PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts.

PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts. Research Abstract Details 

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PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts. Abstract Text:

Md Moksed Ali,Tatsuya Yoshizawa,Osamu Ishibashi,Akio Matsuda,Mika Ikegame,Junko Shimomura,Hisashi Mera,Kazuhisa Nakashima,Hiroyuki Kawashima,Md Moksed Ali,Tatsuya Yoshizawa,Osamu Ishibashi,Akio Matsuda,Mika Ikegame,Junko Shimomura,Hisashi Mera,Kazuhisa Nakashima,Hiroyuki Kawashima,

We recently reported that tensile stress induces osteoblast differentiation and osteogenesis in the mouse calvarial suture in vitro. Using this experimental system, we identified PIASxbeta, a splice isoform of Pias2, as one of the genes most highly upregulated by tensile stress. Further study using cell culture revealed that this upregulation was transient and was accompanied by upregulation of other differentiation markers, including osterix, whereas expression of Runx2 was unaffected. Runx2 and osterix are the two master proteins controlling osteoblast differentiation, with Runx2 being upstream of osterix. Targeted knockdown of PIASxbeta by small interfering RNA (siRNA) markedly suppressed osteoblastic differentiation and matrix mineralization, whereas transient overexpression of PIASxbeta caused the exact opposite effects. Regardless of PIASxbeta expression level, Runx2 expression remained constant. Reporter assays demonstrated that osterix enhanced its own promoter activity, which was further stimulated by PIASxbeta but not by its sumoylation-defective mutant. NFATc1 and NFATc3 additionally increased osterix transcriptional activity when co-transfected with PIASxbeta. Because osterix has no consensus motif for sumoylation, other proteins are probably involved in the PIASxbeta-mediated activation and NFAT proteins may be among such targets. This study provides the first line of evidence that PIASxbeta is indispensable for osteoblast differentiation and matrix mineralization, and that this signaling molecule is located between Runx2 and osterix.

PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts. Publishing Authors By Initials

MM Ali,T Yoshizawa,O Ishibashi,A Matsuda,M Ikegame,J Shimomura,H Mera,K Nakashima,H Kawashima,MM Ali,T Yoshizawa,O Ishibashi,A Matsuda,M Ikegame,J Shimomura,H Mera,K Nakashima,H Kawashima,

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PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of cell science

VOLUME: 120

Page Numbers: 2565-73

Journal Abbreviation: J. Cell. Sci.

ISSN: 0021-9533

DAY: 10

MONTH: 07

YEAR: 2007

PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts. Information

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LANGUAGE: eng

NlmUniqueID: 52457

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Grant and Affiliation Information for PIASxbeta is a key regulator of osterix transcriptional activity and matrix mineralization in osteoblasts.

AFFILIATION: Division of Cell Biology and Molecular Pharmacology, Niigata University Graduate School of Medical and Dental Sciences, 2-5274 Gakkocho-dori, Niigata-city, Niigata 951-8514, Japan.

Country: England

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MEDLINETA: J Cell Sci

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