Human Transforming Growth Factor- β3: Recombinant Expression, Purification, and Biological Activities in Comparison with Transforming Growth Factors-β 1 and -β2

Graycar, Jeannette L.; Miller, Duncan A.; Arrick, Bradley A.; Lyons, Russette M.; Moses, Harold L.; Derynck, Rik

doi:10.1210/mend-3-12-1977

Cited by 258 publications

(113 citation statements)

References 41 publications

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“…Coding sequences for amino-terminally HA-or Flag-tagged, or GAL4-or VP16-fused, Smad and CBP proteins or defined regions were generated by oligonucleotide-or PCR-based techniques and inserted into the ClaI-EcoRI sites of the mammalian expression plasmid pRK5 (Graycar et al 1989) or derivatives. Detailed information on the plasmid constructions will be provided upon request.…”

Section: Expression Plasmidsmentioning

confidence: 99%

The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

Feng

Zhang²,

Wu³

et al. 1998

Genes Dev.

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491

409

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Smads regulate transcription of defined genes in response to TGF-β receptor activation, although the mechanisms of Smad-mediated transcription are not well understood. We demonstrate that the TGF-β-inducible Smad3 uses the tumor suppressor Smad4/DPC4 and CBP/p300 as transcriptional coactivators, which associate with Smad3 in response to TGF-β. The association of CBP with Smad3 was localized to the carboxyl terminus of Smad3, which is required for transcriptional activation, and a defined segment in CBP. Furthermore, CBP/p300 stimulated both TGF-β- and Smad-induced transcription in a Smad4/DPC4-dependent fashion. Smad3 transactivation and TGF-β-induced transcription were inhibited by expressing E1A, which interferes with CBP functions. The coactivator functions and physical interactions of Smad4 and CBP/p300 with Smad3 allow a model for the induction of gene expression in response to TGF-β.

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Section: Expression Plasmidsmentioning

confidence: 99%

The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

Feng

Zhang²,

Wu³

et al. 1998

Genes Dev.

Self Cite

491

409

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“…cDNA cloning from human [37, 381, porcine [37] and chicken [39] libraries have identified a gene, TGFP3, which shares similarity with TGFPl and TGFP2. Expression and production of human recombinant TGFJ13 indicates that this protein has a similar range of in vitro biological activities as that of TGFBl and TGFP2 [40]. TGFJl4 has been cloned from a chicken chondrocyte library [41].…”

Section: Observations) Thementioning

confidence: 99%

Transforming growth factors and the regulation of cell proliferation

Lyons

Moses

1990

European Journal of Biochemistry

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377

164

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“…Three isoforms of TGFß (TGF/31, TGF/32, and TGFß3) have been identified in mammahan cells (Graycar et al, 1989;Cheifetz et al, 1990). TGF/3s can modulate embryonic development, bone formation, hematopoiesis, and cell proliferation and differentiation (Barnard et al, 1990;Lyons and Moses, 1990;Roberts and Sporn, 1990;Fausto, 1991;Sporn and Roberts, 1992;Toru-Delbauffe et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Transforming Growth Factor β1 Regulates the Expression of Cyclooxygenase in Cultured Cortical Astrocytes and Neurons

Luo¹,

Lang²,

Miller

1998

Journal of Neurochemistry

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Abstract:The hypothesis that transforming growth factor ßl (TGFß1) regulates the synthesis of prostaglandins by CNS tissue was tested by using purified cultures of cortical astrocytes or neurons that were obtained from rat pups on postnatal day 4 or 5 or fetuses on gestational day 16, respectively. The cells were exposed to TGFß1 for 2 days. The synthesis of prostaglandins depends upon the production and conversion of arachidonic acid, steps that are catalyzed by phospholipase A 2 (PLA2) and cyclooxygenase (COX), respectively. Prostaglandin E2 (PGE2) concentration was determined by radioimmunoassay. The expression of cytosolic PLA2 and COX (the constitutive COX1 and the inducible COX2) was assessed by using immunohistochemical and quantitative immunoblotting procedures. Astrocytes produced much more PGE2 than neurons, suggesting that glial cells are an important source of PGE2 in the CNS. TGF/31 increased the production of PGE2 by astrocytes and neurons in a concentration-dependent manner. Furthermore, TGFß1 enhanced COX activity; the inhibitor indomethacin completely blocked TGF/31-mediated PGE2 synthesis. Cultured astrocytes and neurons expressed the three enzymes: cytosolic PLA2, COX1, and COX2. Cytosolic PLA2 expression was unaffected by TGFf31 treatment. In contrast, COX expression was altered by TGF~31treatment in a concentration-dependent fashion. COX1 was increased by TGFß1, but only in astrocytes. TGFß1 increased COX2 expression in astrocytes and neurons. Thus, TGFß1 -induced increases in PGE2 concentration are regulated by COX. This study suggests that TGF/31 is an important regulator of immune and inflammatory processes in the CNS. Key Words: Cell culture-Cerebral cortex-Cytokine-Phospholipase A2-Prostaglandin. J. Neurochem. 71, 526-534 (1998).Prostaglandins, thromboxanes, and prostacyclin, collectively called prostanoids, are metabolites of arachidonic acid (AA). The initial step of prostanoid synthesis, the production of AA from fatty acids, is catalyzed by phospholipases, primarily phospholipase A2 (PLA2). AA is then converted to a prostanoid by cyclooxygenase (COX). There are at least two isoforms of COX: the constitutive COX1 and the inducible COX2.Prostanoids are commonly known as pivotal regulators of immune and inflammatory processes (Plescia and Racis, 1988). They are also present in the CNS, where they play important roles in the regulation of diverse CNS functions, i.e., cerebral blood flow, the sleep/wake cycle, and temperature regulation (Wolfe, 1982;Rothwell, 1992; Hayaishi, 1994). Although prostanoid concentrations are low in brain under normal conditions, they are increased in pathological states, such as ischemia, seizures, multiple sclerosis, acquired immunodeficiency syndrome, alcohol intoxication, and inflammation (Chen et al., 1986;George et al., 1986;Shimizu and Wolfe, 1990;Fretland, 1992;Griffin et al., 1994).Various growth factors, e.g., transforming growth factor ß (TGFß), have functions that parallel those of the prostanoids. Three isoforms of TGFß (TGF/31, TGF/32, and TGFß3...

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Human Transforming Growth Factor- β3: Recombinant Expression, Purification, and Biological Activities in Comparison with Transforming Growth Factors-β 1 and -β2

Cited by 258 publications

References 41 publications

The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

The tumor suppressor Smad4/DPC4 and transcriptional adaptor CBP/p300 are coactivators for Smad3 in TGF-β-induced transcriptional activation

Transforming growth factors and the regulation of cell proliferation

Transforming Growth Factor β1 Regulates the Expression of Cyclooxygenase in Cultured Cortical Astrocytes and Neurons

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