Induction of a mitogen-responsive gene after expression of the Ha-ras oncogene in NIH 3T3 fibroblasts.

Werenskiold, Anne Katrin; Hoffmann, Sylvia; Klemenz, Roman

doi:10.1128/mcb.9.11.5207

Cited by 89 publications

(74 citation statements)

References 28 publications

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“…The fact that NIH 3T3 cells that overexpress PKC-E, -(, and -r/, the three isoforms that seem to induce transformation of NIH 3T3 ( [24,40] and Goodnight and Mischak, unpublished), show a strong and prolonged ST2/TI induction after PKC activation by TPA, makes it tempting to speculate that ST2/T1 might contribute to PKC-mediated transformation of NIH 3T3. This hypothesis correlates with reports of Werenskiold et al [36] that ST2/T1 is an inducible gene and that ST2/T1 might be involved in the process of tumorgenicity. Experiments to test this notion involving the overexpression of ST2/TI in NIH 3T3 cells are underway and will be reported elsewhere.…”

Section: Discussionsupporting

confidence: 92%

“…ST2/T1 has been described as a primary response gene to growth stimuli in BALB/c 3T3 cells and as a p21H-r"s-inducible gene in NIH 3T3 fibroblasts [35,36]. Its expression can be induced by serum, growth factors and TPA and peaks after 6-10 h [35,38].…”

Section: Discussionmentioning

confidence: 99%

“…For sequential hybridization of the same blots with different DDRT-PCR-generated probes, membranes were stripped with boiling water. After hybridization with these short cDNA probes, the blots were probed with a full-length cDNA of TI [36] and with a probe specific for the 'housekeeping' gene GAPDH [34] to confirm the identity of the DDRT-PCR probe and to normalize for the amount of mRNA loaded in each lane, respectively.…”

Section: Rna Isolation and Northern Blot Analysismentioning

confidence: 99%

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Identification of the primary growth response gene, ST2/T1, as a gene whose expression is differentially regulated by different protein kinase C isozymes

Kieser¹,

Goodnight²,

Kölch³

et al. 1995

FEBS Letters

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kbstract Individual protein kinase C isozymes have been shown Io play different roles in mediating proliferation, differentiation and transformation, but it is not known to what extent these effects involve induction of expression of particular genes. To explore the differential gene expression that might be induced by activation of different PKC isozymes, we stably transfected NIH 3T3 cells with expression vectors that encode the isozymes PKC-~, -Eli, -V, -~i, -c, -~ and -~l. Using differential display-reverse transcription-polymerase chain reaction we isolated a small eDNA that encodes a portion of the primary response gene, ST2 (also referred to as T1 or DER4), and we confirmed by RNA blot studies that ST2fYI expression is differentially regulated by PKC isozymes. ST2/TI mRNA is undetectable in the unstimulated parental NIH 3T3 cells that express only the a isozyme of PKC, but it can be induced by phorbol ester treatment. Clones that overexpress PKC-a, -5 or -e similarly do not express ST2/TI until they are stimulated with phorbol esters, which induces expression of ST2/TI with kinetics similar to wild-type NIH 3T3 but to different extents. In contrast, ST2/TI mRNA is already present in unstimulated cells that overexpress PKC-~III, -V, -~ and -~l, but phorbol ester greatly enhances ST2frl expression in these cells. These results suggest a differential role for PKC isozymes in mediating the ST2ffl expression that is induced by growth stimuli.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Section: Rna Isolation and Northern Blot Analysismentioning

confidence: 99%

See 1 more Smart Citation

Identification of the primary growth response gene, ST2/T1, as a gene whose expression is differentially regulated by different protein kinase C isozymes

Kieser¹,

Goodnight²,

Kölch³

et al. 1995

FEBS Letters

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“…It was originally detected as a primary response gene in murine fibroblasts [19,20] and as a HA-ras oncogen-responsive gene [21]. Alternative splicing of the gene generates three mRNAs, corresponding to a longer membrane-anchored form (ST2L), a shorter released form (sST2) and a membrane bound variant form (ST2V) [22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Elevated levels of soluble ST2 protein in dengue virus infected patients

et al. 2008

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Levels of the soluble form of the interleukin-1 receptor like 1 protein (IL-1RL-1 / ST2) are elevated in the serum of patients with diseases characterized by an inflammatory response. The objective of this study was to determine the concentration of soluble ST2 (sST2) in dengue infected patients during the course of the disease. Twenty four patients with confirmed dengue infection, classified as dengue fever, and eleven patients with other febrile illness (OFI) were evaluated. Levels of sST2 in serum and laboratory variables usually altered during dengue infections were measured. Dengue infected patients had higher serum sST2 levels than OFI at the end of the febrile stage and at defervescence (p=0.0088 and p=0.0004 respectively). Patients with secondary dengue infections had higher serum sST2 levels compared with patients with primary dengue infections (p=0.047 at last day of fever and p=0.030 at defervescence). Furthermore, in dengue infected patients, we found a significant negative correlation of sST2 with platelet and WBC counts, and positive correlation with thrombin time and transaminases activity. We suggest that sST2 could be a potential marker of dengue infection, could be associated with severity or could play a role in the immune response in secondary dengue virus infection.

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“…P reviously, ST2/T1 was independently identified as an oncogene and serum-responsive gene expressed in fibroblasts (1)(2)(3). It was subsequently found to be expressed by mast cells (4) and by Th2, but not Th1, cells (5)(6)(7).…”

mentioning

confidence: 99%

A Novel Pathway Regulating Lipopolysaccharide-Induced Shock by ST2/T1 Via Inhibition of Toll-Like Receptor 4 Expression

Sweet

Leung

Kang

et al. 2001

The Journal of Immunology

236

205

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ST2/ST2L, a member of the IL-1R gene family, is expressed by fibroblasts, mast cells, and Th2, but not Th1, cells. It exists in both membrane-bound (ST2L) and soluble forms (ST2). Although ST2L has immunoregulatory properties, its ligand, cellular targets, and mode of action remain unclear. Using a soluble ST2-human IgG fusion protein, we demonstrated that ST2 bound to primary bone marrow-derived macrophages (BMM) and that this binding was enhanced by treatment with LPS. The sST2 treatment of BMMs inhibited production of the LPS-induced proinflammatory cytokines IL-6, IL-12, and TNF-α but did not alter IL-10 or NO production. Treatment of BMMs with sST2 down-regulated expression of Toll-like receptors-4 and -1 but induced nuclear translocation of NF-κB. Administration of sST2 in vivo after LPS challenge significantly reduced LPS-mediated mortality and serum levels of IL-6, IL-12, and TNF-α. Conversely, blockade of endogenous ST2 through administration of anti-ST2 Ab exacerbated the toxic effects of LPS. Thus, ST2 has anti-inflammatory properties that act directly on macrophages. We demonstrate here a novel regulatory pathway for LPS-induced shock via the ST2-Toll-like receptor 4 route. This may be of considerable therapeutic potential for reducing the severity and pathology of inflammatory diseases.

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Induction of a mitogen-responsive gene after expression of the Ha-ras oncogene in NIH 3T3 fibroblasts.

Cited by 89 publications

References 28 publications

Identification of the primary growth response gene, ST2/T1, as a gene whose expression is differentially regulated by different protein kinase C isozymes

Identification of the primary growth response gene, ST2/T1, as a gene whose expression is differentially regulated by different protein kinase C isozymes

Elevated levels of soluble ST2 protein in dengue virus infected patients

A Novel Pathway Regulating Lipopolysaccharide-Induced Shock by ST2/T1 Via Inhibition of Toll-Like Receptor 4 Expression

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