| TAF4b controls the granulosa-cell-specific expression of the proto-oncogene c-jun, and together they regulate transcription of ovary-selective promoters. | None |
| Protein phosphatase 2A reverses phosphorylation of c-Jun specified by the delta domain in vitro: correlation with oncogenic activation and deregulated transactivation activity of v-Jun. | None |
| Functional antagonism between oncoprotein c-Jun and steroid hormone receptors. | None |
| Drosophila homolog of the mammalian jun oncogene is expressed during embryonic development and activates transcription in mammalian cells. | None |
| RASSF1A suppresses oncogenic H-Ras-induced c-Jun N-terminal kinase activation. | None |
| STP-A11, an oncoprotein of Herpesvirus saimiri augments both NF-kappaB and AP-1 transcription activity through TRAF6. | None |
| Mechanism of specificity in the Fos-Jun oncoprotein heterodimer. | None |
| Oncogenic and transcriptional cooperation with Ha-Ras requires phosphorylation of c-Jun on serines 63 and 73. | None |
| ds-Oligonucleotide-peptide conjugates featuring peptides from the leucine-zipper region of Fos as switchable receptors for the oncoprotein Jun. | None |
| [Redox regulation of DNA-binding activity of fos and jun oncogene proteins in vitro]. | None |
| [JUN oncogene unmasked: a new role for an old actor]. | None |
| [Functional interaction between estrogen receptor and proto-oncogene products c-Jun and c-Fos]. | None |
| analysis of the structural polymorphism of a 21-bp Pu.Py DNA segment within human c-jun protooncogene 3_-region, a potential target for triplex formation | None |
| Structural polymorphism exhibited by a homopurine.homopyrimidine sequence found at the right end of human c-jun protooncogene. | None |
| Site-specific phosphorylation of raf in cells containing oncogenic ras-p21 is likely mediated by jun-N-terminal kinase. | None |
| Transcriptional co-factor CDCA4 participates in the regulation of JUN oncogene expression. | None |
| an important role of CDCA4 in the context of transcriptional regulation and cell fate determination through the JUN oncogene | None |
| TOJ3, a v-jun target with intrinsic oncogenic potential, is directly regulated by Jun via a novel AP-1 binding motif. | None |
| Growth hormone induces expression of c-jun and jun B oncogenes and employs a protein kinase C signal transduction pathway for the induction of c-fos oncogene expression. | None |
| ablation of AP-1 function disrupts the cellular transformation and proliferation mediated by this oncogene. Data illustrate a novel mechanism required to couple mitogenic signals to the AP-1 gene regulatory program | None |