p300 Acts as a Transcriptional Coactivator for Mammalian Notch-1

Oswald, Franz; Täuber, Birgitt; Dobner, Thomas; Bourteele, Soizic; Kostezka, Ulrike; Adler, Guido; Liptay, Susanne; Schmid, Roland M.

doi:10.1128/mcb.21.22.7761-7774.2001

Cited by 279 publications

(238 citation statements)

References 54 publications

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“…) and overactivation of Notch1 may play a role in tumorigenesis resulting from a loss of functional p53 (Oswald et al, 2001), we speculated that Notch1 activation might be irregular in the thymocytes of Pin1À/Àp53À/À mice. The activated form of Notch1 is the intracellular form (NIC) produced by limited cleavage of full length Notch1 (Fowlkes and Robey, 2002).…”

Section: Resultsmentioning

confidence: 99%

“…Notch1 is expressed at varying levels in developing and mature T cells, from hematopoietic progenitors to peripheral lymphocytes . Both p53 and Notch1 are linked to lymphoid malignancies (Oswald et al, 2001). Pear et al (1996) showed that transduction of bone marrow cells with NIC results in T-cell leukemia, and that Notch1 plays a role in lymphoid oncogenesis in mice.…”

Section: Introductionmentioning

confidence: 99%

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Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1

et al. 2006

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Tumor suppressor p53 is essential for checkpoint control in response to a variety of genotoxic stresses. DNA damage leads to phosphorylation on the Ser/Thr-Pro motifs of p53, which facilitates interaction with Pin1, a pSer/pThr-Prospecific peptidyl prolyl isomerase. Pin1 is required for the timely activation of p53, resulting in apoptosis or cell cycle arrest. To investigate the physiological relationship between Pin1 and p53, we created Pin1À/Àp53À/À mice. These p53-deficient mice spontaneously developed lymphomas, mainly of thymic origin, as well as generalized lymphoma infiltration into other organs, including the liver, kidneys and lungs. Ablation of Pin1, in addition to p53, accelerated the thymic hyperplasia, but the thymocytes in these Pin1À/À p53À/À mice did not infiltrate other organs. The thymocytes in 12-week-old Pin1À/Àp53À/À mice were CD4 À CD8 À (double negative) and had significantly higher levels of the intracellular form of Notch1 (NIC) than the thymocytes of p53À/À or wild-type mice. Presenilin-1, a cleavage enzyme for NIC generation from full-length Notch1 was increased in the thymocytes of Pin1À/Àp53À/À mice. Pin1 depletion also inhibited the degradation of NIC by proteasomes. These results suggest that both Pin1 and p53 control the normal proliferation and differentiation of thymocytes by regulating the NIC level.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1

et al. 2006

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“…The precise mechanisms of epigenetic regulation of Notch target genes are not yet known, although some histone-modifying enzymes have been implicated in the regulation of Notch target genes. The histone acetyltransferase (HAT) p300 has been shown in complex with RBP-J/Notch and is a positive cofactor for Notch dependent transcription [45,46]. Functional interactions between Notch and PCAF and GCN5 have also been observed [47].…”

Section: Epigenetic Regulation Of Notch Target Genesmentioning

confidence: 99%

“…This tool has been exploited to study the physiological role of "canonical" (RBP-J dependent) Notch signaling in detail, reviewed in [107]. The ternary complex of RBP-J/NICD/MAML recruits histone acetyltransferase p300 to activate Notch target genes [45,46,108]. The Capobianco lab set out to purify the endogenous Notch-coactivator complex [109].…”

Section: Coactivators Of Notchmentioning

confidence: 99%

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Borggrefe

Oswald

2009

Cell. Mol. Life Sci.

585

499

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. The Notch gene encodes a transmembrane receptor that gave the name to the evolutionary highly conserved Notch signaling cascade. It plays a pivotal role in the regulation of many fundamental cellular processes such as proliferation, stem cell maintenance and differentiation during embryonic and adult development. After specific ligand binding, the intracellular part of the Notch receptor is cleaved off and translocates to the nucleus, where it binds to the transcription factor RBP-J. In the absence of activated Notch, RBP-J represses Notch target genes by recruiting a corepressor complex. Here, we review Notch signaling with a focus on gene regulatory events at Notch target genes. This is of utmost importance to understand Notch signaling since certain RBP-J associated cofactors and particular epigenetic marks determine the specificity of Notch target gene expression in different cell types. We subsequently summarize the current knowledge about Notch target genes and the physiological significance of Notch signaling in development and cancer.

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“…The last cleavage liberates the intracellular domain of Notch (NIC), which translocates to the nucleus (Struhl and Adachi, 1998). Once in the nucleus, NIC associates with the DNA binding protein CSL/ RBPJj (Fortini and Artavanis-Tsakonas, 1994;Jarriault et al, 1995) thereby recruiting other coactivators and initiates the formation of a functional transcription activation complex driving target gene expression (Kurooka and Honjo, 2000;Oswald et al, 2001;Wallberg et al, 2002;Wu et al, 2000).…”

mentioning

confidence: 99%

Generation and characterization of a Notch1 signaling‐specific reporter mouse line

Smith

Claudinot

Lehal

et al. 2012

Genesis

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Signaling through the Notch1 receptor is essential for the control of numerous developmental processes during embryonic life as well as in adult tissue homeostasis and disease. Since the outcome of Notch1 signaling is highly context‐dependent, and its precise physiological and pathological role in many organs is unclear, it is of great interest to localize and identify the cells that receive active Notch1 signals in vivo. Here, we report the generation and characterization of a BAC‐transgenic mouse line, N1‐Gal4VP16, that when crossed to a Gal4‐responsive reporter mouse line allowed the identification of cells undergoing active Notch1 signaling in vivo. Analysis of embryonic and adult N1‐Gal4VP16 mice demonstrated that the activation pattern of the transgene coincides with previously observed activation patterns of the endogenous Notch1 receptor. Thus, this novel reporter mouse line provides a unique tool to specifically investigate the spatial and temporal aspects of Notch1 signaling in vivo. genesis 50:700–710, 2012. © 2012 Wiley Periodicals, Inc.

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p300 Acts as a Transcriptional Coactivator for Mammalian Notch-1

Cited by 279 publications

References 54 publications

Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1

Ablation of a peptidyl prolyl isomerase Pin1 from p53-null mice accelerated thymic hyperplasia by increasing the level of the intracellular form of Notch1

The Notch signaling pathway: Transcriptional regulation at Notch target genes

Generation and characterization of a Notch1 signaling‐specific reporter mouse line

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