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Titolo:
DIRECTED EXPRESSION OF KERATIN-16 TO THE PROGENITOR BASAL CELLS OF TRANSGENIC MOUSE SKIN DELAYS SKIN MATURATION
Autore:
PALADINI RD; COULOMBE PA;
Indirizzi:
JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM,725 N WOLFE ST BALTIMORE MD21205 JOHNS HOPKINS UNIV,SCH MED,DEPT BIOL CHEM BALTIMORE MD 21205 JOHNS HOPKINS UNIV,SCH MED,DEPT DERMATOL BALTIMORE MD 21205
Titolo Testata:
The Journal of cell biology
fascicolo: 4, volume: 142, anno: 1998,
pagine: 1035 - 1051
SICI:
0021-9525(1998)142:4<1035:DEOKTT>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
EPIDERMAL GROWTH-FACTOR; STRATIFIED SQUAMOUS EPITHELIA; DOMINANT-NEGATIVE MUTANT; INTERMEDIATE FILAMENTS; FACTOR RECEPTOR; HAIR FOLLICLE; TGF-ALPHA; MOLECULAR MARKERS; NETWORK FORMATION; BULLOUS DISEASES;
Keywords:
SKIN; KERATIN; ADHESION; WOUND REPAIR; TRANSGENIC MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
91
Recensione:
Indirizzi per estratti:
Citazione:
R.D. Paladini e P.A. Coulombe, "DIRECTED EXPRESSION OF KERATIN-16 TO THE PROGENITOR BASAL CELLS OF TRANSGENIC MOUSE SKIN DELAYS SKIN MATURATION", The Journal of cell biology, 142(4), 1998, pp. 1035-1051

Abstract

We previously hypothesized that the type I keratin 16 (K16) plays a role in the process of keratinocyte activation that occurs in response to skin injury (Paladini, R.D., K. Takahashi, N,S. Brave, and P.A. Coulombe. 1996. J. Cell Biol. 132:381-397). To further examine its properties in vivo, the human K16 cDNA was constitutively expressed in the progenitor basal layer of transgenic mouse skin using the K14 gene promoter. Mice that express approximately as much K16 protein as endogenous K14 display a dramatic postnatal phenotype that consists of skin that is hyperkeratotic, scaly, and essentially devoid of fur. Histologically, the epidermis is thickened because of hyperproliferation of transgenic basal cells, whereas the hair follicles are decreased in number,poorly developed, and hypoproliferative. Microscopically, the transgenic keratinocytes are hypertrophic and feature an altered keratin filament network and decreased cell-cell adhesion. The phenotype normalizes at,similar to 5 Wk after birth. In contrast, control mice expressinga K16-K14 chimeric protein to comparable levels are normal. The character and temporal evolution of the phenotype in the K16 transgenic mice are reminiscent of the activated EGF receptor-mediated signaling pathway in skin. In fact, tyrosine phosphorylation of the EGF receptor isincreased in the newborn skin of K16 transgenic mice. We conclude that expression of K16 can significantly alter the response of skin keratinocytes to signaling cues, a distinctive property likely resulting from its unique COOH-terminal tail domain.

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Documento generato il 05/12/20 alle ore 07:06:10