Overexpression of Raidd cDNA inhibits differentiation of mouse preadipocytes

Felmer R.; Horvat S.; Clinton M.; Clark A.J.

Keywords: kinetics, sequence, proteins, apoptosis, differentiation, overexpression, dna, mouse, hormone, region, animals, expression, adipocytes, transcription, regions, cells, culture, protein, proliferation, product, cell, gene, chain, mice, transduction, division, cysteine, polymerase, signal, proteinase, drug, carrier, article, factor, promoter, function, genetic, complement, transfection, adaptor, type, controlled, animal, reverse, adipocyte, action, study, nucleotide, Reaction, nonhuman, Animalia, DNA,, Complementary, RNA,, serine, Messenger, (Genetics), unclassified, Murinae, 3t3, D, Endopeptidases, Raidd

Abstract

RAIDD (RIP-associated ICH-1 homologous protein with a death domain) is an adaptor molecule that mediates the action of cysteine proteases involved in apoptosis. To study the possibility of a novel system of cell ablation mediated by RAIDD, a preadipocyte cell line (3T3L1) was stably transfected with a plasmid containing the murine Raidd cDNA under the control of the adipocyte specific promoter aP2. Instead of the expected apoptosis, a blockage to differentiation upon hormonal induction was observed as judged by an absence of lipid accumulation, a lack of expression of adipocyte-specific genes and a fibroblastic appearance. Proliferation rate of Raidd-transfected clones remained unaffected. Overexpression of Raidd cDNA in 3T3L1 cell therefore inhibited differentiation, suggesting that Raidd plays a role in controlling differentiation of mouse preadipocytes and, perhaps, in other cell types, in addition to its established role in apoptosis.

Más información

Título según SCOPUS: Overexpression of Raidd cDNA inhibits differentiation of mouse preadipocytes
Título de la Revista: Cell Proliferation
Volumen: 36
Número: 1
Editorial: Wiley-Blackwell
Fecha de publicación: 2003
Página de inicio: 45
Página final: 54
Idioma: English
URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-0037326751&partnerID=q2rCbXpz
DOI:

10.1046/j.1365-2184.2003.00253.x

Notas: SCOPUS