Apolipoprotein A-1 is a negative target of v-Jun overexpression

Hadman, Martin; Lin, Wen; Bush, Linnette; Bos, Timothy J.

doi:10.1038/sj.onc.1201574

Cited by 27 publications

(42 citation statements)

References 27 publications

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“…However, activation of these genes is not su cient for immediate cell transformation (Miao and Curran, 1994). The putative Jun target gene JTAP-1 encoding a cathepsin-like protein related to the family of cysteine proteases is induced in avian ®broblasts transformed by v-jun, but not in cells transformed by deregulated c-jun or c-fos alleles (Hadman et al, 1996). In contrast, BKJ transcriptional activation is found in all avian ®broblasts containing retroviral or deregulated cellular jun or fos alleles.…”

Section: Target Genes and Cell Transformationmentioning

confidence: 94%

“…Recently, approaches aimed at the identi®cation of genes speci®cally dysregulated in juntransformed ®broblasts have led to the identi®cation of two new potential jun target genes. The JTAP-1 gene encoding a cathepsin-like protein was found to be speci®cally overexpressed in v-jun-transformed avian ®broblasts, but not in cells transformed by a deregulated c-jun allele (Hadman et al, 1996). The BKJ gene encoding a hydrophobic protein (BKJ) structurally related to avian epidermal b-keratins was identi®ed based on its strong and highly speci®c activation in jun-transformed avian ®broblasts, including cells transformed by a deregulated c-jun allele .…”

Section: Introductionmentioning

confidence: 99%

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Structure and transcriptional regulation of BKJ, a novel AP-1 target gene activated during jun- or fos-induced fibroblast transformation

Hartl

Bister

1998

Oncogene

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The BKJ gene was originally identi®ed based on its speci®c transcriptional activation in jun-transformed avian ®broblasts. We now show that BKJ is a direct transcriptional target of the AP-1 transcription factor components Jun and Fos. The complete structural organization of the quail BKJ gene was determined by nucleotide sequence analysis and transcriptional mapping. The gene contains three exons with the coding region con®ned to the third exon. A major mRNA species of 0.8 kb and a minor one of 1.3 kb are produced by variable usage of two transcriptional initiation sites. The BKJ promoter region contains two authentic AP-1 binding sites. By transactivation of reporter gene constructs and direct binding of Jun recombinant protein, the proximal AP-1 element was shown to be essential for BKJ promoter activation. Using polyclonal antiserum directed against recombinant BKJ protein, the activation of BKJ in jun-transformed avian ®broblasts was also demonstrated at the protein level. BKJ is a novel gene related to the avian b-keratin gene family whose members display highly speci®c expression patterns during embryogenesis and epidermal development. Activation of BKJ in ®broblasts by retroviral or deregulated cellular jun or fos alleles may contribute to cell transformation.

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Section: Target Genes and Cell Transformationmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Structure and transcriptional regulation of BKJ, a novel AP-1 target gene activated during jun- or fos-induced fibroblast transformation

Hartl

Bister

1998

Oncogene

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“…Further insights into the mechanism of v-Jun transformation will develop from the identi®cation and functional characterization of aberrantly expressed target genes. Previous e orts have identi®ed several upregulated v-Jun targets including quail bkj, encoding a member of the b-keratin family, chicken jtab-1, encoding a cathepsin-like protein and the genes encoding glutaredoxin, neuromodulin, phenobarbital-induced cytochrome P450 and heparinbinding EGF-like growth factor (HB-EGF) (Fu et al, 1999;Goller et al, 1998;Hadman et al, 1996;Hartl and Bister, 1995). One of these targets, HB-EGF, can induce partial oncogenic transformation.…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of genes upregulated in cells transformed by v-Jun

Waha

Vogt

2000

Oncogene

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“…The migration of the super-shifted complexes is indicated positions, interactions between the AP-1 and CRE DNA binding proteins could be important in establishing patterns of gene expression in the epidermis. Crosstalk in the form of binding of AP-1 or CRE proteins to both AP-1 and CRE target binding sequences has been demonstrated (Masquilier and Sassone-corsi 1992;Hadman et al, 1993;Hai and Curran 1991;Pestell et al, 1994), and the ability of AP-1 and CRE DNA binding proteins to heterodimerize has been indicated in other systems (Hai et al, 1989;Hai and Curran 1991;Chatton et al, 1994;Ryseck and Bravo 1991). This study examines the expression patterns and DNA binding activities of CREB, CREMa and ATF-1 in basal and di erentiating keratinocytes.…”

Section: Introductionmentioning

confidence: 99%

CRE DNA binding proteins bind to the AP-1 target sequence and suppress AP-1 transcriptional activity in mouse keratinocytes

et al. 1999

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Previously, we have shown that nuclear extracts from cultured mouse keratinocytes induced to di erentiate by increasing the levels of extra-cellular calcium contain Fra-1, Fra-2, Jun B, Jun D and c-Jun proteins that bind to the AP-1 DNA binding sequence. Despite this DNA binding activity, AP-1 reporter activity was suppressed in these cells. Here, we have detected the CREB family proteins CREB and CREMa as additional participants in the AP-1 DNA binding complex in di erentiating keratinocytes. AP-1 and CRE DNA binding activity correlated with the induction of CREB, CREMa and ATF-1 and CREB phosphorylation at ser 133 (ser 133 phospho-CREB) in the transition from basal to di erentiating keratinocytes, but the activity of a CRE reporter remained unchanged. In contrast, the CRE reporter was activated in the presence of the dominantnegative (DN) CREB mutants, KCREB and A-CREB, proteins that dimerize with CREB family members and block their ability to bind to DNA. The increase in CRE reporter activity in the presence of these mutants suggests that CRE-mediated transcriptional activity is suppressed in keratinocytes through protein-protein interactions involving a factor that dimerizes with the CREB leucine zipper. In experiments where the A-CREB mutant was co-transfected with an AP-1 reporter construct, transcriptional activity was also increased indicating that a CREB family member binds AP-1 sites and represses AP-1 transcriptional activity as well. Exogenous expression of the transcriptional repressor CREMa down-regulated both CRE and AP-1 reporters in keratinocytes suggesting that this factor may contribute to the suppression of AP-1 transcriptional activity observed in di erentiating keratinocytes.

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Apolipoprotein A-1 is a negative target of v-Jun overexpression

Cited by 27 publications

References 27 publications

Structure and transcriptional regulation of BKJ, a novel AP-1 target gene activated during jun- or fos-induced fibroblast transformation

Structure and transcriptional regulation of BKJ, a novel AP-1 target gene activated during jun- or fos-induced fibroblast transformation

Identification and characterization of genes upregulated in cells transformed by v-Jun

CRE DNA binding proteins bind to the AP-1 target sequence and suppress AP-1 transcriptional activity in mouse keratinocytes

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