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Increased IKKα expression in the basal layer of the epidermis of transgenic mice enhances the malignant potential of skin tumorsTransrepression function of the glucocorticoid receptor regulates eyelid development and keratinocyte proliferation but is not sufficient to prevent skin chronic inflammation.Exocrine pancreatic disorders in transsgenic mice expressing human keratin 8Constitutively active Akt induces ectodermal defects and impaired bone morphogenetic protein signalingSevere abnormalities in the oral mucosa induced by suprabasal expression of epidermal keratin K10 in transgenic mice.IKKalpha enhances human keratinocyte differentiation and determines the histological variant of epidermal squamous cell carcinomas.The expression of keratin k10 in the basal layer of the epidermis inhibits cell proliferation and prevents skin tumorigenesis.Deregulated activity of Akt in epithelial basal cells induces spontaneous tumors and heightened sensitivity to skin carcinogenesis.Glucocorticoid receptor is required for skin barrier competence.Phenotype of hepatic infiltrates and hepatic lymph nodes of lambs primarily and challenge infected with Fasciola hepatica, with and without triclabendazole treatment.Abnormal epidermal differentiation and impaired epithelial-mesenchymal tissue interactions in mice lacking the retinoblastoma relatives p107 and p130.Targeted overexpression of leptin to keratinocytes in transgenic mice results in lack of skin phenotype but induction of early leptin resistance.Context-Dependent Role of IKKβ in Cancer.Glucocorticoid Receptor Counteracts Tumorigenic Activity of Akt in Skin through Interference with the Phosphatidylinositol 3-Kinase Signaling Pathway.IKKβ overexpression leads to pathologic lesions in stratified epithelia and exocrine glands and to tumoral transformation of oral epithelia.Epidermal abnormalities and increased malignancy of skin tumors in human epidermal keratin 8-expressing transgenic mice.Ectoderm-targeted overexpression of the glucocorticoid receptor induces hypohidrotic ectodermal dysplasia.RNAi-mediated knockdown of IKK1 in transgenic mice using a transgenic construct containing the human H1 promoter.IKKβ overexpression together with a lack of tumour suppressor genes causes ameloblastic odontomas in mice
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description
hulumtuese
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researcher
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wetenschapper
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հետազոտող
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name
Ana Bravo
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Ana Bravo
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Ana Bravo
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Ana Bravo
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type
label
Ana Bravo
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Ana Bravo
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Ana Bravo
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Ana Bravo
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altLabel
Bravo A Ana Mª Bravo Moral
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prefLabel
Ana Bravo
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Ana Bravo
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Ana Bravo
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Ana Bravo
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P106
P21
P31
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0000-0002-5282-8921