|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• do not observe any defects in keratinocyte proliferation and differentiation of homeostatic, UV-exposed and regenerating adult skin in mice in which Taf10 is selectively ablated in epidermal keratinocytes of adults
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice exhibit reduced atopic dermatitis-like symptoms when treated with MC903 compared to similarly treated wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• only 50% of tamoxifen treated mice subjected to carcinogens DMBA and TPA formed papillomas after 12 weeks compared to 100% of untreated mice
• mice treated with DMBA and TPA and subsequently treated with tamoxifen after majority of papillomas had formed, showed a reduction in the malignant conversion of papillomas into squamous cell carcinoma (0.6% of papillomas formed carcinoma compared to 4.1% in controls and the 0.6% did not have Ptk2 excised by tamoxifen treatment)
|
|
• substantial reduction in the average number of papillomas formed per tamoxifen treated mouse at 22 weeks when compared to untreated controls
|
|
• loss of normal cell cycle profiles and a substantial amount of cell death in tamoxifen treated primary keratinocytes
|
|
• tamoxifen treated primary keratinocytes were unable to repopulate denuded areas of wounded monolayers and displayed ~50% reduced migration rates, however saw no visible difference in punch biopsy would repair assays
|
|
• only 50% of tamoxifen treated mice subjected to carcinogens DMBA and TPA formed papillomas after 12 weeks compared to 100% of untreated mice
• mice treated with DMBA and TPA and subsequently treated with tamoxifen after majority of papillomas had formed, showed a reduction in the malignant conversion of papillomas into squamous cell carcinoma (0.6% of papillomas formed carcinoma compared to 4.1% in controls and the 0.6% did not have Ptk2 excised by tamoxifen treatment)
|
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• loss of normal cell cycle profiles and a substantial amount of cell death in tamoxifen treated primary keratinocytes
|
|
• tamoxifen treated primary keratinocytes were unable to repopulate denuded areas of wounded monolayers and displayed ~50% reduced migration rates, however saw no visible difference in punch biopsy would repair assays
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants have higher proportions of activated peripheral T cells (CD44high CD62Llow CD25high) than wild-type
|
|
• mutants have higher proportions of activated peripheral T cells (CD44high CD62Llow CD25high) than wild-type
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Rxratm1Ipc/Rxratm4Ipc Rxrbtm1Mma/Rxrbtm1Pcn Tg(KRT14-cre/ERT2)1Ipc/0 mice develop alopecia but no skin inflammation while Rxratm4Ipc/Rxratm4Ipc Rxrbtm1Pcn/Rxrbtm1Pcn Tg(KRT14-cre/ERT2)1Ipc/0 mice show both hair loss and skin inflammation
|
• at week 12, IgG and IgE levels are 5- and 4-fold higher respectively in mutants compared to wild-type
|
|
• mice develop early hair loss observed around the eyes and the dorsal skin at weeks 3 to 5
|
|
• phenotype of adult mutant epidermis is identical to that observed in Rargtm1Ipc newborns
|
|
• at week 5, mice show a dense dermal hyperplasia
|
|
• mutants show a weaker infiltration of the dermis
|
|
• in mutants neutral lipids are distributed unevenly along the cornified layer of the epidermis
• with treatment with the Ppard agonist L165041, epidermis of adult mice is similar to control mice with lipids forming a continuous ribbon on top of the cornified layer
|
|
• granular keratinocytes in mutants contain vesicles devoid of lamellae or with disorganized lamellae
• disorganized lamellae form aggregates at the apical pole of granular keratinocytes
|
|
• at week 5, mice show a dense dermal hyperplasia and hyperplasic epidermis
|
|
• at week 12, IgG and IgE levels are 5- and 4-fold higher respectively in mutants compared to wild-type
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• if tamoxifen given to mothers between E9.5 and 13.5
• if induction with tamoxifen occurred between E12.5 and 16.5 then all limbs are normal
|
|
• malformed in contrast to forelimbs which are normal if tamoxifen given to mothers between E9.5 and 13.5
• if induction with tamoxifen occurred between E12.5 and 16.5 then all limbs are normal
|
|
• regardless of when tamoxifen induction occurred
|
|
• regardless of when tamoxifen induction occurred
|
|
• regardless of when tamoxifen induction occurred
|
|
• 5 fold fewer corneodesmosomes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• regardless of when tamoxifen induction occurred
• very severely affected
|
|
• regardless of when tamoxifen induction occurred
• very severely affected
|
|
• regardless of when tamoxifen induction occurred
|
|
• only 1-2 cornified cell layers present
|
|
• swollen cytoplasm and nuclei
|
|
• swollen cytoplasm and nuclei
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Rxratm4Ipc/Rxratm4Ipc Rxrbtm1Pcn/Rxrbtm1Pcn Tg(KRT14-cre/ERT2)1Ipc/0 mice develop a chronic skin inflammation
|
• after weeks 2-8, mutants develop progressive splenomegaly
|
|
• mutant ears display reddening, swelling and scaling at week 2; by week 24, all mutants have swollen and red ears and 60% have developed ulcerations and crusts in the ear
|
|
• total WBC counts are 24500 cells in mutants compared to 9700 cells in controls; eosinophils and neutrophils are increased relative to control
|
|
• mutants display hyperplasia of regional lymph nodes
|
|
• at weeks 2 and 24, cervical lymph nodes are enlarged 2- and 10-fold respectively
|
|
• adult mice develop a spontaneous dermatitis that occurs predominantly on and behind the ears, on the face, and in the neck and back regions
|
|
• after weeks 2-8, mutants develop progressive splenomegaly
|
|
• total WBC counts are 24500 cells in mutants compared to 9700 cells in controls; eosinophils and neutrophils are increased relative to control
|
|
• at week 20, 50% of mutants have livers that are enlarged up to 2-fold
|
|
• mutant ears display reddening, swelling and scaling at week 2; by week 24, all mutants have swollen and red ears and 60% have developed ulcerations and crusts in the ear
|
|
• adult mice develop a spontaneous dermatitis that occurs predominantly on and behind the ears, on the face, and in the neck and back regions
|
|
• mutants display progressive alopecia that is obvious by 6 weeks after Tamoxifen administration at 6 weeks of age
|
|
• infiltrated cells and dilated blood vessels are present in the dermis; by week 24, there is heavy dermal infiltrate in mutant ears
|
|
• at week 2, ear and dorsal skin biopsies show epidermal hyperplasia; at week 12. ears exhibit high epidermal hyperplasia
|
|
• at week 6-8, mice exhibit scaly skin on the trunk
|
|
• at week 6-8, small lesions are macroscopically visible on the trunk
|
|
• at week 20, 50% of mutants have livers that are enlarged up to 2-fold
|
|
• after weeks 2-8, mutants develop progressive splenomegaly
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after intraperitoneal injection of tamoxifen mice need to be euthanized within 5 days of the development of the abnormal skin phenotype
|
|
• seen after tamoxifen treatment
|
|
• seen after the development of the abnormal skin phenotype induced by intraperitoneal injection of tamoxifen
|
|
• in tamoxifen treated mice, progressive increase in trans epidermal water loss is seen coinciding with the appearance and progression of the scaly skin phenotype
|
|
• moderate inflammation is seen in the early stages of phenotype development after topical treatment with tamoxifen
|
|
• seen after tamoxifen treatment
|
|
• in tamoxifen treated mice, progressive increase in trans epidermal water loss is seen coinciding with the appearance and progression of the scaly skin phenotype
|
|
• moderate inflammation is seen in the early stages of phenotype development after topical treatment with tamoxifen
|
|
• after tamoxifen treatment hair follicles appear distended
|
|
• at later stages after tamoxifen treatment hair follicles disappear
|
|
• seen after tamoxifen treatment
|
|
• seen after tamoxifen treatment
|
|
• seen after tamoxifen treatment
|
|
• after tamoxifen treatment mice develop scales that first appear on the ventral side and snout then extend to the back and whole body
|
|
• after topical tamoxifen treatment ulcerations appear associated with shedding of large scale and complete loss of the epidermis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in tamoxifen- and UVB-treated mice
|
|
• in tamoxifen- and UVB-treated mice
|
|
• tamoxifen- and UVB-treated mice exhibit reduced latency to development of squamous cell and increased number of tumors per mouse compared with similarly treated wild-type mice
|
|
• tamoxifen- and UVB-treated mice exhibit reduced latency to development of squamous cell and increased number of tumors per mouse compared with similarly treated wild-type mice
|
|
• tamoxifen-treated mice exhibit reduced latency to development of squamous cell carcinomas induced by UVB irradiation compared with similarly treated wild-type mice
|
|
• in tamoxifen- and UVB-treated mice
|
|
• in tamoxifen- and UVB-treated mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• survived at least 6 months when not treated with tamoxifen which causes the mice to become sickly
|
|
• benign proliferations derived from hair follicles and follicular cysts
• tamoxifen treatment accelerated cyst formation
|
|
• sparse hair becoming more severe with age
|
|
• abnormal growths under the nails
|
|
• maintained in proliferative state
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• following tamoxifen treatment, mice have increased tongue epidermal hypoplasia and increased cell death
|
|
• following tamoxifen treatment, mice have increased tongue epidermal hypoplasia and increased cell death
|
|
• following tamoxifen treatment, mice have increased epidermal hypoplasia and increased cell death
|
|
• following tamoxifen treatment, mice have increased tongue epidermal hypoplasia and increased cell death
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice die within 6 days of birth
|
|
• severe defect
|
|
• lower zone of the layers are densely packed with lipid-poor interspaces
|
|
• focal
|
|
• severe defect
|
|
• reduced esterified omega-hydroxyacyl-sphingosine and acylglucosylceramide but increased ceramide levels in the epidermis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• increased transepidermal water loss
|
|
• more sensitive to tumor induction using DMBA and TPA
|
|
• hyperkeratinisation leading to drying
|
|
• resulting from hyperkeratinisation
• occasionally results in breakage
|
|
• more sensitive to tumor induction using DMBA and TPA
|
|
• large melanocyte tumors are found
• composed of densely packed melanocytes
• penetrate deeply into the dermis and invading the underlying muscle
• invasive melanocytes are also found in lymph nodes
|
|
• increased numbers of induced squamous cell carcinomas
|
|
• of the foot pads
|
|
• large numbers of suprabasal keratinocytes
• form 4-6 layers rather than the normal 1-2 layers
|
|
• increased transepidermal water loss
|
|
• uniform sparse coat results from the reduced density of hair regrowth
|
|
• hair shafts are shorter and penetrate less deeply into the dermis
• poorly defined morphology
|
|
• hair fails to grow back after experimental depilation of the entire coat
• failure of hair follicles to enter anagen stage
|
|
• extensive scaling only on the foot pads which show inflammation as well
|
|
• many utriculi and closed dermal cysts form
|
|
• large numbers of suprabasal keratinocytes
• form 4-6 layers rather than the normal 1-2 layers
|
|
• many utriculi and closed dermal cysts form
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• phenotype of adult mutant epidermis is identical to that observed in Rargtm1Ipc newborns
• sqaumes from adult mice with Rarg ablation in all epidermal layers display a smooth surface with small or lacking corneodesmosomes (CDs), compared to wild-type which have numerous regularly spaced plaques corresponding to CDs
|
|
• in mutants neutral lipids are distributed unevenly along the cornified layer of the epidermis
|
|
• granular keratinocytes in mutants contain vesicles devoid of lamellae or with disorganized lamellae
• disorganized lamellae form aggregates at the apical pole of granular keratinocytes
|
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 04/30/2024 MGI 6.23 |
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