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Eckert, Dawid; Buhl, Sandra; Weber, Susanne N.; Jäger, Richard; Schorle, Hubert

doi:10.1186/gb-2005-6-13-246

Cited by 372 publications

(225 citation statements)

References 76 publications

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“…In mamma- lian species, e.g. human and rodents, five members of AP-2 factors (␣-⑀) have been reported (11). Among three AP-2 members (AP-2␣, ␤, and ␥) expressed in the nervous system, we show that AP-2␤ specifically regulates development of NA neurons.…”

Section: Ap-2␤ Critically Regulates the Na Neurotransmitter Phenotypementioning

confidence: 75%

“…AP-2 proteins share unique structures consisting of an N-terminal transactivation domain and a C-terminal DNA binding and dimerization domain. Although AP-2 proteins are coexpressed in some developing organs, they show different spatiotemporal expression during development, and gene inactivation studies indicated that they may have quite distinct roles in development (11). Based on initial studies of AP-2␣ and its expression in the neural crest (12,13), it was generally assumed that AP-2␣ regulates differentiation of neural crest-derived cells such as SA cells.…”

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confidence: 99%

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Regulation of the Noradrenaline Neurotransmitter Phenotype by the Transcription Factor AP-2β

Hong

Lardaro

et al. 2008

Journal of Biological Chemistry

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AP-2 family transcription factors are essential for development and morphogenesis of diverse tissues and organs, but their precise roles in specification of neural crest stem cell (NCSC)-derived cell types have not been determined. Among three members known to be expressed in the NCSC (i.e. AP-2␣, AP-2␤, and AP-2␥), we found that only AP-2␤ is predominantly expressed in the sympathetic ganglia of developing mouse embryos, supporting its role in sympathetic development. Indeed, AP-2␤ null mice expressed significantly reduced levels of both noradrenaline (NA) and NA-synthesizing dopamine ␤-hydroxylase in the peripheral nervous system. Strikingly, we also found that NA neuron development was significantly compromised in the locus coeruleus as well. Pharmacological treatment with an NA intermediate during pregnancy significantly rescues the neonatal lethality of AP-2␤ ؊/؊ mice, indicating that NA deficiency is one of the main causes for lethality found in AP-2␤ ؊/؊ mice. We also showed that forced expression of AP-2␤, but not other AP-2 factors, in NCSC favors their differentiation into NA neurons. In summary, we propose that AP-2␤ plays critical and distinctive roles in the NA phenotype specification in both the peripheral and central nervous system during development.

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Section: Ap-2␤ Critically Regulates the Na Neurotransmitter Phenotypementioning

confidence: 75%

mentioning

confidence: 99%

Regulation of the Noradrenaline Neurotransmitter Phenotype by the Transcription Factor AP-2β

Hong

Lardaro

et al. 2008

Journal of Biological Chemistry

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“…AP-2 is a family of transcription factors containing a helixspan-helix motif for DNA binding at the carboxyl terminus with possible roles in development, the control of apoptosis and cell cycling, and oncogenesis (40,41). Its members are clearly distinct from AP-1 family transcription factors, homo/heterodimers composed of c-Fos, c-Jun, or ATF, which share a b-Zip motif for dimerization and DNA binding.…”

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confidence: 99%

Induction of Epstein-Barr Virus Oncoprotein LMP1 by Transcription Factors AP-2 and Early B Cell Factor

Murata

Noda

Narita

et al. 2016

J Virol

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Latent membrane protein 1 (LMP1) is a major oncogene essential for primary B cell transformation by Epstein-Barr virus (EBV).Previous studies suggested that some transcription factors, such as PU.1, RBP-J, NF-B, and STAT, are involved in this expression, but the underlying mechanism is unclear. Here, we identified binding sites for PAX5, AP-2, and EBF in the proximal LMP1 promoter (ED-L1p). We first confirmed the significance of PU.1 and POU domain transcription factor binding for activation of the promoter in latency III. We then focused on the transcription factors AP-2 and early B cell factor (EBF). Interestingly, among the three AP-2-binding sites in the LMP1 promoter, two motifs were also bound by EBF. Overexpression, knockdown, and mutagenesis in the context of the viral genome indicated that AP-2 plays an important role in LMP1 expression in latency II in epithelial cells. In latency III B cells, on the other hand, the B cell-specific transcription factor EBF binds to the ED-L1p and activates LMP1 transcription from the promoter. IMPORTANCE Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) is crucial for B cell transformation and oncogenesis of other EBVrelated malignancies, such as nasopharyngeal carcinoma and T/NK lymphoma.Its expression is largely dependent on the cell type or condition, and some transcription factors have been implicated in its regulation. However, these previous reports evaluated the significance of specific factors mostly by reporter assay. In this study, we prepared point-mutated EBV at the binding sites of such transcription factors and confirmed the importance of AP-2, EBF, PU.1, and POU domain factors. Our results will provide insight into the transcriptional regulation of the major oncogene LMP1. The Epstein-Barr virus (EBV) is a human gammaherpesvirus that mainly infects and establishes latent infection in B lymphocytes, but it can also infect other types of cells, including NK, T, and epithelial cells. EBV infection has been implicated as a causal factor in a variety of malignancies, and the expression pattern of viral latent genes varies depending on the tissue of origin and the state of the tumors. Neoplasms such as Burkitt lymphomas or gastric carcinomas express only EBV-encoded small RNA (EBER) and EBV nuclear antigen 1 (EBNA1) (type I latency), whereas some Hodgkin lymphomas, nasopharyngeal carcinomas (NPC), and NK/T lymphomas express EBER, EBNA1, latent membrane protein 1 (LMP1), and LMP2 genes (type II latency). In addition to the type II genes, EBNA2, EBNA3, and EBNA-LP are also expressed in immunosuppression-related lymphomas or lymphoblastoid cell lines (LCLs; type III latency). LMP1 constitutively activates cellular signaling through NF-B, mitogen-activated protein, JAK/STAT, and AKT and is believed to be a major oncogene encoded by EBV (1-11).Two promoters regulate LMP1 gene transcription, with mechanisms that differ between type II and type III infection. In latency III in B lymphocytes, LMP1 transcription from the proximal ED-L1 promoter is acti...

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“…R. Soc. B 283: 20161712 of chordates including C. intestinalis [18,23,24]. When the AP-2 binding site in the reporter construct was mutated, epidermal expression of the reporter gene was completely abolished (figure 1b-d; electronic supplementary material, figure S2), suggesting that the AP-2 binding site is essential for epidermal expression of Ci-CesA.…”

Section: Resultsmentioning

confidence: 99%

Transcriptional regulation of a horizontally transferred gene from bacterium to chordate

et al. 2016

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The horizontal transfer of genes between distantly related organisms is undoubtedly a major factor in the evolution of novel traits. Because genes are functionless without expression, horizontally transferred genes must acquire appropriate transcriptional regulations in their recipient organisms, although the evolutionary mechanism is not known well. The defining characteristic of tunicates is the presence of a cellulose containing tunic covering the adult and larval body surface. Cellulose synthase was acquired by horizontal gene transfer from Actinobacteria. We found that acquisition of the binding site of AP-2 transcription factor was essential for tunicate cellulose synthase to gain epidermal-specific expression. Actinobacteria have very GC-rich genomes, regions of which are capable of inducing specific expression in the tunicate epidermis as the AP-2 binds to a GCrich region. Therefore, the actinobacterial cellulose synthase could have been potentiated to evolve its new function in the ancestor of tunicates with a higher probability than the evolution depending solely on a spontaneous event.

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Cited by 372 publications

References 76 publications

Regulation of the Noradrenaline Neurotransmitter Phenotype by the Transcription Factor AP-2β

Regulation of the Noradrenaline Neurotransmitter Phenotype by the Transcription Factor AP-2β

Induction of Epstein-Barr Virus Oncoprotein LMP1 by Transcription Factors AP-2 and Early B Cell Factor

Transcriptional regulation of a horizontally transferred gene from bacterium to chordate

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