Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts

Ryseck, Rolf-Peter; Hirai, Syu-ichi; Yaniv, Moshe; Bravo, Rodrigo

doi:10.1038/334535a0

Cited by 564 publications

(297 citation statements)

References 27 publications

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“…A PstI/SalI fragment of v-fos (Curran et al, 1982) was used to detect c-fos mRNA. All other probes were derived from cDNA clones of fos and jun genes, which were generously provided by Rodrigo Bravo (Roche); a 1.7 kb fragment of fosB in pGEM-1 (Promega); an EcoRI/SacII fragment derived from the mouse c-jun pAH119 plasmid (Ryseck et al, 1988); a 1.8 kb fragment of junB in pBluescripts KS + (Stratagene); and a 1.5 kb fragment of junD in pBluescript KS + (Stratagene). The glyceraldehyde 3-phosphate dehydrogenase (GAPDH) probe was a 1 kb fragment of murine cDNA cloned in pBluescript KS 7 (Stratagene), kindly provided by DR Edwards.…”

Section: Northern Blot Analysismentioning

confidence: 99%

Effects of the inhibition of p38/RK MAP kinase on induction of five fos and jun genes by diverse stimuli

et al. 1997

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The ERK, JNK/SAPK and p38/RK MAP kinase subtypes are di erentially activated by physiological, pharmacological and stress stimuli; all three subtypes are implicated in immediate-early (IE) gene induction by these agents. Here, we have asked whether inhibition of a single MAP kinase subtype under these conditions would generally alter induction of several IE genes in a similar way or whether this would di erentially up-and down-regulate particular IE genes, an issue which bears on the question of whether individual MAP kinases are strictly targeted to speci®c IE genes, or whether they might catalyse phosphorylation events that a ect several IE genes in the same way. SB 203580, an inhibitor of p38/RK, has been used to analyse the role of this kinase in the induction of ®ve IE genes (c-fos, fosB, c-jun, junB and junD) under diverse conditions of stimulation. In C3H 10T cells, p38/RK and its downstream kinase MAPKAP K-2 are activated by all stimuli used with the exception of TPA. The speci®city of SB 203580 as a p38/RK inhibitor in these cells is demonstrated; it does not a ect ERKs or JNK/SAPKs but does result in a small increase in the activity of the upstream kinase MKK6, the principal p38/RK activator in these cells. We ®nd that inhibition of p38/RK under these conditions produces general e ects on all ®ve IE genes as a group in three ways. First, induction of all ®ve genes in response to okadaic acid or tumour necrosis factor-a (TNF-a) is not signi®cantly altered by SB 203580. Second, in cells stimulated with anisomycin or U.V. radiation, SB 203580 potently inhibits all of the induced IE genes. Finally, SB 203580 enhances induction of all ®ve IE genes in EGF-treated cells; these enhanced mRNA levels are not due to stabilisation of labile mRNA transcripts. The signi®cance of these results to current thinking on the relationship between distinct MAP kinase subtypes and speci®c IE genes is discussed.

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Section: Northern Blot Analysismentioning

confidence: 99%

Effects of the inhibition of p38/RK MAP kinase on induction of five fos and jun genes by diverse stimuli

et al. 1997

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“…There was a good correlation between the amount of activated Ras and transformation as measured by a soft agar assay (ie: normal NIH3T3 ®broblasts or clone R5 that did not show accumulation of Ras protein do not grow in agar, whereas clones expressing the higher levels of Ras produced the higher number of colonies) Mechta et al, 1989;Ryseck et al, 1988;Lallemand et al, 1997). These observations suggest that, under various conditions, the members of the Jun and Fos families present di erent properties and have distinct functions.…”

Section: Introductionmentioning

confidence: 98%

Transformation by ras modifies AP1 composition and activity

et al. 1997

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The Ras proteins play a central role in regulating cell growth and their mutation can lead to abnormal proliferation. To analyse the potential link betwen AP1 activity, encoded by members of the jun and fos gene families, and Ras-mediated cellular transformation, we have studied several NIH3T3 clones which overexpress the Ha-Ras or Ki-Ras oncogenes. These transformed ®broblasts accumulated higher levels of cJun, JunB, Fra1 and Fra2 proteins relative to their normal counterparts. They also displayed increased AP1 DNA binding activity which was predominantly composed of cJun and Fra1 containing dimers. Following serum stimulation of Ras clones, the elevated levels of cJun and Fra1 remained steady, while the induction of JunB and Fra2 was partially attenuated. Moreover, deregulated Ras signaling resulted in a complete loss of the serum inducibility of cFos and FosB. Ectopic co-expression of cJun and Fra1 in NIH3T3 ®broblasts led to a transformed phenotype, attenuation of cFos serum inducibility, increased AP1 activity and Cyclin D1 accumulation, all characteristics of oncogenic Ras expressing cells. These results demonstrate that cJun and Fra1 are crucial mediators of the Ras-transformation process.

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“…Basically, a transient and rapid activation of these genes occurs within the first few hours of cell activation and does not require de novo protein synthesis. Several immediate-early genes encoding secretory proteins, structural proteins such as actin and transcription factors such as Jun [2], Fos [3] and zinc-finger proteins [4] are probably involved in the regulation of expression of genes at the later point of the cell cycle (called delayed genes). As such, they may have a crucial role in the cell cycle progression and cell growth.…”

Section: Introductionmentioning

confidence: 99%

NOR‐2 (neuron‐derived orphan receptor), a brain zinc finger protein, is highly induced during liver regeneration

Petropoulos¹,

Part²,

Ochoa³

et al. 1995

FEBS Letters

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~,bstraet Zinc-finger proteins are involved in several cellular processes. Some of these proteins are implicated in the primary cellular response in regenerating liver and mitogen-stimulated cells. Using a rat cDNA brain library, we have isolated a clone designated NOR-2, encoding a protein containing two zinc-finger motifs and whose expression is highly induced during G0/GI transition. We analysed the expression of NOR-2 mRNAs during early growth in regenerating liver and in both insulin-stimulated H4-11 cells and pheochromocytoma-derived cell line PCI2 treated by NGF. In these systems, there is an early, rapid and transient accumulation of NOR-2 mRNAs. The induction of NOR-2 mRNAs does not require de novo protein synthesis, since it is not prevented by cycloheximide treatment. Mobility shift assays show that NOR-2 protein binds to NBRE, a target sequence for r-NGFI-B family. Structurally, NOR-2 is closely related to the recently identified NOR-I factor. Therefore, like NOR-I, NOR-2 belongs to the r-NGFI-B sub-family of nuclear receptors superfamily.

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Transcriptional activation of c-jun during the G0/G1 transition in mouse fibroblasts

Cited by 564 publications

References 27 publications

Effects of the inhibition of p38/RK MAP kinase on induction of five fos and jun genes by diverse stimuli

Effects of the inhibition of p38/RK MAP kinase on induction of five fos and jun genes by diverse stimuli

Transformation by ras modifies AP1 composition and activity

NOR‐2 (neuron‐derived orphan receptor), a brain zinc finger protein, is highly induced during liver regeneration

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