FOS

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FOS

abbreviation for
(Biochemistry) fructooligosaccharide: a chain polymer of fructose found in a variety of plants, vegetables, and fruits and used as a sweetener
References in periodicals archive ?
Although estrogen-like molecules are thought to function predominantly through ER-mediated activation of transcription via estrogen-responsive elements (EREs), both ERs, [alpha] and [beta], can interact with various cell-cycle transcription factors such as AP-1. The nature of the ER-AP-1 interaction depends on the ligand, ER subtype, and AP-1 components (37-39).
The weakly estrogenic polychlorinated biphenyl Arochlor 1254 has been reported to induce AP-1 activity (53,54).
Given the ability of the ER to interact with AP-1 signaling and estrogenic compounds to elicit early signaling events, we hypothesized that known estrogenic organochlorines, such as DDT and its metabolites, could induce AP-1-mediated gene expression.
This effect is also seen in other cell lines under different AP-1 promoter contexts.
We used PMA as a positive control because we have previously shown that 20 ng/mL PMA activates protein kinase C, downstream mitogen-activated protein kinases, and AP-1 (65).
Treatment of the estrogen-responsive Ishikawa(AP-1)+ stable cells produced a significant induction of AP-1 activity by all the DDT, DDD, and DDE compounds in a dose-dependent manner at the environmentally relevant concentrations 25 [micro]M and 50 [micro]M (Figure 3A) with 50 [micro]M o,p'-DDT being the most potent (4.2-fold).
Dose-response relationships of transformation, AP-1, SRE, and NF[kappa]B activation by TPA, EGF, or TNF[alpha] revealed activation levels above which there was risk of neoplastic transformation.
AP-1 or NF[kappa]B luciferase reporter plasmids consisting of luciferase reporter gene driven by the promoter harboring the appropriate element were described previously (13,14).
Two independent AP-1 reporter clones (A3 and A9) also showed concentration-dependent activation of AP-1-dependent transcription in response to TPA or EGF treatment (Figure 3A, B).
Because TPA or EGF produced < 2-fold maximal induction of NF[kappa]B activation, and because TNF[alpha] produced less than 2-fold maximal AP-1 activation, dose-response analyses for the respective ligand-induced transcriptional activities were not pursued using the respective cloned reporter cell lines.
These results establish that there are thresholds of activation of ERK-1, ERK-2, AP-1, or NF[kappa]B above which there is risk of transformation by TPA, EGF, or TNF[alpha].
Regression analysis shows the close relationship between SRE activation, AP-1 activation, and transformation responses to TPA or EGF.