normal phenotype
• homozygotes are indistinguishable from wild-type littermates
|
Allele Symbol Allele Name Allele ID |
Stat5btm1Mam targeted mutation 1, Lothar Hennighausen MGI:3055319 |
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Summary |
34 genotypes
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|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• homozygotes are indistinguishable from wild-type littermates
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• splenomegaly starting at the age of 4 weeks
|
• increased ratio of CD4+ versus CD8+ cells in thymus, peripheral blood, spleen, and lymph nodes
|
• reduction of CD8+ T cells in thymus, peripheral blood, spleen and lymph nodes
|
• lymphoid organ infiltration starting at the age of 4 weeks
|
• splenomegaly starting at the age of 4 weeks
|
• increased ratio of CD4+ versus CD8+ cells in thymus, peripheral blood, spleen, and lymph nodes
|
• reduction of CD8+ T cells in thymus, peripheral blood, spleen and lymph nodes
|
• splenomegaly starting at the age of 4 weeks
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• splenomegaly starting at the age of 4 weeks
|
• increased ratio of CD4+ versus CD8+ cells in thymus, peripheral blood, spleen, and lymph nodes
|
• reduction of CD8+ T cells in thymus, peripheral blood, spleen and lymph nodes
|
• lymphoid organ infiltration starting at the age of 4 weeks
|
• splenomegaly starting at the age of 4 weeks
|
• increased ratio of CD4+ versus CD8+ cells in thymus, peripheral blood, spleen, and lymph nodes
|
• reduction of CD8+ T cells in thymus, peripheral blood, spleen and lymph nodes
|
• splenomegaly starting at the age of 4 weeks
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• increase 40% and 20% in male and female mice, respectively at 22 weeks of age
|
• gain more weight than control littermates starting from 8 weeks of age
• more profound after 16 weeks of age
• weigh on the average 65% (males) and 60% (females) more at 26 weeks of age
|
• increased food intake in male at 16 weeks of age
• increased food intake in both male and female at 26 weeks of age
|
• reduced cold tolerance at 26 weeks of age
|
• 8-fold at 22 weeks of age
|
• 4.5-fold at 22 weeks of age
|
• at 22 weeks of age
|
• at 22 weeks of age
|
• reduced oxygen consumption normalized to lean mass in male mice at 26 weeks of age
|
• at 22 weeks of age
|
• at 22 weeks of age
|
• increase 2.5- and 3.5-fold in male and female mice, respectively at 22 weeks of age
• increase in both subcutaneous and visceral fat mass
|
• larger mean cross-sectional areas of adipocytes in inguinal, parametrial and mesenteric fat pads
|
• at least 2 fold increase in weight of all 5 fat pads (inguinal, parametrial, retroperitoneal, mesenteric and perirenal)
|
• 150% and 200% in male and female mice, respectively of that measured in control mice at 22 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• increase 40% and 20% in male and female mice, respectively at 22 weeks of age
|
• gain more weight than control littermates starting from 8 weeks of age
• more profound after 16 weeks of age
• weigh on the average 65% (males) and 60% (females) more at 26 weeks of age
|
• increased food intake in male at 16 weeks of age
• increased food intake in both male and female at 26 weeks of age
|
• reduced cold tolerance at 26 weeks of age
|
• 8-fold at 22 weeks of age
|
• 4.5-fold at 22 weeks of age
|
• at 22 weeks of age
|
• at 22 weeks of age
|
• reduced oxygen consumption normalized to lean mass in male mice at 26 weeks of age
|
• at 22 weeks of age
|
• at 22 weeks of age
|
• increase 2.5- and 3.5-fold in male and female mice, respectively at 22 weeks of age
• increase in both subcutaneous and visceral fat mass
|
• larger mean cross-sectional areas of adipocytes in inguinal, parametrial and mesenteric fat pads
|
• at least 2 fold increase in weight of all 5 fat pads (inguinal, parametrial, retroperitoneal, mesenteric and perirenal)
|
• 150% and 200% in male and female mice, respectively of that measured in control mice at 22 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced body weight starting around 3 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced body weight starting around 3 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced lean mass at 8 weeks of age
• normal fraction of lean mass to total body weight
|
• 12% and 20% smaller for female and male mice respectively, at 8 weeks of age
|
• reduced body length at 8 weeks of age
|
• a trend toward higher total fat mass at 8 weeks of age
|
• 15% decrease in circulating IGF-I level at 8 weeks of age
|
• elevated serum triglycerides at 8 weeks of age
|
• glucose intolerance in male mice at 30- and 60-min after glucose challenge
• a similar trend in female, but less severe
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• a trend toward higher total fat mass at 8 weeks of age
|
• reduced lean mass at 8 weeks of age
• normal fraction of lean mass to total body weight
|
• 12% and 20% smaller for female and male mice respectively, at 8 weeks of age
|
• reduced body length at 8 weeks of age
|
• 15% decrease in circulating IGF-I level at 8 weeks of age
|
• elevated serum triglycerides at 8 weeks of age
|
• glucose intolerance in male mice at 30- and 60-min after glucose challenge
• a similar trend in female, but less severe
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced lean mass at 8 weeks of age
• reduction in fraction of lean mass at 8 weeks of age
|
• 12% and 20% smaller for female and male mice respectively, at 8 wk of age
|
• reduced body length at 8 weeks of age
|
• modest increase in body fat at 8 weeks of age
|
• 60% decrease in circulating IGF-I level at 8 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• modest increase in body fat at 8 weeks of age
|
• reduced lean mass at 8 weeks of age
• reduction in fraction of lean mass at 8 weeks of age
|
• 12% and 20% smaller for female and male mice respectively, at 8 wk of age
|
• reduced body length at 8 weeks of age
|
• 60% decrease in circulating IGF-I level at 8 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• the number of alveoli is reduced, however females are able to successfully nurse their pups
• the alveoli that are present are distended
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
• the number of alveoli is reduced, however females are able to successfully nurse their pups
• the alveoli that are present are distended
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• the number of alveoli is reduced, however females are able to successfully nurse their pups
• the alveoli that are present are distended
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
• the number of alveoli is reduced, however females are able to successfully nurse their pups
• the alveoli that are present are distended
|
• increased apoptosis is seen in the mammary epithelium during late pregnancy
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
• the number of tertiary branches is severely decreased, the lobular units are absent, and at parturition the alveolar compartment is missing
• treatment with estrogen and progesterone induces very little side branching in mammary epithelia unlike in wild-type females
|
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
• the number of tertiary branches is severely decreased, the lobular units are absent, and at parturition the alveolar compartment is missing
• treatment with estrogen and progesterone induces very little side branching in mammary epithelia unlike in wild-type females
|
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
• the number of tertiary branches is severely decreased, the lobular units are absent, and at parturition the alveolar compartment is missing
• treatment with estrogen and progesterone induces very little side branching in mammary epithelia unlike in wild-type females
|
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
• the number of tertiary branches is severely decreased, the lobular units are absent, and at parturition the alveolar compartment is missing
• treatment with estrogen and progesterone induces very little side branching in mammary epithelia unlike in wild-type females
|
• 10 out of 12 dams were unable to secrete milk, while the remaining 2 could secrete only small amounts of milk
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• elevated serum IL-17 concentration
|
• elevated serum IL-17 concentration
|
• increased amounts of IL-17 protein in the culture supernatants of CD4+ T cells activated with anti-CD3 and anti-CD28
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• elevated serum IL-17 concentration
|
• elevated serum IL-17 concentration
|
• increased amounts of IL-17 protein in the culture supernatants of CD4+ T cells activated with anti-CD3 and anti-CD28
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• fewer IL9+ cells in IFN-alpha-treated mice following differentiation towards Th9 lineage
|
• fewer IL9+ cells in IFN-alpha-treated mice following differentiation towards Th9 lineage
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• decreased absolute number of bone marrow mononuclear cells (BMMNCs) from both femora and tibiae per mouse
• decreased absolute number of granulocyte-macrophage progenitors (GMPs) from both femora and tibiae per mouse
• normal percentage of GMPs in BMMNCs
• impaired colony formation of GMPs
• reduced numbers of mutant colonies by more than 50% in the presence of GM-CSF
• the average cell number of a mutant GMP-derived colony is only 11% of that from control GMPs
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• decreased white blood cell counts
|
• decreased absolute number of peripheral neutrophils by 50% in homeostasis 3 weeks after PolyIC injection
|
• decreased lymphocytes counts (70% decrease)
|
• decreased monocytes counts (44% decrease)
|
• only 65% of mutant bone marrow neutrophils, compare with virtually all cells from control animals survive for 36 hours in the presence of GM-CSF
|
• decreased absolute number of bone marrow mononuclear cells (BMMNCs) from both femora and tibiae per mouse
• decreased absolute number of granulocyte-macrophage progenitors (GMPs) from both femora and tibiae per mouse
• normal percentage of GMPs in BMMNCs
• impaired colony formation of GMPs
• reduced numbers of mutant colonies by more than 50% in the presence of GM-CSF
• the average cell number of a mutant GMP-derived colony is only 11% of that from control GMPs
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• decreased white blood cell counts
|
• decreased absolute number of peripheral neutrophils by 50% in homeostasis 3 weeks after PolyIC injection
|
• decreased lymphocytes counts (70% decrease)
|
• decreased monocytes counts (44% decrease)
|
• only 65% of mutant bone marrow neutrophils, compare with virtually all cells from control animals survive for 36 hours in the presence of GM-CSF
|
• increased cell death in GMPs and their progeny during culture with GM-CSF up to the fifth generation
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• longer generation times in every generation (F1 through F4) during culture with GM-CSF compared with control cells
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• disrupted architecture of islets as evidenced by the migration of glucagon-expressing alpha-cells into the central region of the islets
|
• mild glucose intolerance in mice older than 6 months
• slightly more glucose intolerant during pregnancy than their control littermates
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• increased cell death in GMPs and their progeny during culture with GM-CSF up to the fifth generation
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• longer generation times in every generation (F1 through F4) during culture with GM-CSF compared with control cells
|
• decreased absolute number of bone marrow mononuclear cells (BMMNCs) from both femora and tibiae per mouse
• decreased absolute number of granulocyte-macrophage progenitors (GMPs) from both femora and tibiae per mouse
• impaired colony formation of GMPs
• reduced numbers of mutant colonies by more than 50% in the presence of GM-CSF
• the average cell number of a mutant GMP-derived colony is only 11% of that from control GMPs
• normal percentage of GMPs in BMMNCs
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• decreased white blood cell counts
|
• decreased absolute number of peripheral neutrophils by 50% in homeostasis 3 weeks after PolyIC injection
|
• decreased lymphocytes counts (70% decrease)
|
• decreased monocytes counts (44% decrease)
|
• only 65% of mutant bone marrow neutrophils, compare with virtually all cells from control animals survive for 36 hours in the presence of GM-CSF
|
• decreased absolute number of bone marrow mononuclear cells (BMMNCs) from both femora and tibiae per mouse
• decreased absolute number of granulocyte-macrophage progenitors (GMPs) from both femora and tibiae per mouse
• impaired colony formation of GMPs
• reduced numbers of mutant colonies by more than 50% in the presence of GM-CSF
• the average cell number of a mutant GMP-derived colony is only 11% of that from control GMPs
• normal percentage of GMPs in BMMNCs
|
• no elevation of neutrophils 18 days after induced myelosuppression by 5-FU injection
• severely impaired GM-CSF-induced increase of peripheral blood neutrophils
|
• decreased white blood cell counts
|
• decreased absolute number of peripheral neutrophils by 50% in homeostasis 3 weeks after PolyIC injection
|
• decreased lymphocytes counts (70% decrease)
|
• decreased monocytes counts (44% decrease)
|
• only 65% of mutant bone marrow neutrophils, compare with virtually all cells from control animals survive for 36 hours in the presence of GM-CSF
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• disrupted architecture of islets as evidenced by the migration of glucagon-expressing alpha-cells into the central region of the islets
|
• mild glucose intolerance in mice older than 6 months
• slightly more glucose intolerant during pregnancy than their control littermates
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mild obesity
• weigh on the average 20% more than their control littermates by 9 months of age
|
• elevated adipose tissue mass of female mice
• normal lean mass
|
• reduced insulin secretion from isolated islets upon challenge with 16.7 mM of glucose
|
• slightly elevated serum glucose levels at 7 months of age
|
• higher serum leptin levels at 7 months of age
• normal serum insulin levels
|
• higher serum free fatty acids levels at 7 months of age
|
• higher glucose levels than the controls at all time points after glucose injection
• severity of impaired glucose response increases in both female and male mice as they age
• more severe than that seen in Tg(Ins2-cre)25Mgn mice
|
• disrupted architecture of islets as evidenced by the migration of glucagon-expressing alpha-cells into the central region of the islets
|
• reduced insulin secretion from isolated islets upon challenge with 16.7 mM of glucose
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mild obesity
• weigh on the average 20% more than their control littermates by 9 months of age
|
• elevated adipose tissue mass of female mice
• normal lean mass
|
• reduced insulin secretion from isolated islets upon challenge with 16.7 mM of glucose
|
• slightly elevated serum glucose levels at 7 months of age
|
• higher serum leptin levels at 7 months of age
• normal serum insulin levels
|
• higher serum free fatty acids levels at 7 months of age
|
• higher glucose levels than the controls at all time points after glucose injection
• severity of impaired glucose response increases in both female and male mice as they age
• more severe than that seen in Tg(Ins2-cre)25Mgn mice
|
• disrupted architecture of islets as evidenced by the migration of glucagon-expressing alpha-cells into the central region of the islets
|
• reduced insulin secretion from isolated islets upon challenge with 16.7 mM of glucose
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• with doxycycline food during pregnancy female mice develop functional mammary glands during pregnancy and are able to feed their pups
• expanded alveoli lined with differentiated secretory cells, with proteinaceous material and lipid droplets in the lumen after doxycycline treatment
• formation of alveolar structures and functional differentiation of luminal cells after doxycycline treatment
• the mutant mice generate CD61+ luminal progenitor cells during pregnancy to a similar extent as Stat5a/Stat5btm2Mam control mice
|
N |
• with doxycycline food during pregnancy female mice develop functional mammary glands during pregnancy and are able to feed their pups
• expanded alveoli lined with differentiated secretory cells, with proteinaceous material and lipid droplets in the lumen after doxycycline treatment
• formation of alveolar structures and functional differentiation of luminal cells after doxycycline treatment
• the mutant mice generate CD61+ luminal progenitor cells during pregnancy to a similar extent as Stat5a/Stat5btm2Mam control mice
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
N |
• with doxycycline food during pregnancy female mice develop functional mammary glands during pregnancy and are able to feed their pups
• expanded alveoli lined with differentiated secretory cells, with proteinaceous material and lipid droplets in the lumen after doxycycline treatment
• formation of alveolar structures and functional differentiation of luminal cells after doxycycline treatment
• the mutant mice generate CD61+ luminal progenitor cells during pregnancy to a similar extent as Stat5a/Stat5btm2Mam control mice
|
N |
• with doxycycline food during pregnancy female mice develop functional mammary glands during pregnancy and are able to feed their pups
• expanded alveoli lined with differentiated secretory cells, with proteinaceous material and lipid droplets in the lumen after doxycycline treatment
• formation of alveolar structures and functional differentiation of luminal cells after doxycycline treatment
• the mutant mice generate CD61+ luminal progenitor cells during pregnancy to a similar extent as Stat5a/Stat5btm2Mam control mice
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• microcytic, hypochromic anemia
|
• red cell hypoplasia in bone marrow at E18.5
|
• higher ratio of nucleated erythroid cells in fetuses and neonates
|
• greatly reduced number of mature red blood cells in fetuses and neonates
|
• decreased hematocrits of approximately 2.5 (25%) in neonates, compared with 4.7 (47%) in controls
• hematocrits in adult mutant mice remain low at 2.9
• decreased hematocrits of approximately 2.6 in mice that receive a transplant of mutant fetal liver cells, compared with 3.8 in controls
|
• reduced red cell size (mean corpuscular volume) and hemoglobin content in mutant mice and in mice that receive a transplant of mutant fetal liver cells
|
• increased red cell distribution width
|
• elevated serum iron levels and transferrin saturation in mutant mice and in mice that receive a transplant of mutant fetal liver cells
|
• non-heme iron overload in the liver
• periportal hepatocyte iron staining
|
• elevated cell death in survival response of splenic Ter119-positive cells to erythropoietin
|
• non-heme iron overload in the liver
• periportal hepatocyte iron staining
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• microcytic, hypochromic anemia
|
• red cell hypoplasia in bone marrow at E18.5
|
• higher ratio of nucleated erythroid cells in fetuses and neonates
|
• greatly reduced number of mature red blood cells in fetuses and neonates
|
• decreased hematocrits of approximately 2.5 (25%) in neonates, compared with 4.7 (47%) in controls
• hematocrits in adult mutant mice remain low at 2.9
• decreased hematocrits of approximately 2.6 in mice that receive a transplant of mutant fetal liver cells, compared with 3.8 in controls
|
• reduced red cell size (mean corpuscular volume) and hemoglobin content in mutant mice and in mice that receive a transplant of mutant fetal liver cells
|
• increased red cell distribution width
|
• elevated serum iron levels and transferrin saturation in mutant mice and in mice that receive a transplant of mutant fetal liver cells
|
• non-heme iron overload in the liver
• periportal hepatocyte iron staining
|
• elevated cell death in survival response of splenic Ter119-positive cells to erythropoietin
|
• non-heme iron overload in the liver
• periportal hepatocyte iron staining
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced body weight starting around 3 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
• profoundly reduced amount of luminal progenitors (CD61+) in the luminal cell population (CD24hiCD49flo) in mammary tissue of 12 week-old virgin mice and on day 6 of pregnancy
|
• fail to lactate even after five to six pregnancies
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
• profoundly reduced amount of luminal progenitors (CD61+) in the luminal cell population (CD24hiCD49flo) in mammary tissue of 12 week-old virgin mice and on day 6 of pregnancy
|
• fail to lactate even after five to six pregnancies
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• reduced body weight starting around 3 weeks of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
• profoundly reduced amount of luminal progenitors (CD61+) in the luminal cell population (CD24hiCD49flo) in mammary tissue of 12 week-old virgin mice and on day 6 of pregnancy
|
• fail to lactate even after five to six pregnancies
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
|
• the epithelial compartment in stem cell-transplanted hosts fail to develop a full alveolar compartment and devoid of milk in the epithelial lumina at term when mated to induce pregnancy
• produce only a ductal tree with virgin-like characteristics
• profoundly reduced amount of luminal progenitors (CD61+) in the luminal cell population (CD24hiCD49flo) in mammary tissue of 12 week-old virgin mice and on day 6 of pregnancy
|
• fail to lactate even after five to six pregnancies
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• impaired NK cell maturation
|
• impaired NK cell maturation
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• homozygotes are indistinguishable from wild-type littermates
|
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 12/10/2024 MGI 6.24 |
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