Analysis Tools
vision/eye
| N |
• mice exhibit normal intraocular pressure and iridocorneal angle
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Allele Symbol Allele Name Allele ID |
Vav3tm1Swat targeted mutation 1, Wojciech Swat MGI:2683642 |
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| Summary |
9 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice exhibit normal intraocular pressure and iridocorneal angle
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice appear healthy and fertile, have normal lymphocyte development and show no major abnormalities
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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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• ephrin-A1-induced angiogenesis is impaired compared to in similarly exposed wild-type mice
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• murine pulmonary microvascular endothelial cells (MPMECs) exhibit reduced ephrin-A1 migration compared with wild-type cells
• however, migration in response to serum is normal
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• on Matrigel, organization of murine pulmonary microvascular endothelial cells (MPMECs) into capillary-like structures is inhibited compared with similarly treated wild-type cells
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• murine pulmonary microvascular endothelial cells (MPMECs) exhibit reduced ephrin-A1 migration compared with wild-type cells
• however, migration in response to serum is normal
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• mouse embryonic fibroblasts exhibit decreased spreading on an ephrin-A1-coated surface compared with wild-type cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in culture, growth cones respond poorly to ephrin-A1 treatment compared to in wild-type cells
• however, growth cones respond normally to other repulsive guidance factors
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• ipsilateral projections from the retinal ganglion cells (RGCs) to the dorsal lateral geniculate nucleus are reduced in number and shifted ventrally compared to in wild-type
• RGC projections along the long axis are distorted compared to in wild-type mice
• ipsilateral RGC projections are shifted ventrolaterally and have a sloping distribution compared to in wild-type mice
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• in culture, growth cones respond poorly to ephrin-A1 treatment compared to in wild-type cells
• however, growth cones respond normally to other repulsive guidance factors
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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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• 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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• 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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• 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
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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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• 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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• even after 10 days, mice fail to exhibit complete healing of colonic mucosa injury unlike similarly treated wild-type mice
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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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• 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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• 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
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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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• 50 to 100 fold reduction relative to wild-type
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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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• 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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• B cells show diminished proliferation in response to Ig receptor stimulation
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• T cells are unable to generate blasts when stimulated, indicating a proliferation defect
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• small decrease in mature IgMloIgDhi B cells
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• T cell numbers are reduced more than in single Vav1 homozygotes
• reduction in peripheral T cells
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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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• B cells show diminished proliferation in response to Ig receptor stimulation
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• T cells are unable to generate blasts when stimulated, indicating a proliferation defect
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• small decrease in mature IgMloIgDhi B cells
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• T cell numbers are reduced more than in single Vav1 homozygotes
• reduction in peripheral T cells
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• B cells show diminished proliferation in response to Ig receptor stimulation
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• T cells are unable to generate blasts when stimulated, indicating a proliferation defect
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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 04/23/2024 MGI 6.23 |
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