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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2003-2-4
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pubmed:abstractText |
PTEN is a tumor suppressor gene mutated in many human cancers. We used the Cre-loxP system to generate a keratinocyte-specific null mutation of Pten in mice (k5Pten(flox/flox) mice). k5Pten(flox/flox) mice exhibit wrinkled skin because of epidermal hyperplasia and hyperkeratosis and ruffled, shaggy, and curly hair. Histological examination revealed that skin morphogenesis is accelerated in k5Pten(flox/flox) mice. Within 3 weeks of birth, 90% of k5Pten(flox/flox) mice die of malnutrition possibly caused by hyperkeratosis of the esophagus. All k5Pten(flox/flox) mice develop spontaneous tumors within 8.5 months of birth, and chemical treatment accelerates the onset of tumors. k5Pten(flox/flox) keratinocytes are hyperproliferative and resistant to apoptosis and show increased activation of the Pten downstream signaling mediators Akt/protein kinase B (PKB) and extracellular signal-regulated kinase. Pten is thus an important regulator of normal development and oncogenesis in the skin.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0008-5472
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pubmed:author |
pubmed-author:HamadaKoichiK,
pubmed-author:InoueTaeT,
pubmed-author:ItamiSatoshiS,
pubmed-author:KomazawaNobuyasuN,
pubmed-author:MakTak WahTW,
pubmed-author:ManabeMotomuM,
pubmed-author:NakanoToruT,
pubmed-author:OhishiMinakoM,
pubmed-author:SasakiTakehikoT,
pubmed-author:SenooHarukiH,
pubmed-author:SuzukiAkiraA,
pubmed-author:TakedaJunjiJ
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
63
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
674-81
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12566313-Animals,
pubmed-meshheading:12566313-Apoptosis,
pubmed-meshheading:12566313-Cell Division,
pubmed-meshheading:12566313-Cell Transformation, Neoplastic,
pubmed-meshheading:12566313-Enzyme Activation,
pubmed-meshheading:12566313-Female,
pubmed-meshheading:12566313-Hair Follicle,
pubmed-meshheading:12566313-Hyperplasia,
pubmed-meshheading:12566313-Keratinocytes,
pubmed-meshheading:12566313-Male,
pubmed-meshheading:12566313-Mice,
pubmed-meshheading:12566313-Mice, Inbred C57BL,
pubmed-meshheading:12566313-Mice, Transgenic,
pubmed-meshheading:12566313-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12566313-PTEN Phosphohydrolase,
pubmed-meshheading:12566313-Phosphoric Monoester Hydrolases,
pubmed-meshheading:12566313-Protein-Serine-Threonine Kinases,
pubmed-meshheading:12566313-Proto-Oncogene Proteins,
pubmed-meshheading:12566313-Proto-Oncogene Proteins c-akt,
pubmed-meshheading:12566313-Skin,
pubmed-meshheading:12566313-Skin Abnormalities,
pubmed-meshheading:12566313-Skin Neoplasms,
pubmed-meshheading:12566313-Tumor Suppressor Proteins
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pubmed:year |
2003
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pubmed:articleTitle |
Keratinocyte-specific Pten deficiency results in epidermal hyperplasia, accelerated hair follicle morphogenesis and tumor formation.
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pubmed:affiliation |
Department of Biochemistry, Akita University School of Medicine, Akita 010-8543, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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