Mechanisms of nickel carcinogenesis.

Fw, Sunderman

doi:10.5271/sjweh.1888

Cited by 148 publications

(91 citation statements)

References 66 publications

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“…Nickel (Sunderman 1989) ions have been implicated as chemical reagents that disturb signal transduction. It has been shown that intracellular signaling mediated by calcium ions is involved in the differentiation of oral-aboral ectoderms (Akasaka et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Hbox1 and Hbox7 are involved in pattern formation in sea urchin embryos

et al. 1999

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In spite of their potential importance in evolution, there is little information about Hox genes in animal groups that are related to ancestors of deuterostome. It has been reported that only two Hox genes (Hbox1 and Hbox7) are expressed significantly in sea urchin embryos. Expression of Hbox1 protein is restricted to the aboral ectoderm, and Hbox7 expression is restricted to oral ectoderm, endoderm and secondary mesenchyme cells in sea urchin embryos after the gastrula stage. With the aim of gaining insight into the role of Hbox1 and Hbox7 in sea urchin development, Hbox1 and Hbox7 overexpression experiments were performed. Overexpression of Hbox1 repressed the development of oral ectoderm, endoderm and mesenchyme cells. On the contrary, overexpression of Hbox7 repressed the development of aboral ectoderm and primary mesenchyme cells. The data suggest that Hbox1 and Hbox7 are expressed in distinct non‐overlapping territories, and overexpression of either one inhibits territory‐specific gene expression in the domain of the other. It is proposed that an important function of both Hbox1 and Hbox7 genes is to maintain specific territorial gene expression by each one, in its domain of expression, while repressing the expression of the other in this same domain.

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Section: Discussionmentioning

confidence: 99%

Hbox1 and Hbox7 are involved in pattern formation in sea urchin embryos

et al. 1999

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“…The amino acid sequence indicates that Ep45 is a secreted glycoprotein and a member of the serine protease inhibitor (serpin) superfamily. Moreover, Ep45 is a Ni 2ϩ binding protein and is implicated in Ni 2ϩ -induced teratogenesis (25,26). In this report, we performed functional analyses of Ep45 in the interaction between BMP and its antagonist follistatin and found that Ep45 blocked the binding of BMP to follistatin.…”

mentioning

confidence: 85%

Isolation and Characterization of Bone Morphogenetic Protein-binding Proteins from the Early Xenopus Embryo

Iemura

Yamamoto

Takagi

et al. 1999

Journal of Biological Chemistry

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Using a surface plasmon resonance biosensor as a sensitive and specific monitor, we have isolated two distinct bone morphogenetic protein (BMP)-binding proteins, and identified them as lipovitellin 1 and Ep45, respectively. Lipovitellin 1 is an egg yolk protein that is processed from vitellogenin. Both vitellogenin and Ep45 are synthesized under estrogen control in the liver, secreted, and taken up by developing oocytes. In this paper, we have shown that of the TGF-␤ family members tested, Ep45 can bind only to BMP-4, whereas lipovitellin 1 can bind to both BMP-4 and activin A. Because of this difference in specificity, we have focused on and further studied Ep45. Kinetic parameters were determined by surface plasmon resonance studies and showed that Ep45 associated rapidly with BMP-4 (k a ‫؍‬ 1.06 ؋ 10 4 M ؊1 s ؊1 ) and dissociated slowly (k d ‫؍‬ 1.6 ؋ 10 ؊4 s ؊1 ). In Xenopus embryos microinjected with Ep45 mRNA, Ep45 blocked the ability of follistatin to inhibit BMP activity and to induce a secondary body axis in a dose-dependent manner, whereas it had no effect on other BMP antagonists, chordin and noggin. These results support the possibility that Ep45 interacts with BMP to modulate its activities in vivo.

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“…A model for nickel carcinogenesis can be based on the assessment of the bioavailability of nickel ion at nuclear sites of respiratory target cells (7,(43)(44)(45). This model predicts that it is not just the presence of nickel in a given inhaled substance that determines its carcinogenic potential but rather whether this nickel is bioavailable in sufficient amounts at nuclear sites of epithelial cells to result in respiratory tumor induction.…”

Section: Respiratory Model For Nickel Carcinogenesismentioning

confidence: 99%