Negative regulation of the major histocompatibility complex class I promoter in embryonal carcinoma cells.

Flanagan, James R.; Morimoto, Masahiro; Burke, Patricia A.; Shirayoshi, Yasuaki; Appella, Ettore; Sharp, Phillip A.; Ozato, Keiko

doi:10.1073/pnas.88.8.3145

Cited by 41 publications

(18 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CAT, presumably because of modest activity of a downstream regulatory element(s) present in pLdl23.CAT (23) or lack of negative control by an upstream repressor element. Negative regulation of pLdl23.CAT was observed in F9 EC cells (25). In NT2 cells treated with RA for 7 days, however, pLdl400.CAT and pLd237.CAT gave much higher activity than pLd123.CAT.…”

Section: Methodsmentioning

confidence: 89%

Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers.

Segars¹,

Nagata²,

Bours³

et al. 1993

Mol. Cell. Biol.

View full text Add to dashboard Cite

Retinoic acid (RA) treatment of human embryonal carcinoma (EC) NTera-2 (NT2) cells induces expression of major histocompatibility complex (MHC) class I and 13-2 microglobulin surface molecules. We found that this induction was accompanied by increased levels of MHC class I mRNA, which was attributable to the activation of the two conserved upstream enhancers, region I (NF-KB like) and region H. This activation coincided with the induction of nuclear factor binding activities specific for the two enhancers. Region I binding activity was not present in undifferentiated NT2 cells, but binding of an NF-KB heterodimer, p50-p65, was induced following RA treatment. The p50-p65 heterodimer was produced as a result of de novo induction of p50 and p65 mRNAs. Region H binding activity was present in undifferentiated cells at low levels but was greatly augmented by RA treatment because of activation of a nuclear hormone receptor heterodimer composed of the retinoid X receptor (RXR3) and the RA receptor (RARI3). The RXR,-RARj3 heterodimer also bound RA responsive elements present in other genes which are likely to be involved in RA triggering of EC cell differentiation. Furthermore, transfection of p50 and p65 into undifferentiated NT2 cells synergistically activated region I-dependent MHC class I reporter activity. A similar increase in MHC class I reporter activity was demonstrated by cotransfection of RXRI3 and RAR(3. These data show that following RA treatment, heterodimers of two transcription factor families are induced to bind to the MHC enhancers, which at least partly accounts for RA induction of MHC class I expression in NT2 EC cells.

show abstract

Section: Methodsmentioning

confidence: 89%

Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers.

Segars¹,

Nagata²,

Bours³

et al. 1993

Mol. Cell. Biol.

View full text Add to dashboard Cite

show abstract

“…This complex was sensitive to competition with all three silencer elements (Fig. 9B, lanes 10 to 12) The relationship between the K18 silencer element and the previously described NRE of mouse major histocompatibility complex (MHC) locus class I genes (13) was investigated further by gel mobility shift experiments. After incubation with F9 nuclear proteins, a radioactive NRE probe was found to form a complex with the same mobility as the K18 silencer complex I (Fig.…”

Section: Resultsmentioning

confidence: 99%

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.

View full text Add to dashboard Cite

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.

show abstract

“…Such transcription initiating factors have been vari ously termed 8 (Hariharan et al, 1991), YYI , TFII-I (Roy et al, 1991), NF-E1 (Park and Atchi son, 1991), UCRBP (Flanagan et al, 1991), and are either identical binding factors or belong to a similar classes of factors (Roy et al, 1991;Seto et al, 1991). These factors interact wife TFIID, and they can bind DNA and initiate transcription even in the absence of a TATA box.…”

Section: Molecular Controls Of Epidermal Gene Expressionmentioning

confidence: 99%

Epidermal differentiation and keratin gene expression

Fuchs

1993

Journal of Cell Science

157

101

View full text Add to dashboard Cite

SUMMARYThe epidermis of the skin is a stratified squamous epithelium, which plays an important protective role. It manifests this role by building an extensive cytoskeletal architecture, the unique feature of which is the presence of keratin filaments. There are two major pairs of ker atins in the epidermis: one pair is expressed in dividing cells and the other expressed in terminally differentiat ing cells. As such, keratins provide useful biochemical markers to explore the molecular mechanisms underly-

show abstract

Negative regulation of the major histocompatibility complex class I promoter in embryonal carcinoma cells.

Cited by 41 publications

References 37 publications

Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers.

Retinoic acid induction of major histocompatibility complex class I genes in NTera-2 embryonal carcinoma cells involves induction of NF-kappa B (p50-p65) and retinoic acid receptor beta-retinoid X receptor beta heterodimers.

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

Epidermal differentiation and keratin gene expression

Contact Info

Product

Resources

About