Disease relevance of Genes, jun

• Transcriptional regulation of c-jun gene expression by arabinofuranosylcytosine in human myeloid leukemia cells [1].
• Transcription of the c-jun gene is up-regulated by either retinoic acid (RA) or adenovirus E1A during the differentiation of F9 cells [2].
• Induction of jun gene family members by transforming growth factor alpha but not 17 beta-estradiol in human breast cancer cells [3].
• The c-jun proto-oncogene down-regulates the rat alpha-fetoprotein promoter in HepG2 hepatoma cells without binding to DNA [4].
• These results suggest that the c-fos and c-jun genes may suppress the expression of BGP mRNA relevant to differentiation and osteoid formation in rat osteosarcomas [5].

High impact information on Genes, jun

• AP-1 consists of the products of the fos and jun oncogenes, which associate as dimers to bind TPA-responsive promoter elements (TRE) efficiently [6].
• One consequence of MEF2C activation is increased c-jun gene transcription [7].
• Because of the similarity between the recognition sites for GCN4 and AP-1, we examined the possibility that AP-1 could be the product of the c-jun proto-oncogene [8].
• The protein products of the fos and jun proto-oncogenes form a heterodimeric complex that participates in a stable high affinity interaction with DNA elements containing AP-1 binding sites [9].
• Transcriptional run-on assays revealed that treatment of serum-starved NKM-1 with 50 ng/ml G-CSF or M-CSF increased the transcription rate of the junB gene and the c-fos gene by 1.8-fold and 2.9-fold, respectively, but did not induce any transcript of the c-jun gene [10].

Chemical compound and disease context of Genes, jun

• Doxorubicin-induced alterations of c-myc and c-jun gene expression in rat glioblastoma cells: role of c-jun in drug resistance and cell death [11].
• The effects of vitamin E succinate on the expression of c-jun gene and protein in human gastric cancer SGC-7901 cells [12].

Biological context of Genes, jun

• We also found factors, designated DRF1 and DRF2, that bound specifically to a sequence element that is necessary and sufficient for RA- and E1A-mediated up-regulation of the c-jun gene [2].
• The c-jun proto-oncogene encodes a transcription factor which is activated by mitogens both transcriptionally and by phosphorylation by Jun N-terminal kinase (JNK) [13].
• This preferential response of the c-jun gene is mediated by its 5' control region and requires the TPA response element, suggesting that this element also serves as an early target for the signal transduction pathway elicited by DNA damage [14].
• HDRP also interacts with histone deacetylase 1 (HDAC1) and recruits it to the c-Jun gene promoter, resulting in an inhibition of histone H3 acetylation at the c-Jun promoter [15].
• In the present study, we tested for such selectivity of stimulated gene expression by monitoring the expression of fos/jun gene mRNAs in the striatum in rats treated in vivo with the indirect dopamine agonist cocaine [16].

Anatomical context of Genes, jun

• Protein kinase C regulates proliferation of mast cells and the expression of the mRNAs of fos and jun proto-oncogenes during activation by IgE-Ag or calcium ionophore A23187 [17].
• Moreover, treatment of T cells with actinomycin D to block further transcription before their culture with PWM suggests that the increase in c-jun gene expression by PWM is also regulated at least in part by a posttranscriptional mechanism [18].
• Using the factor-dependent myelogenous leukemia cell lines GF-D8 and Mo7, we show that TGF-beta interferes with stem cell factor (SCF)-induced proliferation by downmodulating c-jun gene expression [19].
• These results show transient induction of immediate-early response genes in B cells and support a potential role for the c-jun gene product in regulation of IL-6 transcription and secretion [20].
• In accordance with the results obtained by analysis of the mRNA, we found that estrogen increases 3- to 4-fold c-jun gene transcription in the uterus, at the same time it induces its mRNA accumulation [21].

Associations of Genes, jun with chemical compounds

• We found that As3+, but not As5+, which is toxic but not carcinogenic, is a potent stimulator of AP-1 transcriptional activity and an efficient inducer of c-fos and c-jun gene expression [22].
• The jun gene lacks preserved coding domains of tyrosine-specific protein kinases [23].
• Both proteins were found to contain a peptide sequence reminiscent of a leucine-repeat motif ("leucine-zipper") that is also found in the myc, fos, and jun oncogenes [24].
• The DNA binding activity of the c-jun proto-oncogene product is inhibited by oxidation of a specific cysteine residue (Cys-252) in the DNA binding domain [25].
• Platelet-derived growth factor-beta receptor was not phosphorylated on Ang II stimulation, and Ang II-induced c-jun gene expression was not affected by tyrphostin AG1478 [26].

Gene context of Genes, jun

• Furthermore, we observed significant time-dependent increases in the expression of the c-fos and c-jun proto-oncogenes after addition of IGF-I (n = 5 per group, P <.05) [27].
• Differential regulation of fos and jun gene expression and AP-1 cis-element activity by endothelin isopeptides. Possible implications for mitogenic signaling by endothelin [28].
• In addition, although the c-jun proto-oncogene product was detected in stimulated human T cells, two additional T cell-specific proteins (45 and 43 kDa) bind to the GM-CSF, IL-3, and IL-5 promoters and are functionally and immunologically distinct from c-jun or OAP40 (jun-D) [29].
• Because HDAC inhibitors suppressed the induction of c-jun gene expression, resulting in reduced COX-2 transcription, it was important to determine whether other known AP-1 target genes were also modulated [30].
• Tumor necrosis factor-alpha induces expression of monocyte chemoattractant JE via fos and jun genes in clonal osteoblastic MC3T3-E1 cells [31].

Analytical, diagnostic and therapeutic context of Genes, jun

• Nonetheless, the ligation-mediated PCR technology was used here to demonstrate, at nucleotide resolution, that p53-/-p21+/+ DLD1 excises UVB-induced cyclobutane pyrimidine dimers from the c-jun proto-oncogene at a significantly lower rate than the isogenic p53-/-p21-/- derivative [32].
• Western blotting analysis of c-Fos and c-Jun suggested that up-regulation of c-fos and c-jun gene expression does not directly contribute to the induction of AP-1 activation [33].
• Northern blot analysis revealed that lack of BGP mRNA expression was associated with expression of both c-fos and c-jun proto-oncogenes in SOS [5].
• Coronal hypothalamic sections and control ovarian tissues were incubated with 45-mer oligonucleotide probes complementary to porcine c-fos and c-jun genes using standard in situ hybridization histochemistry techniques [34].
• DNA array analysis revealed that expression of genes such as the RhoG and D4-GDI genes was down-regulated in TEL-overexpressing cells, while that of the representative growth-related genes such as the c-myc, c-fos and c-jun genes was not remarkably changed [35].

References