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Titolo:
Overexpression of Smad2 reveals its concerted action with Smad4 in regulating TGF-beta-mediated epidermal homeostasis
Autore:
Ito, Y; Sarkar, P; Mi, QG; Wu, N; Bringas, P; Liu, YH; Reddy, S; Maxson, R; Deng, CX; Chai, Y;
Indirizzi:
Univ So Calif, Sch Dent, Ctr Craniofacial Mol Biol, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 ol Biol, Los Angeles, CA 90033 USA Univ So Calif, Keck Sch Med, Inst Med Genet, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 d Genet, Los Angeles, CA 90033 USA NIDDK, Genet Dev & Dis Branch, NIH, Bethesda, MD 20892 USA NIDDK BethesdaMD USA 20892 Dev & Dis Branch, NIH, Bethesda, MD 20892 USA Univ So Calif, Norris Hosp & Res Inst, Dept Biochem & Mol Biol, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 ol Biol, Los Angeles, CA 90089 USA
Titolo Testata:
DEVELOPMENTAL BIOLOGY
fascicolo: 1, volume: 236, anno: 2001,
pagine: 181 - 194
SICI:
0012-1606(20010801)236:1<181:OOSRIC>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSFORMING-GROWTH-FACTOR; TRANSGENIC MICE; TOOTH FORMATION; II RECEPTOR; IN-VITRO; EXPRESSION; SKIN; DIFFERENTIATION; INHIBITION; LACKING;
Keywords:
skin; Smad2 transgenic; Smad4; TGF-beta signaling; tooth;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
62
Recensione:
Indirizzi per estratti:
Indirizzo: Chai, Y Univ So Calif, Sch Dent, Ctr Craniofacial Mol Biol, 2250 Alcazar St,CSA 103, Los Angeles, CA 90033 USA Univ So Calif 2250 Alcazar St,CSA 103 Los Angeles CA USA 90033 USA
Citazione:
Y. Ito et al., "Overexpression of Smad2 reveals its concerted action with Smad4 in regulating TGF-beta-mediated epidermal homeostasis", DEVELOP BIO, 236(1), 2001, pp. 181-194

Abstract

Members of the transforming growth factor-beta (TGF-beta) superfamily are critical regulators for epithelial growth and can alter the differentiationof keratinocytes. Transduction of TGF-beta signaling depends on the phosphorylation and activation of Smad proteins by heteromeric complexes of ligand-specific type I and II receptors. To understand the function of TGF-beta and activin-specific Smad, we generated transgenic mice that overexpress Smad2 in epidermis under the control of keratin 14 promoter. Overexpression of Smad2 increases endogenous Smad4 and TGF-beta1 expression while heterozygous loss of Smad2 reduces their expression levels, suggesting a concerted action of Smad2 and -4 in regulating TGF-beta signaling during skin development. These transgenic mice have delayed hair growth, underdeveloped ears, and shorter tails. In their skin, there is severe thickening of the epidermis with disorganized epidermal architecture, indistinguishable basement membrane, and dermal fibrosis. These abnormal phenotypes are due to increased proliferation of the basal epidermal cells and abnormalities in the program of keratinocyte differentiation. The ectodermally derived enamel structure is also abnormal. Collectively, our study presents the first in vivo evidence that, by providing an auto-feedback in TGF-beta signaling, Smad2 plays apivotal role in regulating TGF-beta -mediated epidermal homeostasis. (C) 2001 Academic Press.

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Documento generato il 01/04/20 alle ore 11:24:03