A quantitative analysis of nuclear factor I/DNA interactions

Meisterernst, Michael; Gander, Irene; Rogge, Lars; Winnacker, Ernst‐Ludwig

doi:10.1093/nar/16.10.4419

Cited by 109 publications

(75 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The (p50)2 form, and perhaps (p52)2 in some cells, detected in the nuclei of many cell types as KBF-1 (Isra61 et al 1987), activates certain KB sites constitutively and should be subject to coactivation by BCL-3. Because the p50 homodimer has an extremely high affinity for DNA binding (Kd --5 pM) (Zabel et al 1991;Fujita et al 1992), as compared with other eukaryotic DNA-binding proteins (Kd --10--100 riM) (Chodosh et al 1986;Meisterernst et al 1988;Harada et al 1989;Cao et al 1991), it might bind effectively to chromosomal DNA but not function as a strong activator. The coactivator BCL-3 could then easily recognize the bound (p50)2 and interact with it.…”

Section: Gene Regulation By P50 and Bcl-3mentioning

confidence: 99%

The candidate proto-oncogene bcl-3 encodes a transcriptional coactivator that activates through NF-kappa B p50 homodimers.

Fujita¹,

Nolan²,

Liou³

et al. 1993

Genes & Development

382

356

View full text Add to dashboard Cite

The candidate proto-oncogene bcl-3 encodes a protein that shares structural features with IKB-~ and other proteins that bind to members of the Rel protein family. Here, we show that in contrast to the inhibitory activity of IKB-a, the bcl-3 gene product superactivates NF-KB p50 homodimer-mediated gene expression both in vivo and in vitro. BCL-3 protein can, as well, selectively associate with p50 homodimers in the presence of DNA containing a KB motif. These results strongly suggest that BCL-3 can act as a transcriptional coactivator, acting through DNA-bound pS0 homodimers.[Key Words: NF-KB; p50; IKB; transcription; coactivator]Received January 8, 1993; revised version accepted May 21, 1993.The candidate proto-oncogene bcl-3 was identified by the cloning of chromosomal breakpoints from chronic lymphocytic leukemia cells containing a t(14;19) translocation (Ohno et al. 1990). bcl-3 expression is activated by translocation without apparent alteration of the encoded protein structure. The deduced primary structure of BCL-3 contains seven repeats of an -30-amino-acid motif (ankyrin repeat) found in several other proteins (Nolan and Baltimore 1992). These include erythrocyte ankyrin, a cytoskeletal protein; yeast cell cycle regulatory proteins, such as cdclO and SWI6; and the transmembrane receptors notch, TAN1, and int-3.

show abstract

Section: Gene Regulation By P50 and Bcl-3mentioning

confidence: 99%

The candidate proto-oncogene bcl-3 encodes a transcriptional coactivator that activates through NF-kappa B p50 homodimers.

Fujita¹,

Nolan²,

Liou³

et al. 1993

Genes & Development

382

356

View full text Add to dashboard Cite

show abstract

“…Purification of crude extracts by DEAE-cellulose and Mono-Q chromatography has been described recently (Meisterernst et al 1988a). Fractions were monitored by gel retardation assays using end-labeled synthetic oligonucleotides or isolated DNA fragments.…”

Section: Preparation and Purification Of Nuclear Extractsmentioning

confidence: 99%

Nuclear factor E2F mediates basic transcription and trans-activation by E1a of the human MYC promoter.

Thalmeier

Synovzik²,

Mertz³

et al. 1989

Genes Dev.

248

183

View full text Add to dashboard Cite

Transcription from one of the two initiation sites, P1 and P2, of the dual human MYC promoter seems to be essential in all proliferating cells. To identify proteins and target structures for MYC regulation, a DNA region was analyzed that is critical for P2 promoter activity. Here, we show that a nuclear factor binds to a DNA element within P2, which is conserved perfectly between mouse and man and displays a striking homology to the Ela-inducible E2 promoter of adenovirus type 5 (AdS}. We demonstrate that the same transcription factor, defined recently as E2F, which plays an essential role in the activation of adenovirus early promoters and enhancers, also interacts as a dominant nuclear factor with the MYC promoter. The presence of an intact E2F binding site is required for basic expression and for trans-activation of the P2 promoter by Ela proteins. The human MYC promoter is the first cellular target described for E2F. The results suggest that expression of MYC might be regulated via modulation of E2F by cellular 'Ela-like' factors.

show abstract

“…The four members of this family, Nfia, Nfib, Nfic and Nfix, share a common DNA binding sequence. The NF-I transcription factors bind to the dyad symmetric consensus sequence TTGGCNNNNNGCCAA and to individual half-sites with reduced affinity (Gronostajski et al, 1985;Meisterernst et al, 1988). Previous studies have found that NF-I transcription factors preferentially bind DNA target sites that are located close to transcription start sites and mainly act as activators of transcription of downstream target genes (Pjanic et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

An Nfic-hedgehog signaling cascade regulates tooth root development

Liu

Feng

et al. 2015

Development

View full text Add to dashboard Cite

Coordination between the Hertwig's epithelial root sheath (HERS) and apical papilla (AP) is crucial for proper tooth root development. The hedgehog (Hh) signaling pathway and Nfic are both involved in tooth root development; however, their relationship has yet to be elucidated. Here, we establish a timecourse of mouse molar root development by histological staining of sections, and we demonstrate that Hh signaling is active before and during root development in the AP and HERS using Gli1 reporter mice. The proper pattern of Hh signaling activity in the AP is crucial for the proliferation of dental mesenchymal cells, because either inhibition with Hh inhibitors or constitutive activation of Hh signaling activity in transgenic mice leads to decreased proliferation in the AP and shorter roots. Moreover, Hh activity is elevated in Nfic −/− mice, a root defect model, whereas RNA sequencing and in situ hybridization show that the Hh attenuator Hhip is downregulated. ChIP and RNAscope analyses suggest that Nfic binds to the promoter region of Hhip. Treatment of Nfic −/− mice with Hh inhibitor partially restores cell proliferation, AP growth and root development. Taken together, our results demonstrate that an NficHhip-Hh signaling pathway is crucial for apical papilla growth and proper root formation. This discovery provides insight into the molecular mechanisms regulating tooth root development.

show abstract

A quantitative analysis of nuclear factor I/DNA interactions

Cited by 109 publications

References 37 publications

The candidate proto-oncogene bcl-3 encodes a transcriptional coactivator that activates through NF-kappa B p50 homodimers.

The candidate proto-oncogene bcl-3 encodes a transcriptional coactivator that activates through NF-kappa B p50 homodimers.

Nuclear factor E2F mediates basic transcription and trans-activation by E1a of the human MYC promoter.

An Nfic-hedgehog signaling cascade regulates tooth root development

Contact Info

Product

Resources

About