Mechanism of c-Myb–C/EBPβ Cooperation from Separated Sites on a Promoter

Tahirov, T.H.; Sato, Ko; Ichikawa-Iwata, Emi; Sasaki, Motoko; Inoue-Bungo, Taiko; Shiina, Masaaki; Kimura, Kazumi; Takata, Shioka; Fujikawa, Atsushi; Morii, Hisayuki; Kumasaka, Takashi; Yamamoto, Masaki; Ishii, Shunsuke; Ogata, Kazuhiro

doi:10.1016/s0092-8674(01)00636-5

Cited by 158 publications

(159 citation statements)

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“…It is possible that C/EBP b could influence transcription from this location either by interacting with NF-kB through long-range interactions with the promoter as has been shown for c-Myb 31 or through interaction with components of the RNA transcriptassociated heterogeneous nuclear ribonucleoprotein (hnRNP) complexes such as hnRNP K. 32 Further experiments are needed to address the specificity and functionality of C/EBP b binding to the þ 781T polymorphism in vivo. 6) and þ 781C allele (lanes 7-12) in EMSA with nuclear extracts from A549 cells harvested after no activation (NA) and after stimulation with TNF.…”

Section: Upregulation Of Ilmentioning

confidence: 99%

Increased in vivo transcription of an IL-8 haplotype associated with respiratory syncytial virus disease-susceptibility

et al. 2004

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Section: Upregulation Of Ilmentioning

confidence: 99%

Increased in vivo transcription of an IL-8 haplotype associated with respiratory syncytial virus disease-susceptibility

et al. 2004

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“…Thus, the DNA-binding domain of B-Myb is not only required for protein-DNA interaction but also stimulates transcription via specific protein-protein interactions involving at leat two coactivators. That the Myb DNA-binding domain is involved in protein-protein interactions has also been shown in case of v-Myb and cMyb (Mink et al, 1996;Tahirov et al, 2002), whose interaction with members of the C/EBP transcription factor family is mediated by their DNA-binding domain. Previous work has shown that B-Myb directly interacts with the coactivator p300/CBP via the central part of B-Myb, which contains the transactivation domain (Horstmann et al, 2000b).…”

Section: Discussionmentioning

confidence: 72%

Transactivation mediated by B-Myb is dependent on TAFII250

Bartusel

Klempnauer

2003

Oncogene

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B-Myb is a highly conserved member of the Myb family of transcription factors, which has been implicated in cell cycle regulation. B-Myb is expressed in most proliferating cells and its activity is highly regulated around the G1/Sphase border of the cell cycle. It is generally assumed that B-Myb regulates the expression of genes that are crucial for cell proliferation; however, the identity of these genes, the molecular mechanisms by which B-Myb stimulates their expression and the involvement of other proteins have not been sufficiently clarified. We have employed the hamster cell line ts13 as a tool to demonstrate a functional link between B-Myb and the coactivator TAF II 250, a key component of the transcriptional machinery which itself is essential for cell proliferation. ts13 cells express a pointmutated version of TAF II 250 whose intrinsic histone acetyl transferase activity is temperature sensitive. Transactivation of Myb-responsive reporter genes by BMyb is temperature-dependent in ts13 cells but not in ts13 cells, which have been rescued by transfection with an expression vector for wild-type TAF II 250. Furthermore, B-Myb and TAF II 250 can be coprecipitated, suggesting that both proteins are present in a complex. The formation of this complex is dependent on the DNA-binding domain of B-Myb and not on its transactivation domain. Taken together, these observations provide the first evidence that the coactivator TAF II 250 is involved in the activation of Myb responsive promoters by B-Myb. The finding that BMyb transactivation is dependent on a key coactivator involved in cell cycle control is consistent with and strengthens the idea that B-Myb plays a crucial role as a transcription factor in proliferating cells.

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“…Alternatively, it is possible that the B cell specificity of the Ikaros and C/EBP complex may be mediated by a B cell-specific factor that was not detected in the current approach. In this respect, the synergistic interactions of Ikaros or C/EBP with other transcription factors have been previously observed in active regulation of different enhancers and promoters in lymphoid as well as other tissues [36,39]. Therefore, it will be necessary to identify this B cell-specific factor.…”

Section: Discussionmentioning

confidence: 96%

Characterization of the proximal enhancer element and transcriptional regulatory factors for murine recombination activating gene‐2

et al. 2005

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Recombination-activating gene (RAG)-1 and RAG-2 are essential for V(D)J recombination and are expressed specifically in lymphoid cells. We previously identified two putative enhancer elements, the proximal and distal enhancers, located at -2.6 and -8 kb, respectively, 5 0 upstream of mouse RAG-2, and characterized the distal enhancer element in detail. In this study, to characterize the proximal enhancer in vitro as well as in vivo, we first defined a 170-bp core enhancer element within the proximal enhancer (Ep) and determined its activity in various cells. Ep conferred enhancer activity only in B-lymphoid cell lines, but not in T-or non-lymphoid cell lines. Analysis of the transgenic mice carrying an EGFP reporter gene linked with Ep revealed that Ep activated the transcription of the reporter gene in bone marrow and spleen, but not in thymus or non-lymphoid tissues. Ep was active in both B220 + IgM -and B220 + IgM + subpopulations in the bone marrow and in the B220 + subpopulation in the spleen. Using electrophoretic mobility shift assays and mutational assays, we found that Ikaros and CCAAT/enhancer binding protein cooperatively bind Ep and function as the transcription factors responsible for B cell-specific enhancer activity. These results demonstrate the role of Ep as a cis-regulatory enhancer element for RAG-2-specific expression in B-lymphoid lineages. IntroductionAssembly of Ig and TCR genes by V(D)J recombination is mediated by the products of recombination-activating gene (RAG)-1 and RAG-2 [1, 2]. RAG proteins act together to recognize recombination signal sequences that flank V, D, and J gene segments and introduce the double-stranded DNA breaks between the recombination signal sequences and the gene segments [3]. The expression of RAG-1 and RAG-2 is restricted to lymphoid cells undergoing V(D)J rearrangement [4, 5]. In the absence of either RAG-1 or RAG-2 gene products, the development of mature lymphocytes is completely abrogated and hence results in severe combined immune deficiency in mouse and human [6][7][8]. In human, missense mutations in either RAG-1 or RAG-2 result in the Omenn syndrome, which is characterized by a poor T lymphocyte repertoire [9].There are two waves of RAG-1 and RAG-2 expression in bone marrow B cell precursors. RAG are expressed first in pro-B cell progenitors undergoing Ig heavy-chain gene rearrangement, and the second expression of RAG is seen during Ig j or k light-chain gene rearrangement occurring in pre-B cells [4,10]. In T cell development, RAG areThe first two authors contributed to this work equally. first expressed in pro-T cells when rearrangement of the TCRb chain gene occurs, and secondary expression of RAG occurs when the TCRa chain loci undergo V-J rearrangement to produce mature T cells [11,12]. The transcription of RAG is regulated at different levels. At the chromatin level, Fuller et al. and we reported that a DNase I-hypersensitive (HS) site was identified in the promoter region of mouse and human RAG-1 only in RAG-expressing lymphocytes [13,14]. We a...

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Mechanism of c-Myb–C/EBPβ Cooperation from Separated Sites on a Promoter

Cited by 158 publications

References 50 publications

Increased in vivo transcription of an IL-8 haplotype associated with respiratory syncytial virus disease-susceptibility

Increased in vivo transcription of an IL-8 haplotype associated with respiratory syncytial virus disease-susceptibility

Transactivation mediated by B-Myb is dependent on TAFII250

Characterization of the proximal enhancer element and transcriptional regulatory factors for murine recombination activating gene‐2

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