JunB does not inhibit the induction of <i>c</i>‐Jun during the retinoic acid induced differentiation of F9 cells

Kwon, Moosik; Oshima, Robert G.

doi:10.1002/aja.1001930211

Cited by 4 publications

(4 citation statements)

References 36 publications

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“…The low levels of ETS-1 and AP-1 components and the induced levels of ETS-2 mRNAs that we observe in differentiating ES cell cultures (Fig. 3) parallel similar findings for F9 cells (30,34). Recently ETS-related transcription factors were implicated in the expression of the mouse K8 gene (EndoA) in extraembryonic endodermal cells (2,56).…”

Section: Discussionsupporting

confidence: 73%

AP-1, ETS, and transcriptional silencers regulate retinoic acid-dependent induction of keratin 18 in embryonic cells.

Pankov¹,

Neznanov²,

Umezawa³

et al. 1994

Mol. Cell. Biol.

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The differentiation of both embryonal carcinoma (EC) and embryonic stem (ES) cells can be triggered in culture by exposure to retinoic acid and results in the transcriptional induction of both the endogenous mouse keratin 18 (mK18) intermediate filament gene and an experimentally introduced human keratin 18 (K18) gene as well as a variety of other markers characteristic of extraembryonic endoderm. The induction of K18 in EC cells is limited, in part, by low levels of ETS and AP-1 transcription factor activities which bind to sites within a complex enhancer element located within the first intron of K18. RNA levels of ETS-2, c-Jun, and JunB increase upon the differentiation of ES cells and correlate with increased expression of K18. Occupancy of the ETS site, detected by in vivo footprinting methods, correlates with K18 induction in ES cells. In somatic cells, the ETS and AP-1 elements mediate induction by a variety of oncogenes associated with the ras signal transduction pathway. In EC cells, in addition to the induction by these limiting transcription factors, relief from negative regulation is mediated by three silencer elements located within the first intron of the K18 gene. These silencer elements function in F9 EC cells but not their differentiated derivatives, and their activity is correlated with proteins in F9 EC nuclei which bind to the silencers and are reduced in the nuclei of differentiated F9 cells. The induction of K18, associated with the differentiation of EC cells to extraembryonic endoderm, is due to a combination of relief from negative regulation and activation by members of the ETS and AP-1 transcription factor families.

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Section: Discussionsupporting

confidence: 73%

AP-1, ETS, and transcriptional silencers regulate retinoic acid-dependent induction of keratin 18 in embryonic cells.

Pankov¹,

Neznanov²,

Umezawa³

et al. 1994

Mol. Cell. Biol.

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“…However, unlike the cjun gene, levels of jun-B mRNAs decreased during development of young odontoblasts to mature odontoblasts. It is reported that the jun-B gene has a role different from that of the c-jun gene (Chiu et al, 1989;Schutte et al, 1989;Yang-Yen et al, 1990;Kwon and Oshima, 1992). We did not examine the function of the jun-B gene in odontoblasts, but this difference in expression pattem between c-jun and jun-B genes in the odontoblastic lineage suggests the difference in function between these genes during odontoblast differentiation.…”

Section: Discussioncontrasting

confidence: 50%

“…Because many cells contain low stable levels of c-Jun protein, and because c-jun gene itself contains a consensus DNA sequence recognized by AP-1 transcription factor, c-Jun protein is also an efficient activator of its own promoter, and the transcription of the c-jun gene is autoregulated by the pre-existing c-Jun protein modified post-translationally by cell-surface stimulation (Angel et al, 1988a;Serfling, 1989;Franklin et al, 1993 Expressions of c-jun and jun-B Genes in Odontoblasts the c-Jun protein (Nakabeppu et al, 1988;Ryder et al, 1988;Zerial et al, 1989). However, the c-Jun and Jun-B proteins are very different in their ability to affect transcription (Schiitte et al, 1989;Kwon and Oshima, 1992). One paper has reported that the Jun-B protein has an ineffective activity in comparison with the c-Jun protein (Yang-Yen et al, 1990).…”

Section: Introductionmentioning

confidence: 96%

Expressions of c-jun and jun-B Proto-oncogenes in Odontoblasts during Development of Bovine Tooth Germs

Kitamura

Terashita

1997

J Dent Res

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c-jun and jun-B genes are among the nuclear proto-oncogenes induced by growth factors such as the TGF-beta superfamily and play important roles in cell differentiation. These gene products enhance expressions of proteins including osteocalcin, alkaline phosphatase, and collagens. On the other hand, it is well-known that the TGF-beta superfamily affects odontoblast differentiation, and that differentiated odontoblasts express extracellular and membrane proteins as described above. However, there are few reports of factors that participate in the transcriptional regulation of odontoblasts. Especially, little is known about the expression of c-jun and jun-B genes. In this study, we focused on the examination of expressions of c-jun and jun-B genes in dental papillae of bovine tooth germs. Using in situ hybridization, we found that these genes were expressed only in the odontoblastic lineage, but not in other dental papilla cells. Levels of c-jun and jun-B mRNAs increased along the gradient of differentiation of odontoblasts. These levels of c-jun mRNAs were maintained in both young and mature odontoblasts. However, unlike the c-jun gene, expression of the jun-B gene became sparse in mature odontoblasts compared with young odontoblasts. For further analysis, Northern hybridization of total RNA extracted from differentiated odontoblasts was performed for the examination of levels of jun-B mRNAs, indicating that levels of jun-B mRNAs of mature odontoblasts were clearly less than those of young odontoblasts. These results suggest that c-jun and jun-B genes may participate in the transcriptional regulation of odontoblasts of bovine tooth germs, and may control the odontoblast phenotype. Furthermore, our results suggest that these genes can be markers of odontoblasts during dentinogenesis; especially, high expression of jun-B gene can be a marker of young odontoblasts that start to form the new dentin matrix.

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“…In F9 EC cells, which have very low endogenous AP-1 activity but constitutively express JunD [67], forced expression of either cJun [67] or cFos [61, 68] results in the induction of mK18/EndoB expression. However, overexpression of JunB in F9 cells neither induces nor inhibits inK8 or mK18 expression by retinoic acid [69]. Both cJun and JunB are induced in EC and ES cells treated with retinoic acid [57,67].…”

Section: A Cryptic Promoter and Regulatory Element In The K18 Genementioning

confidence: 99%

Oncogenic regulation and function of keratins 8 and 18

1996

Self Cite

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Keratin 8 (K8) and keratin 18 (K18) are the most common and characteristic members of the large intermediate filament gene family expressed in 'simple' or single layer epithelial tissues of the body. Their persistent expression in tumor cells derived from these epithelia has led to the wide spread use of keratin monoclonal antibodies as aids in the detection and identification of carcinomas. Oncogenes which activate ras signal transduction pathways stimulate expression of the K18 gene through transcription factors including members of the AP-1 (jun and fos) and ETS families. The persistent expression of K8 and K18 may reflect the integrated transcriptional activation of such transcription factors and, in the cases of ectopic expression, an escape from the suppressive epigenetic mechanisms of DNA methylation and chromatin condensation. Comparison of the mechanisms of transcriptional control of K18 expression with expression patterns documented in both normal and pathological conditions leads to the proposal that persistent K8 and K18 expression is a reflection of the action of multiple different oncogenes converging on the nucleus through a limited number of transcription factors to then influence the expression of a large number of genes including these keratins. Furthermore, correlation of various tumor cell characteristics including invasive behavior and drug sensitivity with K8 and K18 expression has stimulated consideration of the possible functions of these proteins in both normal development and in tumorigenesis. Recent developments in the analysis of the functions of these intermediate filament proteins provide new insights into diverse functions influenced by K8 and K18.

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JunB does not inhibit the induction of c‐Jun during the retinoic acid induced differentiation of F9 cells

Cited by 4 publications

References 36 publications

AP-1, ETS, and transcriptional silencers regulate retinoic acid-dependent induction of keratin 18 in embryonic cells.

AP-1, ETS, and transcriptional silencers regulate retinoic acid-dependent induction of keratin 18 in embryonic cells.

Expressions of c-jun and jun-B Proto-oncogenes in Odontoblasts during Development of Bovine Tooth Germs

Oncogenic regulation and function of keratins 8 and 18

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