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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/12/09 18:42:07」(JST)

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In molecular biology and genetics, transactivation is increased rate of gene expression triggered either by biological processes or by artificial means, through expressing an intermediate (transactivator) protein.

Natural transactivation

Transactivation can be triggered either by endogenous cellular or viral proteins, so-called transactivators. These protein factors act in trans (i.e., intermolecularly). HIV and HTLV are just two of the many viruses that encode transactivators to enhance their own gene expression. These transactivators can also be associated with cancer if they start interacting and increasing expression of a cellular proto-oncogene. HTLV for instance has been associated with causing leukemia primarily through this process. Its transactivator (named tax) can interact with p40, causing overexpression of interleukin 2, interleukin receptors, GM-CSF and the transcription factor c-Fos. HTLV infects T-cells and so, with increased expression of these stimulatory cytokines and transcription factors, leads to uncontrolled proliferation of T-cells and hence lymphoma.

Artificial transactivation

Artificial transactivation of a gene is achieved by inserting into the genome at the appropriate area a transactivator gene and special promoter regions of DNA. The transactivator gene expresses a transcription factor that binds to specific promoter region of DNA. By binding to the promoter region of a gene, the transcription factor causes that gene to be expressed. The expression of one transactivator gene can activate multiple genes, as long as they have the specific promoter region attached. Because the expression of the transactivator gene can be controlled, transactivation can be used to turn genes on and off. If this specific promoter region is also attached to a reporter gene, we can see when the transactivator is being expressed.

External links

Transactivation at the US National Library of Medicine Medical Subject Headings (MeSH)
Transactivators at the US National Library of Medicine Medical Subject Headings (MeSH)

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English Journal

Lysophosphatidic Acid Increases Proximal Tubule Cell Secretion of Profibrotic Cytokines PDGF-B and CTGF through LPA2- and Gαq-Mediated Rho and αvβ6 Integrin-Dependent Activation of TGF-β.

Geng H, Lan R, Singha PK, Gilchrist A, Weinreb PH, Violette SM, Weinberg JM, Saikumar P, Venkatachalam MA.SourceDepartment of Pathology, University of Texas Health Science Center, San Antonio, Texas.
The American journal of pathology.Am J Pathol.2012 Oct;181(4):1236-49. doi: 10.1016/j.ajpath.2012.06.035. Epub 2012 Aug 10.
After ischemia-reperfusion injury (IRI), kidney tubules show activated transforming growth factor β (TGF-β) signaling and increased expression of profibrotic peptides, platelet-derived growth factor-B (PDGF-B) and connective tissue growth factor (CTGF). If tubule repair after IRI is incomplete, su
PMID 22885106

Synergistic roles of scleraxis and Smads in the regulation of collagen 1α2 gene expression.

Bagchi RA, Czubryt MP.AbstractCardiac fibrosis is marked by increased deposition of extracellular matrix components including fibrillar collagens, leading to impaired cardiac contractility and function. We recently demonstrated that the transcription factor scleraxis is expressed in collagen-producing cardiac fibroblasts and myofibroblasts, is up-regulated in the collagen-rich scar following myocardial infarction and is sufficient to transactivate the human collagen 1α2 (COL1A2) gene, suggesting a central role in fibrosis. Here we describe the mechanism of scleraxis-mediated regulation of the COL1A2 promoter. Using chromatin immunoprecipitation in primary human cardiac fibroblasts in combination with luciferase assays, we demonstrate that two E box sequences within the proximal COL1A2 promoter are required for scleraxis-mediated transactivation. Expression of scleraxis itself was induced by receptor Smad3, an effector of the pro-fibrotic growth factor TGF-β(1), and attenuated by inhibitory Smad7. TGF-β(1) augmented the effect of scleraxis on COL1A2 transactivation, an effect which was due to synergy between scleraxis and Smad3. Mutation of the COL1A2 Smad-binding element significantly attenuated the ability of scleraxis to transactivate the promoter, while mutation of the scleraxis-interacting E boxes attenuated the effect of Smad3, suggesting that these factors form a common signaling complex at the promoter. COL1A2 promoter transactivation and Col1α2 gene expression in cardiac fibroblasts were completely abrogated by a scleraxis basic domain deletion mutant in a dominant negative fashion, blocking the ability of TGF-β(1) to activate collagen synthesis and suggesting that scleraxis-DNA interaction is absolutely required for this process. Scleraxis thus appears to play a key role in the transcriptional regulation of type I collagen synthesis.
Biochimica et biophysica acta.Biochim Biophys Acta.2012 Oct;1823(10):1936-44. Epub 2012 Jul 13.
Cardiac fibrosis is marked by increased deposition of extracellular matrix components including fibrillar collagens, leading to impaired cardiac contractility and function. We recently demonstrated that the transcription factor scleraxis is expressed in collagen-producing cardiac fibroblasts and myo
PMID 22796342

Japanese Journal

DNA-binding and transcriptional activation properties of tobacco NIC2-locus ERF189 and related transcription factors

SHOJI Tsubasa,HASHIMOTO Takashi
Plant biotechnology 29(1), 35-42, 2012-03-25
… Five group IXa ERFs (tobacco ERF189, tobacco ERF163, Catharanthus ORCA3, Arabidopsis AtERF13, and Arabidopsis AtERF1) were examined whether they bind to the ERF189-recognition site in the promoter of the tobacco putrescine N-methyltransferase gene in vitro, and transactivate the promoter in a transient expression assay using cultured tobacco cells. …
NAID 10030561328

異物応答に関与する核内受容体Ｃｏｎｓｔｉｔｕｔｉｖｅ　ａｎｄｒｏｓｔａｎｅ　ｒｅｃｅｐｔｏｒ　（ＣＡＲ）の局在調節機構

菅野裕一朗,井上義雄
薬学雑誌 131(3), 359-365, 2011
… Following xenobiotic stimuli, receptors translocate into the nucleus and transactivate its target genes. …
NAID 130000678898

61.イネにおけるJA応答性bHLH型転写因子RERJ1の生理機能(口頭発表)

岡田憲典,宮本皓司,清水崇史,北島竜也,河本晃一,宮尾安藝雄,廣近洋彦,野尻秀昭,山根久和
植物化学調節学会研究発表記録集 (45), 78, 2010-10-01
… These results suggest that RERJ1 is induced by synthesized JA at injured sites, then functions to transactivate many PR genes, including the OsLS gene in rice plants. …
NAID 110007767161