Tiul1 and TGIF are Involved in Downregulation of TGFbeta1-induced IgA Isotype Expression
Immune Network
;
: 248-254, 2009.
Artigo
em Inglês
| WPRIM
| ID: wpr-60580
ABSTRACT
TGF-beta1 is well known to induce Ig germ-line alpha (GLalpha) transcription and subsequent IgA isotype class switching recombination (CSR). Homeodomain protein TG-interacting factor (TGIF) and E3-ubiquitin ligases TGIF interacting ubiquitin ligase 1 (Tiul1) are implicated in the negative regulation of TGF-beta signaling. In the present study, we investigated the roles of Tiul1 and TGIF in TGFbeta1-induced IgA CSR. We found that over-expression of Tiul1 decreased TGFbeta1-induced GLalpha promoter activity and strengthened the inhibitory effect of Smad7 on the promoter activity. Likewise, overexpression of TGIF also diminished GLalpha promoter activity and further strengthened the inhibitory effect of Tiul1, suggesting that Tiul1 and TGIF can down-regulate TGFbeta1-induced GLalpha expression. In parallel, overexpression of Tiul1 decreased the expression of endogenous IgA CSR-predicitive transcripts (GLT(alpha), PST(alpha), and CT(alpha)) and TGFbeta1-induced IgA secretion, but not GLT(gamma3) and IgG3 secretion. Here, over-expressed TGIF further strengthened the inhibitory effect of Tiul1. These results suggest that Tiul1 and TGIF act as negatively regulators in TGFbeta1-induced IgA isotype expression.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Recombinação Genética
/
Imunoglobulina A
/
Imunoglobulina G
/
Regulação para Baixo
/
Fator de Crescimento Transformador beta
/
Switching de Imunoglobulina
/
Ubiquitina
/
Fator de Crescimento Transformador beta1
/
Ligases
Idioma:
Inglês
Revista:
Immune Network
Ano de publicação:
2009
Tipo de documento:
Artigo
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