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Titolo:
TGF-beta 1 regulates the expression of multiple max-interacting transcription factors in Balb/MK cells: Implications for understanding the mechanism of action of TGF-beta 1
Autore:
Satterwhite, DJ; White, RL; Aakre, ME; Moses, HL;
Indirizzi:
Univ Utah, Sch Med, Dept Pediat, Div Neonatol, Salt Lake City, UT 84132 USA Univ Utah Salt Lake City UT USA 84132 natol, Salt Lake City, UT 84132 USA Univ Utah, Sch Med, Dept Oncol Sci, Salt Lake City, UT 84132 USA Univ Utah Salt Lake City UT USA 84132 l Sci, Salt Lake City, UT 84132 USA Vanderbilt Univ, Sch Med, Dept Cell Biol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Cell Biol, Nashville, TN 37232 USA Vanderbilt Univ, Sch Med, Ctr Canc, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Ctr Canc, Nashville, TN 37232 USA
Titolo Testata:
PEDIATRIC RESEARCH
fascicolo: 1, volume: 50, anno: 2001,
pagine: 67 - 75
SICI:
0031-3998(200107)50:1<67:T1RTEO>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; N-MYC EXPRESSION; PROTO-ONCOGENE EXPRESSION; CYCLIN D1 EXPRESSION; C-MYC; TGF-BETA; TRANSFORMING GROWTH-FACTOR-BETA-1; BRANCHING MORPHOGENESIS; GENE-EXPRESSION; MURINE KERATINOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Satterwhite, DJ Univ Utah, Sch Med, Dept Pediat, Div Neonatol, 50 N Med Dr, Salt Lake City, UT 84132 USA Univ Utah 50 N Med Dr Salt Lake City UT USA 84132 4132 USA
Citazione:
D.J. Satterwhite et al., "TGF-beta 1 regulates the expression of multiple max-interacting transcription factors in Balb/MK cells: Implications for understanding the mechanism of action of TGF-beta 1", PEDIAT RES, 50(1), 2001, pp. 67-75

Abstract

Appropriate transforming growth factor-beta1 (TGF-beta1) signaling is required to preserve homeostasis of diverse tissues during development, At the cellular level, one function of TGF-beta1 that is critical for preserving homeostasis is the ability to arrest cell growth. TGF-beta1 arrests growth by blocking the function of the c-myc proto-oncogene. c-myc function is determined by the level of c-myc expression relative to other Max-interacting transcription factors, and TGF-beta1 has been shown to inhibit c-myc expression by inhibiting c-myc transcription. However, whether TGF-beta1 might also increase the expression of a Max-interacting factor that blocks myc function by competing with myc for Max binding is not known. Therefore, we determined the effect of TGF-beta1 on the expression of Max-interacting transcription factors in Balb/MK cells, We found unexpectedly that Balb/MK cells express both N-myc and c-myc, The pattern of N-myc expression during the cellcycle differs from that of c-myc, indicating that mRNA accumulation is controlled by mechanisms specific to each gene, TGF-beta1 rapidly inhibits N-myc mRNA expression; thus N-myc is a novel target of TGF-beta1 in Balb/NK cells. More importantly, we found that TGF-beta1 induces the expression of the putative tumor suppressor genes Mad4 and Mxi1 in both the Balb/MK and Mv1Lu cell lines. Mad4 and Mxi1 are novel targets of TGF-beta1, known to inhibit cell growth by antagonizing the interaction of Myc with Max. Thus, our results suggest that the induction of Mad4 and Mxi1 may function in tandem with the inhibition of N-myc and c-myc to mediate the growth inhibitory function of TGF-beta1.

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Documento generato il 29/09/20 alle ore 04:26:12