The Type II Transforming Growth Factor (TGF)-β Receptor-interacting Protein TRIP-1 Acts as a Modulator of the TGF-β Response

Choy, Lisa; Derynck, Rik

doi:10.1074/jbc.273.47.31455

Cited by 116 publications

(73 citation statements)

References 43 publications

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“…It is a WD40 repeat-containing protein that is a phosphorylation substrate for the type II TGF␤ receptor. TRIP-1, when phosphorylated, represses TGF␤-driven reporter activity from the plasminogen activator inhibitor-1 (PAI-1) promoter but has no effect on the TGF␤-driven cyclin A promoter (16). Our data indicate that when TRAP associates with TRIP-1, there is an activation of TGF␤ signaling.…”

Section: Discussionmentioning

confidence: 57%

“…TRIP-1 has been characterized as a modulator of the TGF␤ response (16). It is a WD40 repeat-containing protein that is a phosphorylation substrate for the type II TGF␤ receptor.…”

Section: Discussionmentioning

confidence: 99%

“…TRIP-1 has been previously described in other cell types and has been shown to modulate TGF␤ signaling in both a stimulatory and inhibitory fashion (16,17). In osteoblast systems TGF␤ signaling pathways control osteo-…”

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confidence: 99%

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A Phage Display Technique Identifies a Novel Regulator of Cell Differentiation

Sheu¹,

Schwarz²,

Martinez³

et al. 2003

Journal of Biological Chemistry

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The formation of new bone during the process of bone remodeling occurs almost exclusively at sites of prior bone resorption. In an attempt to discover what regulatory pathways are utilized by osteoblasts to effect this site-specific formation event we probed components of an active bone resorption surface with an osteoblast phage expression library. In these experiments primary cultures of rat osteoblasts were used to construct a phage display library in T7 phage. Tartrate-resistant acid phosphatase (type V) (TRAP) was used as the bait in a biopanning procedure. 40 phage clones with very high affinity for TRAP were sequenced, and of the clones with multiple consensus sequences we identified a regulatory protein that modulates osteoblast differentiation. This protein is the TGF␤ receptor-interacting protein (TRIP-1). Our data demonstrate that TRAP activation of TRIP-1 evokes a TGF␤-like differentiation process. Specifically, TRIP-1 activation increases the activity and expression of osteoblast alkaline phosphatase, osteoprotegerin, collagen, and Runx2. Moreover, we show that TRAP interacts with TRIP intracellularly, that activation of the TGF␤ type II receptor by TRIP-1 occurs in the presence of TRAP and that the differentiation process is mediated through the Smad2/3 pathway. A final experiment demonstrates that osteoblasts, when cultured in osteoclast lacunae containing TRAP, rapidly and specifically differentiate into a mature bone-forming phenotype. We hypothesize that binding to TRAP may be one mechanism by which the full osteoblast phenotype is expressed during the process of bone remodeling.The formation of new bone during the process of bone remodeling occurs almost exclusively at sites of prior bone resorption. As there are 1-2 million active remodeling sites in an adult skeleton at any point in time (1), this spatial localization of formation plays a key role in maintaining skeletal architecture. Aberrant or disorganized formation could lead to architectural changes that would weaken skeletal structure.The observation that osteoclastic bone resorption precedes osteoblastic bone formation has been a well known characteristic of the cell activity in the basal metabolic unit (BMU) described by Frost (2), nearly 40 years ago. In a BMU, osteoclastic activation is followed by a reversal phase in which the osteoclast either migrates to another bony site or dies by apoptosis. Osteoblast bone formation then proceeds directly on the reversal line and if the two activities are matched in amount, a constant skeletal mass is preserved. Activation of osteoprogenitor cells in the immediate area of a resorption event has been attributed to the release of growth factors from the bone during osteoclast activity. This process, first termed coupling by Harris and Heany in 1969 (3, 4), accounts for the temporal sequence of resorption preceding formation. However, what has not been appreciated is that the formation occurs at the immediate sites were osteoclast activity occurred.In work performed by Gray, Jones, and Boyde (5,...

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Section: Discussionmentioning

confidence: 57%

“…TRIP-1 has been characterized as a modulator of the TGF␤ response (16). It is a WD40 repeat-containing protein that is a phosphorylation substrate for the type II TGF␤ receptor.…”

Section: Discussionmentioning

confidence: 99%

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A Phage Display Technique Identifies a Novel Regulator of Cell Differentiation

Sheu¹,

Schwarz²,

Martinez³

et al. 2003

Journal of Biological Chemistry

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“…eIF3f binds directly to mTOR, but whether or not the mTOR-dependent insulin stimulation of eIF3-eIF4G association requires this interaction is not clear. Finally, eIF3i binds to, and is phosphorylated by, the type II TGF-ß receptor (53).…”

Section: Regulation Of Eif3 Is Important In Controlling Cell Prolifermentioning

confidence: 99%

Regulation of protein synthesis and the role of eIF3 in cancer

Hershey¹

2010

Braz J Med Biol Res

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“…As Trip1 interacts with the TGFβ receptor (Chen et al, 1995) with a potential role in modulating TGFβ signalling (Choy and Derynck, 1998) and the rabbit Trip1 cDNA was not previously described, we cloned and sequenced the full length rabbit cDNA to confirm its identity. Rabbit Trip1 encoded an open reading frame composed of 999 nucleotides encoding a predicted protein sequence of 333 amino acids (GenBank accession no.…”

Section: Validation Of Trip1 Identifymentioning

confidence: 99%

Representational difference analysis of cDNA identifies novel genes expressed following preconditioning of the heart

Fauchon

Pell²,

Baxter³

et al. 2005

Exp Mol Med

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Preconditioning of the myocardium rapidly induces a number of transcription factors, which are likely to be responsible for a cascade of transcriptional changes underlying the development of delayed adaptation. Identifying these changes provides insight into the molecular pathways elicited by sub-lethal ischaemia and the mechanism leading to delayed adaptation. Genes up-regulated in rabbit myocardium in vivo by ischaemic preconditioning following reperfusion for 2 h, 4 h and 6 h posttreatment were identified by representational difference analysis of cDNA (cDNA. RDA). The area of the left ventricle rendered ischaemic by preconditioning or the equivalent area of sham-treated animals was isolated and cDNA.RDA performed. Three novel genes and six genes with known function where identified, including the TGFβ receptor interacting protein 1, the α isoform of the A subunit of PP2 and the cap binding protein NCBP1. To determine whether expression of these genes correlated with preconditioning per se, expression was measured in myocardium after both ischaemic as well as heat shock induced preconditioning following 2 h, 4 h, and 6 h reperfusion. These genes were induced in rabbit myocardium in vivo by both ischaemia and heat shock, consistent with a fundamental role in the development of delayed adaptation. The well described role of PP2 in modulating the mitogen-activated protein kinase pathway and promoting cell survival is consistent with our previous work, which identified the reperfusion injury salvage kinase pathway in mediating the protective effects of ischaemic preconditioning. Expression of Trip1 and Ncbp1 also implicates TGFβ signalling pathways and RNA processing and transport in delayed adaptation to stress in the myocardium.

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The Type II Transforming Growth Factor (TGF)-β Receptor-interacting Protein TRIP-1 Acts as a Modulator of the TGF-β Response

Cited by 116 publications

References 43 publications

A Phage Display Technique Identifies a Novel Regulator of Cell Differentiation

A Phage Display Technique Identifies a Novel Regulator of Cell Differentiation

Regulation of protein synthesis and the role of eIF3 in cancer

Representational difference analysis of cDNA identifies novel genes expressed following preconditioning of the heart

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