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Allele Symbol Allele Name Allele ID |
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy targeted mutation 1, Andras Nagy MGI:3583817 |
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| Summary |
30 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice die shortly after birth
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• at E18.5, myofibroblasts in the lungs of doxycycline-treated mice exhibit reduced differentiation, as determined by sma+ expression, compared to in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice develop lethal liver dysplasia
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• doxycycline-treated mice develop lethal liver dysplasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice develop lethal liver dysplasia
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• doxycycline-treated mice develop lethal liver dysplasia
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• local bone and marrow tissue in doxycycline-treat mice are replaced with massively enlarged vascular structures (hemangiomas) unlike in wild-type mice
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| N |
• doxycycline-treat mice exhibit normal bone density, osteoclastic bone remodeling, and bone degradation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in mice exposed to deoxycycline treatment at E16.5
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• enlarged
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• increased anterior chamber depth
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• eyes begin to protrude by 21 to 28 days of age in mice exposed to deoxycycline treatment at E16.5
• difficulty closing eyelids by 8 weeks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• capillary loops extend into the cornea
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• in mice exposed to deoxycycline treatment at E16.5
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• lymphatic vasculature develops in the corneal limbus
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• capillary loops extend into the cornea
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• enlarged
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• increased anterior chamber depth
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• eyes begin to protrude by 21 to 28 days of age
• difficulty closing eyelids by 8 weeks of age
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• reduced thickness of retinal cell layer
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• reduced thickness
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• becoming worse toward periphery
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• in mice exposed to deoxycycline treatment at E16.5
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• elevated
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• severely impaired vision
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• lymphatic vessels are sparse in the dermis of the ear
• abnormal branching of lymphatic vessels
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age
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• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:186194 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro
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• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:186194 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die between 8 and 18 weeks after doxycycline (dox) treatment to induce Kras2 expression due to pancreatic ductal adenocarinoma
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• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
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• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma
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• adult mice treated with dox for 5 weeks prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis exhibit a small, translucent remnant of pancreatic tissue, without fibrosis or PanIN lesions
• when dox is removed after pancreatitis induction, mice show show normal acini interspersed with dilated ducts and acinar-ductal metaplasia, fibrosis and occasional lipomatosis, but with minimal inflammatory infiltrate, and reduced proliferation
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• mice develop invasive adenocarcinoma between 8 and 18 weeks after dox treatment, with some cases showing hemorrhagic ascites, with admixed poorly differentiated and well-differentiated areas and duodenal invasion
• mice in which dox is removed recover their health and show pancreatic tumor regression resulting in a small pancreatic remnant
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• adult mice treated with dox 72 hours prior to injection with cholecystokinin analog cerulein to induce acute pancreatitis develop PanINs, dilated ducts with the presence of intracellular mucins, and extensive fibroinflammatory stroma
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:184378 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• small kidney in mice induced with doxycycline from E14.5 until the end of the experiment
• however, cap mesenchyme differentiates normally in doxycycline induced mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• all mice develop kidney tumors within the first 2 weeks of life following doxycycline (Dox) induction during embryonic development at E0, E14.5 or E18.5
• tumors resemble Wilms tumor
• mice treated with doxycycline at P10 do not develop tumors
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• mice treated with doxycycline at P10 develop cystic kidneys
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• all mice develop kidney tumors within the first 2 weeks of life following doxycycline (Dox) induction during embryonic development at E0, E14.5 or E18.5
• tumors resemble Wilms tumor
• mice treated with doxycycline at P10 do not develop tumors
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• doxycycline induced mice exhibit persistent proliferation of cap mesenchyme cells in adults
• however, cap mesenchyme cells within tumors retain a differentiation capacity that recapitulates normal kidney development
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• timing of kidney development is prolonged in doxycycline induced mice, with sustaining proliferation of the cap mesenchyme cells into adulthood
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• mice treated with doxycycline at P10 develop cystic kidneys
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| nephroblastoma | DOID:2154 |
OMIM:194070 |
J:211179 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop hydronephrosis following doxycycline induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• skin grafts on nude mice treated with doxycycline exhibit stunted hair growth unlike control grafts
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• doxycycline-treated mice exhibit multi-layered epithelium unlike control mice
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• skin grafts on nude mice treated with doxycycline exhibit hyperkeratosis unlike control grafts
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• skin grafts on nude mice treated with doxycycline exhibit hyperkeratosis unlike control grafts
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• 8 days after doxycycline treatment
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• 8 days after doxycycline treatment
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• skin from doxycycline-treated mice exhibit a greater than 5-fold increase in the number of colony-forming cells compared with skin from control mice
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• in nude mice receiving skin grafts and treated with doxycycline
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• thickened and dysplastic in doxycycline-treated mice
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• in nude mice receiving skin grafts and treated with doxycycline
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• doxycycline-treated mice exhibit increased cell proliferation of basal cells and an extension of the proliferative domain into the suprabasal layers of back skin compared with control mice
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• thickened and dysplastic in doxycycline-treated mice
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• thickened and dysplastic in doxycycline-treated mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop cystic kidneys when transgene expression is induced with doxycycline early in embryonic development or in adult mice
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• mice develop cystic kidneys when transgene expression is induced with doxycycline early in embryonic development or in adult mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors
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• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors
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• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| prostate cancer | DOID:10283 |
OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959 |
J:222916 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• no kidney pathology is seen in mice induced with doxycycline
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in the right ventricle and out flow tract
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• thickening of the myocardium
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• thickening of the myocardium
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• in the right ventricle and out flow tract
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the vascular network of the limbs is denser and more complex
• metacarpal centers are enriched for thicker vessels originating from the axial artery
• metacarpal centers are wider and split into a denser and more complex network of small capillaries in the interdigital areas
• however, formation of avascular areas is not affected
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decrease in airway spaces at E18.5
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• develop large, cyst-like structures at the distal epithelial branch tips
• cystic buds appear to collapse by E18.5
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• noticeable by E14.5 and more significant by E16.5
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• develop large, cyst-like structures at the distal epithelial branch tips
• cystic buds appear to collapse by E18.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline (Dox)-treated mice show a gradual reduction in the volume of adipose tissue
• when mice are taken off the Dox-containing diet, the fat tissue volume increases
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• increase in serum free fatty acids in the fed state after 72 hours of induction with Dox
• however, Dox-treated mice maintain the same rate of fatty acid and cholesterol synthesis as controls in a biochemical assay for de novo lipid synthesis
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• mice fed a doxycycline (Dox)-containing diet show a higher respiratory exchange ratio than wild-type mice during the dark phase
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• mice exhibit a reduction in hepatic glucose release when exposed to Dox for 48 hours
• metabolic cage studies indicate higher glucose utilization in Dox-treated mice
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• a 6-hour fast causes severe hypoglycemia within 48 hours after induction with Dox
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• serum glucose levels start to decrease by 72 hours after induction with Dox under fed conditions
• administration of a PPAR-alpha agonist exacerbates the hypoglycemia in Dox-treated mice
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• fed insulin levels start to decrease upon induction with Dox and are significantly lower by 72 hours of induction
• 96 hours after Dox-induction, fasted insulin levels are lower
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• hepatic glycogen is severely depleted after 48 hours of induction with Dox
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• livers of Dox-treated mice show a faster response to insulin exposure and isolated hepatocytes induced with Dox show an enhanced insulin response indicating hepatic insulin sensitivity
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• hepatic triglyceride content is increased in Dox-treated mice
• a 6-hour fast increases liver triglyceride content acutely within 24 hours of Dox exposure
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• the fasting effects of adipocyte lipolysis on hepatic triglyceride content are exacerbated in Dox-treated mice compared to wild-type mice
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• liver mass is increased 1.7-fold within 48 hours of induction with Dox
• Dox-treated mice show reduced dry mass content per wet liver
• increase in total liver protein in Dox-treated mice
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• hepatic glycogen is severely depleted after 48 hours of induction with Dox
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• hepatic triglyceride content is increased in Dox-treated mice
• a 6-hour fast increases liver triglyceride content acutely within 24 hours of Dox exposure
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• Dox-treated mice show an increase in hepatic lipid levels
• when mice are taken off the Dox-containing diet, the liver steatosis decreases rapidly
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop acinar-to-ductal metaplasia within 2 weeks of doxycycline induction
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• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment
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• mice develop PanIN lesions within 2 weeks of doxycycline induction
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• infrequently, mice exhibit occurrence of invasive pancreatic ductal adenocarcinoma after long latency (35-70 weeks) following doxycline treatment
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• mice develop PanIN lesions within 2 weeks of doxycycline induction
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• doxycycline-treated mice exhibit a increase metaphyseal microvascular density compared to in wild-type mice
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• following doxycycline treatment for the first 2 weeks of life, growing long bones are abnormal in shape and morphology with abundant stromal cells and blood vessels surrounding numerous trabeculae unlike in wild-type mice
• adult mice treated with doxycycline for 14 days exhibit disrupted bone architecture with abundant peritrabecular mesenchymal stromal cells in the metaphyseal and epiphyseal regions compared with wild-type mice
• adult mice treated with doxycycline for 14 days exhibit lamellar cortical bone is replaced with trabecular-like porous bone structure with abundant intercalating mesenchymal tissue components and osteoclast-rich remodelling units unlike in wild-type mice
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• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
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• in doxycycline-treated mice, bone marrow blood vessels exhibit hemangioma-like morphology and are filled with erythrocytes unlike in wild-type mice
• in doxycycline-treated mice, hematopoietic bone marrow is replaced with new bone, marrow fibrosis, and aberrant blood vessels displaying paucity of myeloid cells unlike in wild-type mice
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• doxycycline-treated mice exhibit bone marrow fibrosis unlike in wild-type mice
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• adult mice treated with doxycycline for 14 days exhibit a 70% increase in trabecular density compared with wild-type mice
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• adult mice treated with doxycycline for 14 days exhibit increased metaphyseal trabecular bone mass compared with wild-type mice
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• at E16.5, doxycycline-treated mice exhibit increased cell proliferation in the perichondrium/periosteum and throughout the primary ossification center compared with wild-type mice
• adult mice treated with doxycycline exhibit increased proliferation of the mesenchymal cells in the metaphysis, epiphysis, and periosteum compared with wild-type mice
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• in doxycycline-treated mice as determined by marker expression
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• doxycycline-treated mice exhibit a increase in growth plate mineralization compared to in wild-type mice
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• doxycycline-treated mice exhibit a mild decrease in growth plate thickness compared to in wild-type mice
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• increased following doxycycline treatment
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• doxycycline-treated mice exhibit reduced bone resorption in the diaphyses and metaphysis compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
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• doxycycline-treated mice exhibit an increase in CFU-Cs (colony-forming units in culture) in the peripheral blood and spleen compared with wild-type mice
• however, bone marrow CFUs of doxycycline-treated mice are normal
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• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis
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• as indicated by enlarged spleen size in 25% of doxycycline-treated mice
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• in the spleen of doxycycline-treated mice
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• the number of megakarypcyte and progenitor cells in the spleens of doxycycline-treated mice is increased compared to in wild-type mice
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• small after 2 weeks of doxycycline treatment
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• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
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• in the peripheral blood of doxycycline-treated mice
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• following doxycycline treatment, bone vasculogenesis is increased compared to in wild-type mice
• in doxycycline treated mice, bone marrow blood vessels exhibit hemangioma-like morphology and are filled with erythrocytes unlike in wild-type mice
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• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis
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• doxycycline-treated mice exhibit reduced osteoclast numbers in regions of excessive bone and vascularization compared with wild-type mice
• however, osteoclast coverage and bone remodeling are normal in the cortical regions of bone following doxycycline treatment
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• in doxycycline-treated mice as determined by marker expression
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• in 25% of doxycycline-treated mice indicating extramedullary hematopoiesis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
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• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks
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• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show impaired recovery from pancreatitis, showing acinar-ductal metaplasia with progressive accumulation of fibrotic stroma at 1 week after induction, replacement of the whole pancreatic parenchyma with ductal structures and signs of PanINs at 3 weeks after induction, and low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction compared to adult mice without dox which show completely resolved damage
• mice kept on dox for 5 weeks prior to induction of pancreatitis and then dox removal for 2 weeks show incomplete repair process resulting in a small, fibrotic pancreas with fewer acini; after 5 weeks of dox removal, no PanINs are observed however, the pancreas appears fibrotic and is small
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• mice kept on dox for 5 weeks following pancreatitis induction show an increase in apoptotic cells and small pancreas size upon removal of dox
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• mice treated with dox at 4-6 weeks of age begin to show acinar-ductal metaplasia beginning at 3 weeks after dox treatment
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• 1 of 2 mice treated with doxycycline (dox) at 4-6 weeks of age show frank adenocarcinoma by 23 weeks on dox
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein to induce acute pancreatitis show low- and high-grade PanIN lesions interspersed with areas of carcinoma in situ at 5 weeks after induction
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• mice treated with doxycycline (dox) at 4-6 weeks of age to induce Kras2 expression begin to show low-grade pancreatic intraepithelial neoplasia (PanIN) beginning at 3 weeks after dox treatment
• mice treated with dox at 4-6 weeks of age show PanIN, surrounded by areas of fibrosis and embedded in the acinar parenchyma after 18 weeks on dox and by 23 weeks, large areas of the pancreatic parenchyma are substituted with PanIN lesions of different grade, with frank adenocarcinoma seen in 1 of 2 mice
• mice kept on dox for 23 weeks show reversion of PanINs when dox is removed for 2 weeks
• adult mice treated with dox 72 hours prior to injection with the cholecystokinin analog cerulein, to induce acute pancreatitis, develop low- and high-grade PanIN lesions at 5 weeks after induction
• mice treated with dox 72 hours prior to induction of pancreatitis also show reversion of PanINs when dox is removed for 2 weeks
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• forelimbs and hindlimbs of pups exhibit a reduction in the number of digits following doxycycline administration to dams from E4.5 to E11.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• administration of doxycycline in the drinking water to 4 month old mice and consequent VEGF-A164 expression in podocyte of glomerulus caused proteinuria after 7 days of treatment
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• administration of doxycycline in the drinking water to 4 month old mice and consequent VEGF-A164 expression in podocyte of glomerulus caused proteinuria after 7 days of treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused death in 3 out of 8 and moribund appearance in rest of animals after 5 days of treatment
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• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in all embryonic cell caused lethality at E9.5 with no primitive red blood cells in the developing yolk sac and abnormal blood island
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused edema of the face, ears and feet after 2 days of treatment
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused "peliosis-like" liver characterized by an extended blood filed enlarged hepatic sinusoids and a total disruption of the normal liver architecture and blood in the intestine after 5 days of treatment
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused enlarged lymph nodes after 5 days of treatment
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused erythema of the face, ears and feet after 2 days of treatment
|
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused a decrease in cellularity and decreased size in thymus after 5 days of treatment
|
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• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in all cell caused "peliosis-like" liver characterized by an extended blood filed enlarged hepatic sinusoids and a total disruption of the normal liver architecture and blood in the intestine after 5 days of treatment
|
|
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• following doxycycline treatment at E10.5 a strong reduction in rostral bony elements is seen and multiple translucent areas are seen in the skull bones
• later treatment with doxycycline has less dramatic effects on bone morphology
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• enlarged following doxycycline treatment at E12.5
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• reduced or absent following doxycycline treatment at E12.5
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• following doxycycline treatment at E12.5
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• following doxycycline treatment at E12.5
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• doxycycline treatment at E11.5 or E10.5 results in a shorter mandible with a more pointed appearance
• doxycycline treatment at E13.5 results in a mandible with a more pointed appearance
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• reduced following doxycycline treatment at E13.5
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• following doxycycline treatment at E12.5, E11.5 or at E10.5
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• doxycycline treatment at E10.5 results in a shorter maxilla with a more pointed appearance
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• following doxycycline treatment at E10.5
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• following doxycycline treatment at E12.5 in some mice
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• following doxycycline treatment at E10.5, E12.5, or E13.5
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• shortened face following doxycycline treatment at E10.5
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• following doxycycline treatment at E12.5
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• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
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• following doxycycline treatment at E10.5 the overall shape of the head is more rounded
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• following doxycycline treatment at E10.5 the orientation of the eyes is more anterior
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• following doxycycline treatment at E12.5 in some mice
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• following doxycycline treatment at E10.5, E12.5, or E13.5
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• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
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• following doxycycline treatment at E12.5
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• following doxycycline treatment at E10.5 a strong reduction in rostral bony elements is seen and multiple translucent areas are seen in the skull bones
• later treatment with doxycycline has less dramatic effects on bone morphology
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• enlarged following doxycycline treatment at E12.5
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• reduced or absent following doxycycline treatment at E12.5
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• following doxycycline treatment at E12.5
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• following doxycycline treatment at E12.5
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• doxycycline treatment at E11.5 or E10.5 results in a shorter mandible with a more pointed appearance
• doxycycline treatment at E13.5 results in a mandible with a more pointed appearance
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• reduced following doxycycline treatment at E13.5
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• following doxycycline treatment at E12.5, E11.5 or at E10.5
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• doxycycline treatment at E10.5 results in a shorter maxilla with a more pointed appearance
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• following doxycycline treatment at E10.5
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• following doxycycline treatment at E12.5 in some mice
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• following doxycycline treatment at E10.5, E12.5, or E13.5
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• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
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• following doxycycline treatment at E12.5 in some mice
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• following doxycycline treatment at E10.5, E12.5, or E13.5
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• shortened face following doxycycline treatment at E10.5
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• following doxycycline treatment at E12.5
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• enlarged nasal cartilages following doxycycline treatment at E12.5 or E10.5
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• following doxycycline treatment at E10.5 the overall shape of the head is more rounded
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tamoxifen treated mice administered doxycycline in the diet develop melanoma with a median latency of 60 days and with 85% penetrance
• withdrawal of doxycycline leads to rapid tumor regression
• treatment with PLX4720 BRAF inhibitor results in tumor growth inhibition in mutants, however, after continual administration of this inhibitor, mice develop drug resistance
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
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• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
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• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
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• administration of doxycycline to pregnant dam starting at day E1.5 and consequent VEGF-A164 expression in neural cell lineage caused vascular abnormalities by E12.5 associated with spinal cord and brain hemorrhages
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| N |
• administration of doxycycline in the drinking water to 3-4 month old mice and consequent VEGF-A164 expression in neural cell lineage did not cause obvious gross behavioral or phenotypic abnormalities in brain after 5 days of treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• doxycycline-treated mice exhibit normal kidney architecture
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• doxycycline-treated mice exhibit some of segmental glomerulus basement membrane thickening observed in Col4a3tm1Jhm homozygotes
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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 04/16/2024 MGI 6.23 |
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