UV-induced early-domain binding factor as the limiting component of simian virus 40 DNA amplification in rodent cells.

Lücke‐Huhle, Christine; Mai, Sabine; Herrlich, Peter

doi:10.1128/mcb.9.11.4812

Cited by 21 publications

(15 citation statements)

References 40 publications

(31 reference statements)

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“…The protein component of the more slowly migrating complex is referred to as IRF-A, and that of the faster-migrating complex is referred to as IRF-B. Consistent with the results of LuckeHuhle et al (28), UV doses of 3 and 6 J/m2 enhanced IRF-B binding activity in cytosolic extracts (Fig. 2, lanes 5 and 6).…”

supporting

confidence: 77%

“…4). The addition of a 50-fold molar excess of a nonspecific competitor, the synl6-1 fragment of a hepatocyte-specific cis-acting element (28,45), diminished the IRF-B complex by only 49%. A 50-fold molar excess of the Epstein-Barr virus (EBV) oriP fragment (nucleotides 8922 to 8944), containing sequence homology to SV40 IR2 (Fig.…”

Section: A B C T C G C -A C T T C C C T a A T A A A T Cg Jcv C T T A mentioning

confidence: 99%

“…Furthermore, cytosolic extracts from MNNG-treated SV40-transformed Chinese hamster cells supported SV40 DNA replication in vitro in the presence of exogeneous T antigen, whereas replication by extracts from untreated cells was inefficient (4). Treatment of irradiated cells with duplex oligonucleotides corresponding to the SV40 IR domain inhibited DNA amplification, presumably because the duplex oligonucleotides sequestered a DNA damage-activated factor needed for amplification in vivo (28). In addition, a monkey cell factor binding to sequence encompassing the IR domain has been described (52).…”

mentioning

confidence: 99%

“…Similarly, Lucke-Huhle et al (28) reported induction of a factor(s) binding to the SV40 origin imperfect inverted repeat domain (IR domain, as defined by Parsons et al [35]) (see Fig. 1A) in response to cell exposure to UV radiation and correlated this increase with DNA damage-induced viral DNA replication (28). Furthermore, cytosolic extracts from MNNG-treated SV40-transformed Chinese hamster cells supported SV40 DNA replication in vitro in the presence of exogeneous T antigen, whereas replication by extracts from untreated cells was inefficient (4).…”

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confidence: 99%

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confidence: 99%

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Binding of a sequence-specific single-stranded DNA-binding factor to the simian virus 40 core origin inverted repeat domain is cell cycle regulated.

Carmichael¹,

Roome²,

Wahl³

1993

Mol. Cell. Biol.

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supporting

confidence: 77%

Section: A B C T C G C -A C T T C C C T a A T A A A T Cg Jcv C T T A mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Binding of a sequence-specific single-stranded DNA-binding factor to the simian virus 40 core origin inverted repeat domain is cell cycle regulated.

Carmichael¹,

Roome²,

Wahl³

1993

Mol. Cell. Biol.

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Retinoic‐acid‐induced differentiation prevents gene amplification in teratocarcinoma stem cells

Lücke‐Huhle¹,

Herrlich²

1991

Intl Journal of Cancer

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In an attempt to study the regulatory properties of cells required for gene amplification, the capacity for amplification of the dehydrofolate reductase gene (dhfr) was determined in F9 teratocarcinoma stem cells during differentiation. By stepwise selection of surviving cells exposed to progressively increasing concentrations of methotrexate (MTX) up to 1,000 microM within 4 months, non-differentiated F9 cells reached a more than 40-fold amplification of their dhfr gene, elevated levels of dhfr mRNA and a 5-log increase in MTX resistance. Exposure to 5 Gy of 60Co-gamma-irradiation accelerated the process of amplification. In contrast, F9 cells that had been differentiated to endodermal cells by treatment with retinoic acid (RA) did not grow in MTX concentrations above 0.1 microM, either with or without radiation pretreatment and did not amplify the dhfr gene to any measurable extent over the same period of time. Upon treatment of methotrexate-resistant (F9-MTXr) cells with retinoic acid, loss of the amplified DNA in the absence of selection was significantly retarded. The ability to amplify the dhfr gene was correlated with the occurrence of origin binding activity in vitro (early domain of SV40 minimal origin of replication). These data indicate an increase in genomic stability and rigorous control of origin activity by differentiation.

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Cross-coupling of the NF-kappa B p65 and Fos/Jun transcription factors produces potentiated biological function.

et al. 1993

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NF‐kappa B and AP‐1 represent distinct mammalian transcription factors that target unique DNA enhancer elements. The heterodimeric NF‐kappa B complex is typically composed of two DNA binding subunits, NF‐kappa B p50 and NF‐kappa B p65, which share structural homology with the c‐rel proto‐oncogene product. Similarly, the AP‐1 transcription factor complex is comprised of dimers of the c‐fos and c‐jun proto‐oncogene products or of closely related proteins. We now demonstrate that the bZIP regions of c‐Fos and c‐Jun are capable of physically interacting with NF‐kappa B p65 through the Rel homology domain. This complex of NF‐kappa B p65 and Jun or Fos exhibits enhanced DNA binding and biological function via both the kappa B and AP‐1 response elements including synergistic activation of the 5′ long terminal repeat of the human immunodeficiency virus type 1. These findings support a combinatorial mechanism of gene regulation involving the unexpected cross‐coupling of two different classes of transcription factors to form novel protein complexes exhibiting potentiated biological activity.

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UV-induced early-domain binding factor as the limiting component of simian virus 40 DNA amplification in rodent cells.

Cited by 21 publications

References 40 publications

Binding of a sequence-specific single-stranded DNA-binding factor to the simian virus 40 core origin inverted repeat domain is cell cycle regulated.

Binding of a sequence-specific single-stranded DNA-binding factor to the simian virus 40 core origin inverted repeat domain is cell cycle regulated.

Retinoic‐acid‐induced differentiation prevents gene amplification in teratocarcinoma stem cells

Cross-coupling of the NF-kappa B p65 and Fos/Jun transcription factors produces potentiated biological function.

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