at 12 to 16 weeks, 80% of mice exhibit closed iridocorneal angles unlike wild-type mice
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• between 18 days and 16 weeks, some mice exhibit peripheral anterior synechiae unlike wild-type mice
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• beginning at 6 to 12 weeks unilaterally then spreading bilaterally over the next 1 to 2 months with continued enlargement until 6 months of age
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• 6 weeks, mice exhibit increased intraocular pressure compared with wild-type mice that increases further by 10 weeks of age
• mice with increased intraocular pressure exhibit closed iridocorneal angles
• however, treatment with ocular hypotensives such as latanoprost, dorzolamide and timolol produces a greater reduction in intraocular pressure than in similarly treated wild-type mice
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• treatment with Y27632 fails to lower intraocular pressure unlike in wild-type mice
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• treatment with ocular hypotensives such as latanoprost, dorzolamide and timolol produces a greater reduction in intraocular pressure than in similarly treated wild-type mice
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• at 15 and 30 weeks
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• at 10, 15, and 30 weeks
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• B cells show reduced proliferation in response to Ig receptor stimulation
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• ability of T cells to generate blasts when stimulated is reduced by 3- to 4-fold, indicating a proliferation defect
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• 2- to 3-fold reduction in mature IgMloIgDhi B cells
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• few peripheral T cells
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• production of IFN-gamma by T cells in response to TCR stimulation is reduced
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• production of IL-2 by T cells in response to TCR stimulation is reduced
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• B cells show reduced proliferation in response to Ig receptor stimulation
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• ability of T cells to generate blasts when stimulated is reduced by 3- to 4-fold, indicating a proliferation defect
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• 2- to 3-fold reduction in mature IgMloIgDhi B cells
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• few peripheral T cells
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• B cells show reduced proliferation in response to Ig receptor stimulation
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• ability of T cells to generate blasts when stimulated is reduced by 3- to 4-fold, indicating a proliferation defect
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• LPS- or peptidoglycan-stimulated reactive oxygen intermediate (ROI) production by neutrophils is blocked compared to in similarly treated wild-type cells
• however, ROI production in response to PMA stimulation is normal
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• NK cells exhibit reduced conjugation with RMA-S cells compared with wild-type cells
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• LPS-stimulated bone marrow-derived macrophages fail to generate oxidative burst unlike similarly treated wild-type cells
• however, mice exhibit normal bone marrow-derived macrophages response to PMA stimulation and reactive nitrogen and prostaglandin production in response to LPS
• despite normal phagocytosis, bone marrow-derived macrophages stimulated with unopsonized heat-killed E. coli fail to generate reactive oxygen intermediate unlike similarly treated wild-type cells
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• from LPS-stimulated bone marrow-derived macrophages
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• from LPS-stimulated bone marrow-derived macrophages
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• LPS- or peptidoglycan-stimulated reactive oxygen intermediate (ROI) production by neutrophils is blocked compared to in similarly treated wild-type cells
• however, ROI production in response to PMA stimulation is normal
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• NK cells exhibit reduced conjugation with RMA-S cells compared with wild-type cells
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• LPS-stimulated bone marrow-derived macrophages fail to generate oxidative burst unlike similarly treated wild-type cells
• however, mice exhibit normal bone marrow-derived macrophages response to PMA stimulation and reactive nitrogen and prostaglandin production in response to LPS
• despite normal phagocytosis, bone marrow-derived macrophages stimulated with unopsonized heat-killed E. coli fail to generate reactive oxygen intermediate unlike similarly treated wild-type cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• B cells fail to proliferate in response to Ig receptor stimulation
• mature B cells that are present in mutants fail to proliferate in response to stimulation with anti-Ig antibodies
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• T2 cells are reduced approximately 2-fold
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• increase in the proportion of immature cells
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• numbers of transitional 1 (T1) and newly formed B cells are increased
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• immature B lineage cells accumulate in the periphery and development is arrested at a late transitional (T1/T2) stage
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• blocked at an early stage in the thymus, at the DN3 to DN4 transition
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• 2- to 3-fold reduction in mature IgMloIgDhi B cells
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• few peripheral T cells
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• 50 to 100 fold reduction relative to wild-type
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• anti-Ig induced calcium responses are severely disrupted in B cells
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• calcium fluxes induced by anti-CD3 antibody cross-linking are completely disrupted in T cells
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• T cells do not exhibit proliferative responses to stimulation with anti-CD3 with or without anti-CD28 antibodies
• T cells are unable to generate blasts when stimulated
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• failure to mount either T-dependent or T-independent humoral responses
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• fail to produce any anti-TNP antibodies in response to TI-2 antigen
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• fail to produce anti-TNP-specific IgG1 antibodies after immunization
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• fail to produce anti-TNP-specific IgG2b antibodies after immunization
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• fail to produce anti-TNP-specific IgG3 antibodies after immunization
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• fail to produce anti-TNP-specific IgM antibodies after immunization
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• mutant T cells do not produce IFN-gamma in response to TCR stimulation
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• mutant T cells do not produce IL-2 in response to TCR stimulation
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• the upper zone surface of epithelial cells in the cecum and ascending colon are shorted than in wild-type mice
• epithelial cell heights in the cecum and ascending colon decrease between the middle and upper zones unlike in wild-type mice
• upper zone enterocyte differentiation, as determined by marker staining, is incomplete compared to in wild-type mice
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• beyond 6 weeks, mice develop spontaneous mucosal ulcers in the cecum and colon unlike wild-type mice
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• anti-Ig induced calcium responses are severely disrupted in B cells
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• even after 10 days, mice fail to exhibit complete healing of colonic mucosa injury unlike similarly treated wild-type mice
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• B cells fail to proliferate in response to Ig receptor stimulation
• mature B cells that are present in mutants fail to proliferate in response to stimulation with anti-Ig antibodies
|
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• T2 cells are reduced approximately 2-fold
|
|
• increase in the proportion of immature cells
|
|
• numbers of transitional 1 (T1) and newly formed B cells are increased
|
|
• immature B lineage cells accumulate in the periphery and development is arrested at a late transitional (T1/T2) stage
|
|
• blocked at an early stage in the thymus, at the DN3 to DN4 transition
|
|
• 2- to 3-fold reduction in mature IgMloIgDhi B cells
|
|
• few peripheral T cells
|
|
• 50 to 100 fold reduction relative to wild-type
|
|
• anti-Ig induced calcium responses are severely disrupted in B cells
|
|
• fail to produce any anti-TNP antibodies in response to TI-2 antigen
|
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• fail to produce anti-TNP-specific IgG1 antibodies after immunization
|
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• fail to produce anti-TNP-specific IgG2b antibodies after immunization
|
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• fail to produce anti-TNP-specific IgG3 antibodies after immunization
|
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• fail to produce anti-TNP-specific IgM antibodies after immunization
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• calcium fluxes induced by anti-CD3 antibody cross-linking are completely disrupted in T cells
|
|
• T cells do not exhibit proliferative responses to stimulation with anti-CD3 with or without anti-CD28 antibodies
• T cells are unable to generate blasts when stimulated
|
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• 50 to 100 fold reduction relative to wild-type
|
|
• B cells fail to proliferate in response to Ig receptor stimulation
• mature B cells that are present in mutants fail to proliferate in response to stimulation with anti-Ig antibodies
|
|
• T cells do not exhibit proliferative responses to stimulation with anti-CD3 with or without anti-CD28 antibodies
• T cells are unable to generate blasts when stimulated
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• do not exhibit any obvious T cell abnormalities
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced by about 80% compared to controls
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• partial block in B cell differentiation
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• partial block in differentiation of double positive T cells into single positive T cells
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• about an 80% reduction in the number of B cells in the spleen
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• marked decrease in the number of B220hiIgMlo B cells in the bone marrow
• this decrease is more severe than in mice homozygous null for Vav2 alone
• pronounced decrease in the number of mature B cells in the spleen
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• in the peritoneal cavity
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• splenic and lymph node T cell populations are reduced by about 90% and 50% compared to wild-type controls and mice homozygous null for Vav1 alone, respectively
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• decreased compared to wild-type controls and mice homozygous null for Vav1 alone
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• relative increase in the number of immature B cells compared to mature B cells
|
|
• fail to produce IgM following TNP-Ficoll stimulation
|
|
• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• B cells are also virtually insensitive to stimulation with a stronger antigen (polyclonal anti-IgM antibody)
• cells fail to proliferate in response to LPS stimulation
• proliferation defect is seen in both mature and immature B cells
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• basal levels of IgG1 are reduced
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• basal levels of IgG2b are reduced
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• virtually no IgG3 is produced following TNP-Ficoll stimulation
• basal levels of IgG3 are reduced
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• fail to produce IgM following TNP-Ficoll stimulation
• basal levels of IgM are reduced
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• the ratio of IgMhiIgDhi to IgMloIgDhi is about 1:0.7
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• reduced by about 80% compared to controls
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• partial block in B cell differentiation
|
|
• partial block in differentiation of double positive T cells into single positive T cells
|
|
• about an 80% reduction in the number of B cells in the spleen
|
|
• marked decrease in the number of B220hiIgMlo B cells in the bone marrow
• this decrease is more severe than in mice homozygous null for Vav2 alone
• pronounced decrease in the number of mature B cells in the spleen
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• in the peritoneal cavity
|
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• splenic and lymph node T cell populations are reduced by about 90% and 50% compared to wild-type controls and mice homozygous null for Vav1 alone, respectively
|
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• decreased compared to wild-type controls and mice homozygous null for Vav1 alone
|
|
• relative increase in the number of immature B cells compared to mature B cells
|
|
• fail to produce IgM following TNP-Ficoll stimulation
|
|
• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• B cells are also virtually insensitive to stimulation with a stronger antigen (polyclonal anti-IgM antibody)
• cells fail to proliferate in response to LPS stimulation
• proliferation defect is seen in both mature and immature B cells
|
|
• basal levels of IgG1 are reduced
|
|
• basal levels of IgG2b are reduced
|
|
• virtually no IgG3 is produced following TNP-Ficoll stimulation
• basal levels of IgG3 are reduced
|
|
• fail to produce IgM following TNP-Ficoll stimulation
• basal levels of IgM are reduced
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• reduced by about 80% compared to controls
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• proliferation in response to stimulation with a weak antigen (monoclonal antibody to IgM, B7.6) barely exceeds background
• B cells are also virtually insensitive to stimulation with a stronger antigen (polyclonal anti-IgM antibody)
• cells fail to proliferate in response to LPS stimulation
• proliferation defect is seen in both mature and immature B cells
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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 12/17/2024 MGI 6.24 |
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