cDNA Cloning and Chromosomal Mapping of Rat Smad2 and Smad4 and Their Expression in Cultured Rat Articular Chondrocytes

Abstract. Smad proteins are known to transduce signalling of TGF-β receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and...

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Published in:ENDOCRINE JOURNAL 1999, Vol.46 (5), p.695-701
Main Authors: MAKOTO OSAKI, TOMOO TSUKAZAKI, NORIO ONO, AKIHIKO YONEKURA, YASUHIRO HIROTA, YOUICHI MIYAZAKI, HIROYUKI SHINDO, SHIN-ICHI SONTA, SHUNICHI YAMASHITA
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container_end_page 701
container_issue 5
container_start_page 695
container_title ENDOCRINE JOURNAL
container_volume 46
creator MAKOTO OSAKI
TOMOO TSUKAZAKI
NORIO ONO
AKIHIKO YONEKURA
YASUHIRO HIROTA
YOUICHI MIYAZAKI
HIROYUKI SHINDO
SHIN-ICHI SONTA
SHUNICHI YAMASHITA
description Abstract. Smad proteins are known to transduce signalling of TGF-β receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and 5' RACE. The predicted amino acid sequences of rat Smad2 and Smad4 are highly conserved among rat, human and mouse. We also mapped these Smads to chromosome 18q. 12.3. Unlike endothelial cells, TGF-β1 stimulates articular chondrocyte proliferation as well as extracellular matrix production, and acts as a repairing agent against cartilage destruction. Since both Smad2 and Smad4 are essential factors for TGF-β signalling, we examined their expression and regulation in cultured articular chondrocytes. Northern blot analysis showed that TGF-β1 significantly increased the mRNA level of Smad2 but not of Smad4 in a dose- and time-dependent manner, suggesting that the augmentation of TGF-β1 action is caused by increasing the expression of the downstream signahing molecule.
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Smad proteins are known to transduce signalling of TGF-β receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and 5' RACE. The predicted amino acid sequences of rat Smad2 and Smad4 are highly conserved among rat, human and mouse. We also mapped these Smads to chromosome 18q. 12.3. Unlike endothelial cells, TGF-β1 stimulates articular chondrocyte proliferation as well as extracellular matrix production, and acts as a repairing agent against cartilage destruction. Since both Smad2 and Smad4 are essential factors for TGF-β signalling, we examined their expression and regulation in cultured articular chondrocytes. 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Smad proteins are known to transduce signalling of TGF-β receptor superfamily. We report here the entire sequences of rat Smad2 and Smad4 which have not been identified yet. Entire sequences were identified by degenerated polymerase chain reaction and following phage library screening and 5' RACE. The predicted amino acid sequences of rat Smad2 and Smad4 are highly conserved among rat, human and mouse. We also mapped these Smads to chromosome 18q. 12.3. Unlike endothelial cells, TGF-β1 stimulates articular chondrocyte proliferation as well as extracellular matrix production, and acts as a repairing agent against cartilage destruction. Since both Smad2 and Smad4 are essential factors for TGF-β signalling, we examined their expression and regulation in cultured articular chondrocytes. 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title cDNA Cloning and Chromosomal Mapping of Rat Smad2 and Smad4 and Their Expression in Cultured Rat Articular Chondrocytes
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