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Hormone-regulatable neoplastic transformation induced by a Jun-estrogen receptor chimera.
Proc Natl Acad Sci U S A. 1997 Nov 11;94(23):12396-400. doi: 10.1073/pnas.94.23.12396.
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Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation.
Proc Natl Acad Sci U S A. 1999 May 11;96(10):5716-21. doi: 10.1073/pnas.96.10.5716.
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Identification and characterization of genes upregulated in cells transformed by v-Jun.
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Directed mutation of the basic domain of v-Jun alters DNA binding specificity and abolishes its oncogenic activity in chicken embryo fibroblasts.
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Artificial oncoproteins: modified versions of the yeast bZip protein GCN4 induce cellular transformation.
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Hormone-regulated v-rel estrogen receptor fusion protein: reversible induction of cell transformation and cellular gene expression.
EMBO J. 1992 Dec;11(12):4641-52. doi: 10.1002/j.1460-2075.1992.tb05566.x.
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The inhibitory activity of a transdominant c-jun mutant fused to the ligand binding domain of the estrogen receptor.
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A chicken c-Rel-estrogen receptor chimeric protein shows conditional nuclear localization, DNA binding, transformation and transcriptional activation.
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In vitro transforming capacities of mouse c-jun:junD chimeric genes.
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Chimeric c-Jun containing an heterologous homodimerization domain transforms primary chick embryo fibroblasts.
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引用本文的文献
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v-Jun overrides the mitogen dependence of S-phase entry by deregulating retinoblastoma protein phosphorylation and E2F-pocket protein interactions as a consequence of enhanced cyclin E-cdk2 catalytic activity.
Mol Cell Biol. 2000 Apr;20(7):2529-42. doi: 10.1128/MCB.20.7.2529-2542.2000.
2
Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation.
Proc Natl Acad Sci U S A. 1999 May 11;96(10):5716-21. doi: 10.1073/pnas.96.10.5716.
3
Nuclear endpoint of Wnt signaling: neoplastic transformation induced by transactivating lymphoid-enhancing factor 1.
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):139-44. doi: 10.1073/pnas.96.1.139.
本文引用的文献
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AP-1 function and regulation.
Curr Opin Cell Biol. 1997 Apr;9(2):240-6. doi: 10.1016/s0955-0674(97)80068-3.
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Differential and antagonistic effects of v-Jun and c-Jun.
Cancer Res. 1996 Sep 15;56(18):4229-35.
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The inhibitory activity of a transdominant c-jun mutant fused to the ligand binding domain of the estrogen receptor.
Oncogene. 1996 Mar 7;12(5):1043-53.
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The estrogen-dependent c-JunER protein causes a reversible loss of mammary epithelial cell polarity involving a destabilization of adherens junctions.
J Cell Biol. 1996 Mar;132(6):1115-32. doi: 10.1083/jcb.132.6.1115.
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Isolation and cloning of JTAP-1: a cathepsin like gene upregulated in response to V-Jun induced cell transformation.
Oncogene. 1996 Jan 4;12(1):135-42.
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Specific activation in jun-transformed avian fibroblasts of a gene (bkj) related to the avian beta-keratin gene family.
Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11731-5. doi: 10.1073/pnas.92.25.11731.
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Suppression of oncogene-induced transformation by a deletion mutant of c-jun.
Oncogene. 1993 Apr;8(4):877-86.
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A null mutation at the c-jun locus causes embryonic lethality and retarded cell growth in culture.
Genes Dev. 1993 Jul;7(7B):1309-17. doi: 10.1101/gad.7.7b.1309.
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