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Relevant bibliographies by topics / Protein P300

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Academic literature on the topic 'Protein P300'

Author: Grafiati

Published: 7 September 2023

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Journal articles on the topic "Protein P300"

1

Shikama, Noriko, Ho Man Chan, Marija Krstic-Demonacos, Linda Smith, Chang-Woo Lee, William Cairns, and Nicholas B. La Thangue. "Functional Interaction between Nucleosome Assembly Proteins and p300/CREB-Binding Protein Family Coactivators." Molecular and Cellular Biology 20, no. 23 (December 1, 2000): 8933–43. http://dx.doi.org/10.1128/mcb.20.23.8933-8943.2000.

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ABSTRACT The p300/CREB-binding protein (CBP) family of proteins consists of coactivators that influence the activity of a wide variety of transcription factors. Although the mechanisms that allow p300/CBP proteins to achieve transcriptional control are not clear, it is believed that the regulation of chromatin is an important aspect of the process. Here, we describe a new level of p300-dependent control mediated through the functional interaction between p300/CBP and members of the family of nucleosome assembly proteins (NAP), which includes NAP1, NAP2, and TAF1. We find that NAP proteins, which have previously been implicated in the regulation of transcription factor binding to chromatin, augment the activity of different p300 targets, including p53 and E2F, through a process that is likely to involve the physical interaction between p300 and NAP. NAP proteins can form oligomers, and the results show that NAP proteins can bind to both core histones and p300 coactivator proteins, perhaps in a multicomponent ternary complex. We also provide data in support of the idea that histones can influence the interaction between p300 and NAP protein. These results argue that NAP is a functionally important component of the p300 coactivator complex and suggest that NAP may serve as a point of integration between transcriptional coactivators and chromatin.

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Kaida, Atsushi, Yasuo Ariumi, Keiko Baba, Masami Matsubae, Toshifumi Takao, and Kunitada Shimotohno. "Identification of a novel p300-specific-associating protein, PRS1 (phosphoribosylpyrophosphate synthetase subunit 1)." Biochemical Journal 391, no. 2 (October 10, 2005): 239–47. http://dx.doi.org/10.1042/bj20041308.

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CBP [CREB (cAMP-response-element-binding protein)-binding protein] and p300 play critical roles in transcriptional co-activation, cell differentiation, proliferation and apoptosis. Multiple transcription factors associate with CBP/p300. With the exception of the SYT oncoprotein, no proteins have been identified that specifically associate with p300, but not CBP. In the present study, we isolated a novel p300-associated protein for which no interaction with CBP was observed by GST (glutathione S-transferase) pull-down assay using Jurkat cell lysates metabolically labelled with [35S]methionine. This protein bound the KIX (kinase-inducible) domain of p300. Following resolution by two-dimensional acrylamide gel electrophoresis, we identified the KIX-domain-bound protein by MS analysis as PRS1 (phosphoribosylpyrophosphate synthetase subunit 1), a protein essential for nucleoside biosynthesis. This is the first report to demonstrate the existence of a p300 KIX-domain-specific-interacting protein that does not interact with CBP. Thus p300 may play a role in the regulation of DNA synthesis through interactions with PRS1.

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Dallas, Peter B., Ian Wayne Cheney, Da-Wei Liao, Valerie Bowrin, Whitney Byam, Stephen Pacchione, Ryuji Kobayashi, Peter Yaciuk, and Elizabeth Moran. "p300/CREB Binding Protein-Related Protein p270 Is a Component of Mammalian SWI/SNF Complexes." Molecular and Cellular Biology 18, no. 6 (June 1, 1998): 3596–603. http://dx.doi.org/10.1128/mcb.18.6.3596.

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ABSTRACT p300 and the closely related CREB binding protein (CBP) are transcriptional adaptors that are present in intracellular complexes with TATA binding protein (TBP) and bind to upstream activators including p53 and nuclear hormone receptors. They have intrinsic and associated histone acetyltransferase activity, suggesting that chromatin modification is an essential part of their role in regulating transcription. Detailed characterization of a panel of antibodies raised against p300/CBP has revealed the existence of a 270-kDa cellular protein, p270, distinct from p300 and CBP but sharing at least two independent epitopes with p300. The subset of p300/CBP-derived antibodies that cross-reacts with p270 consistently coprecipitates a series a cellular proteins with relative molecular masses ranging from 44 to 190 kDa. Purification and analysis of various proteins in this group reveals that they are components of the human SWI/SNF complex and that p270 is an integral member of this complex.

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Kadeppagari, Ravi-Kumar, Natesan Sankar, and Bayar Thimmapaya. "Adenovirus Transforming Protein E1A Induces c-Myc in Quiescent Cells by a Novel Mechanism." Journal of Virology 83, no. 10 (March 11, 2009): 4810–22. http://dx.doi.org/10.1128/jvi.02145-08.

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ABSTRACT Previously we showed that the E1A binding proteins p300 and CBP negatively regulate c-Myc in quiescent cells and that binding of E1A to p300 results in the induction of c-Myc and thereby induction of S phase. We demonstrated that p300 and HDAC3 cooperate with the transcription factor YY1 at an upstream YY1 binding site and repress the Myc promoter. Here we show that the small E1A protein induces c-Myc by interfering with the protein-protein interaction between p300, YY1, and HDAC3. Wild-type E1A but not the E1A mutants that do not bind to p300 interfered in recruitment of YY1, p300, and HDAC3 to the YY1 binding site. As E1A started to accumulate after infection, it transiently associated with promoter-bound p300. Subsequently, YY1, p300, and HDAC3 began to dissociate from the promoter. Later in infection, E1A dissociated from the promoter as well as p300, YY1, and HDAC3. Removal of HDAC3 from the promoter correlated with increased acetylation of Myc chromatin and induction. In vivo E1A stably associated with p300 and dissociated YY1 and HDAC3 from the trimolecular complex. In vitro protein-protein interaction studies indicated that E1A initially binds to the p300-YY1-HDAC3 complex, briefly associates with it, and then dissociates the complex, recapitulating somewhat the in vivo situation. Thus, E1A binding to the C-terminal region of p300 disrupts the important corepressor function provided by p300 in repressing c-Myc. Our results reveal a novel mechanism by which a viral oncoprotein activates c-Myc in quiescent cells and raise the possibility that the oncoproteins encoded by the small-DNA tumor viruses may use this mechanism to induce c-Myc, which may be critical for cell transformation.

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Sánchez-Molina, Sara, José Luis Oliva, Susana García-Vargas, Ester Valls, José M. Rojas, and Marian A. Martínez-Balbás. "The histone acetyltransferases CBP/p300 are degraded in NIH 3T3 cells by activation of Ras signalling pathway." Biochemical Journal 398, no. 2 (August 15, 2006): 215–24. http://dx.doi.org/10.1042/bj20060052.

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The CBP [CREB (cAMP-response-element-binding protein)-binding protein]/p300 acetyltransferases function as transcriptional co-activators and play critical roles in cell differentiation and proliferation. Accumulating evidence shows that alterations of the CBP/p300 protein levels are linked to human tumours. In the present study, we show that the levels of the CBP/p300 co-activators are decreased dramatically by continuous PDGF (platelet-derived growth factor) and Ras signalling pathway activation in NIH 3T3 fibroblasts. This effect occurs by reducing the expression levels of the CBP/p300 genes. In addition, CBP and p300 are degraded by the 26 S proteasome pathway leading to an overall decrease in the levels of the CBP/p300 proteins. Furthermore, we provide evidence that Mdm2 (murine double minute 2), in the presence of active H-Ras or N-Ras, induces CBP/p300 degradation in NIH 3T3 cells. These findings support a novel mechanism for modulating other signalling transduction pathways that require these common co-activators.

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Lee, J. S., R. H. See, T. Deng, and Y. Shi. "Adenovirus E1A downregulates cJun- and JunB-mediated transcription by targeting their coactivator p300." Molecular and Cellular Biology 16, no. 8 (August 1996): 4312–26. http://dx.doi.org/10.1128/mcb.16.8.4312.

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Transcription factors and cofactors play critical roles in cell growth and differentiation. Alterations of their activities either through genetic mutations or by viral oncoproteins often result in aberrant cell growth and tumorigenesis. The transcriptional cofactor p300 has recently been shown to be complexed with transcription factors YY1 and CREB. Adenovirus E1A oncoproteins target these transcription complexes via physical interactions with p300, resulting in alterations of transcription mediated by these transcription factors. Here we show that p300 is also critical for repression by E1A of the activities of cJun and JunB, two members of the AP-1 transcriptional complexes. This repressive effect of E1A is dependent on the p300-binding domain of E1A and can be relieved by overexpression of p300. These results suggest that p300 serves as a mediator protein for downregulation of AP-1 activity by E1A. This hypothesis was further supported by the following observations: (i) in the absence of E1A, overexpression of p300 stimulated transcription both through an AP-1 site present in the collagenase promoter and through Jun proteins in GAL4 fusion protein-based assays; and (ii) overexpression of a mutant p300 lacking the E1A-interacting domain reduced the responsiveness of Jun-dependent transcription to E1A repression. As predicted from the functional results, p300 physically interacted with the Jun proteins. These findings thus established that p300 is a cofactor for cJun and JunB. We propose that p300 is a common mediator protein through which E1A gains control over multiple transcriptional regulatory pathways in the host cells.

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Thompson, Paul R., Hisanori Kurooka, Yoshihiro Nakatani, and Philip A. Cole. "Transcriptional Coactivator Protein p300." Journal of Biological Chemistry 276, no. 36 (July 9, 2001): 33721–29. http://dx.doi.org/10.1074/jbc.m104736200.

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Kasper, Lawryn H., Tomofusa Fukuyama, Michelle A. Biesen, Fayçal Boussouar, Caili Tong, Antoine de Pauw, Peter J. Murray, Jan M. A. van Deursen, and Paul K. Brindle. "Conditional Knockout Mice Reveal Distinct Functions for the Global Transcriptional Coactivators CBP and p300 in T-Cell Development." Molecular and Cellular Biology 26, no. 3 (February 1, 2006): 789–809. http://dx.doi.org/10.1128/mcb.26.3.789-809.2006.

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ABSTRACT The global transcriptional coactivators CREB-binding protein (CBP) and the closely related p300 interact with over 312 proteins, making them among the most heavily connected hubs in the known mammalian protein-protein interactome. It is largely uncertain, however, if these interactions are important in specific cell lineages of adult animals, as homozygous null mutations in either CBP or p300 result in early embryonic lethality in mice. Here we describe a Cre/LoxP conditional p300 null allele (p300 flox ) that allows for the temporal and tissue-specific inactivation of p300. We used mice carrying p300 flox and a CBP conditional knockout allele (CBP flox ) in conjunction with an Lck-Cre transgene to delete CBP and p300 starting at the CD4− CD8− double-negative thymocyte stage of T-cell development. Loss of either p300 or CBP led to a decrease in CD4+ CD8+ double-positive thymocytes, but an increase in the percentage of CD8+ single-positive thymocytes seen in CBP mutant mice was not observed in p300 mutants. T cells completely lacking both CBP and p300 did not develop normally and were nonexistent or very rare in the periphery, however. T cells lacking CBP or p300 had reduced tumor necrosis factor alpha gene expression in response to phorbol ester and ionophore, while signal-responsive gene expression in CBP- or p300-deficient macrophages was largely intact. Thus, CBP and p300 each supply a surprising degree of redundant coactivation capacity in T cells and macrophages, although each gene has also unique properties in thymocyte development.

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Asahara, Hiroshi, Sophie Tartare-Deckert, Takeya Nakagawa, Tsuyoshi Ikehara, Fumiko Hirose, Tony Hunter, Takashi Ito, and Marc Montminy. "Dual Roles of p300 in Chromatin Assembly and Transcriptional Activation in Cooperation with Nucleosome Assembly Protein 1 In Vitro." Molecular and Cellular Biology 22, no. 9 (May 1, 2002): 2974–83. http://dx.doi.org/10.1128/mcb.22.9.2974-2983.2002.

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ABSTRACT In a yeast two-hybrid screen to identify proteins that bind to the KIX domain of the coactivator p300, we obtained cDNAs encoding nucleosome assembly protein 1 (NAP-1), a 60-kDa histone H2A-H2B shuttling protein that promotes histone deposition. p300 associates preferentially with the H2A-H2B-bound form of NAP-1 rather than with the unbound form of NAP-1. Formation of NAP-1-p300 complexes was found to increase during S phase, suggesting a potential role for p300 in chromatin assembly. In micrococcal nuclease and supercoiling assays, addition of p300 promoted efficient chromatin assembly in vitro in conjunction with NAP-1 and ATP-utilizing chromatin assembly and remodeling factor; this effect was dependent in part on the intrinsic histone acetyltransferase activity of p300. Surprisingly, NAP-1 potently inhibited acetylation of core histones by p300, suggesting that efficient assembly requires acetylation of either NAP-1 or p300 itself. As p300 acted cooperatively with NAP-1 in stimulating transcription from a chromatin template in vitro, our results suggest a dual role of NAP-1-p300 complexes in promoting chromatin assembly and transcriptional activation.

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Kannan, Srinivasaraghavan, Anthony W. Partridge, David P. Lane, and Chandra S. Verma. "The Dual Interactions of p53 with MDM2 and p300: Implications for the Design of MDM2 Inhibitors." International Journal of Molecular Sciences 20, no. 23 (November 28, 2019): 5996. http://dx.doi.org/10.3390/ijms20235996.

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Proteins that limit the activity of the tumour suppressor protein p53 are increasingly being targeted for inhibition in a variety of cancers. In addition to the development of small molecules, there has been interest in developing constrained (stapled) peptide inhibitors. A stapled peptide ALRN_6924 that activates p53 by preventing its interaction with its negative regulator Mdm2 has entered clinical trials. This stapled peptide mimics the interaction of p53 with Mdm2. The chances that this peptide could bind to other proteins that may also interact with the Mdm2-binding region of p53 are high; one such protein is the CREB binding protein (CBP)/p300. It has been established that phosphorylated p53 is released from Mdm2 and binds to p300, orchestrating the transcriptional program. We investigate whether molecules such as ALRN_6924 would bind to p300 and, to do so, we used molecular simulations to explore the binding of ATSP_7041, which is an analogue of ALRN_6924. Our study shows that ATSP_7041 preferentially binds to Mdm2 over p300; however, upon phosphorylation, it appears to have a higher affinity for p300. This could result in attenuation of the amount of free p300 available for interacting with p53, and hence reduce its transcriptional efficacy. Our study highlights the importance of assessing off-target effects of peptide inhibitors, particularly guided by the understanding of the networks of protein-protein interactions (PPIs) that are being targeted.

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Dissertations / Theses on the topic "Protein P300"

1

Chan, Ho Man. "Molecular basis of cell cycle control : p300 and pRb." Thesis, University of Glasgow, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326430.

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Jayatunga, Madura Kelum Perera. "Modulation of the hypoxic response in cancer : inhibition of the HIF-1α/p300 protein-protein interaction." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:a3ae9d39-f7cc-4ba5-b921-2a7855ee1512.

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Hypoxia inducible factor (HIF)-1α is a heterodimerically-activated transcription factor central to the cellular response to hypoxic environments and is often upregulated in cancer. Binding of HIF-1α to the co-activator p300 is necessary for the hypoxia-induced transcription of many oncogenic proteins. The aim of this project was to develop novel small molecule inhibitors of the HIF-1α/p300 protein-protein interaction (PPI). Initial work focused on designing, validating and optimising two high-throughput competition binding assays to screen for inhibitors of the PPI (Chapter 2). Alongside these, zinc ejector assays for both p300 and KDM4A proteins were developed to probe the mechanism of action and selectivity. Analysis of hits from a natural product high-throughput screen (HTS) revealed two compound classes; benzoquinones and 2-substituted indandiones, which modulate the PPI. The potency of these series correlated with the reactivity of the core functional groups, which act as electrophiles to covalently modify reactive cysteines, ejecting structural zinc and disrupting the p300/KDM4A protein fold (Chapter 3). Conjugating electrophilic groups to putative HIF-1α/p300 inhibitors did not replicate the activity of the zinc ejecting HTS hits (Chapter 4). Further work focused on non-covalent inhibitors of the HIF-1α/p300 interaction, first with peptide truncates, and then rationally designed α-helix peptidomimetics. An 11mer truncate showed encouraging activity (IC50 ≈ 70 μM), and corresponded to a key α-helix in the HIF-1α C-terminal transactivation domain. Three distinct double-sided scaffolds were used to imitate up to five hot-spot ampiphilic residues on this α-helix (Chapter 6 and 7). Of the 35 compounds screened, only modest inhibition was observed (IC50 ≈ 200-500 μM). Future work will look to conjugate electrophilic functionality onto the 11mer peptide in an attempt to gain potency from zinc ejection, while maintaining selectivity for p300.

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Kyle, Hannah Frances. "Biophysical and structural characterisation of protein-protein interactions, HIF-1α/p300 and eIF4E/eIF4G to inform inhibitor rational design." Thesis, University of Leeds, 2015. http://etheses.whiterose.ac.uk/10404/.

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Protein-protein interactions (PPIs) are an important class of therapeutic target, however due to their large interaction interface they are considered difficult to inhibit. The two PPIs of interest in this thesis are the HIF-1α (hypoxia inducible factor-1α)/p300 and eIF4E (eukaryotic initiation factor 4E)/eIF4G interactions, both of which have been shown to be involved in many different cancers and are hypothesised to be good targets for targeted therapy. A rational design approach is favoured for PPIs, however for this to be possible a detailed understanding of the binding interface is required. Biophysical assessment of the HIF-1α CTAD/p300 CH1 interface has revealed a key binding “hot-spot” of p300 where the helix three region of HIF-1α binds to p300, this area has subsequently been targeted using oligoamide α-helix mimetics to disrupt the interaction. This binding site was found by two approaches, used to probe the HIF-1α binding surface on p300, first, by analysis of the binding of shorter HIF-1α peptide fragments; and second, by phage display experiments. The HIF-1α fragment study demonstrated that HIF-1α helix 3 region binds to p300 with a higher affinity than any of the short (<20 amino acids) peptide regions of HIF-1α and a peptide containing helices 2 and 3 binds with a higher affinity than a peptide containing helices 1 and 2, this importance of the helix 3 binding site was validated using mutagenesis. The phage display experiment found 12mer peptides that bind to p300 with a higher affinity than any short peptide region of HIF-1α. Structural techniques and mutagenesis were the used to verify that this binding site was similar to that of HIF-1α helix 3. The rationally designed mimetics of HIF-1α helix 3 were able to disrupt the interaction with low micromolar affinity. A second phage display experiment found Adhirons which bound with low nanomolar affinity and were able to disrupt the interaction with low micromolar affinity, docking of the crystal structure of this Adhiron indicated that it may be acting at a different site to the HIF-1α helix 3 region. This is a proof of principle that a detailed understanding of an interaction, using both biophysical and structural techniques, can directly lead to the development of inhibitors of challenging and therapeutically relevant PPIs.

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Shi, Dingding. "Defining the Roles of p300/CBP (CREB Binding Protein) and S5a in p53 Polyubiquitination, Degradation and DNA Damage Responses: A Dissertation." eScholarship@UMMS, 2010. https://escholarship.umassmed.edu/gsbs_diss/452.

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p53, known as the “guardian of the genome”, is the most well-characterized tumor suppressor gene. The central role of p53 is to prevent genome instability. p53 is the central node in an incredibly elaborate genome defense network for receiving various input stress signals and controlling diverse cellular responses. The final output of this network is determined not only by the p53 protein itself, but also by other p53 cooperating proteins. p300 and CBP (CREB-Binding Protein) act as multifunctional regulators of p53 via acetylase and ubiquitin ligase activities. Prior work in vitro has shown that the N-terminal 595 aa of p300 encode both generic ubiquitin ligase (E3) and p53-directed E4 functions. Analysis of p300 or CBP-deficient cells revealed that both coactivators were required for endogenous p53 polyubiquitination and the normally rapid turnover of p53 in unstressed cells. Unexpectedly, p300/CBP ubiquitin ligase activities were absent in nuclear extracts and exclusively cytoplasmic. In the nucleus, CBP and p300 exhibited differential regulation of p53 gene target expression, C-terminal acetylation, and biologic response after DNA damage. p300 activated, and CBP repressed, PUMA expression, correlating with activating acetylation of p53 C-terminal lysines by p300, and a repressive acetylation of p53 lysine-320 induced by CBP. Consistent with their gene expression effects, CBP deficiency augmented, and p300 deficiency blocked, apoptosis after doxorubicin treatment. Subcellular compartmentalization of p300/CBP’s ubiquitination and transcription activities reconciles seemingly opposed functions—cytoplasmic p300/CBP E4 activities ubiquitinate and destabilize p53, while nuclear p300/CBP direct p53 acetylation, target gene activation, and biological outcome after genotoxic stress. p53 is a prominent tumor suppressor gene and it is mutated in more than 50% of human tumors. Reactivation of endogenous p53 is one therapeutic avenue to stop cancer cell growth. In this thesis, we have identified S5as a critical regulator of p53 degradation and activity. S5a is a non-ATPase subunit in the 19S regulatory particle of the 26S proteasome. Our preliminary data indicates that S5a is required for p53 instability and is a negative regulator of p53 tranactivation. As a negative regulator of p53, S5a may therefore also represent a new target for cancer drug development against tumors that specifically maintain wild type p53.

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Chou, Yu-Ting. "Cited2, an autoregulated transcriptional modulator, in TGF-beta signaling." Connect to text online, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1147147222.

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Silk, Rhiannon Nicola. "Studies into host macrophage transcriptional control by the African Swine Fever Virus protein A238L." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4808.

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African swine fever virus (ASFV) is a large double-stranded DNA virus which causes a lethal haemorrhagic fever in domestic pigs. This virus primarily infects cells from the monocyte/macrophage lineage and its ability to manipulate the function of these cells is key to the pathogenesis of this disease. ASFV encodes several proteins involved in immune evasion. One of these proteins, A238L, has been shown to inhibit host macrophage gene transcription. This protein has been shown to interact with several cellular proteins involved in signal transduction: a serine/threonine protein phosphatase, calcinerurin (CaN), the transcription factor NF-кB, and most recently the transcriptional co-activator CREB binding protein (CBP/P300). However its exact mechanism of action is not fully understood. Previous work has been limited to the investigation of individual signaling pathways and/or the expression of individual host genes. The aim of this study was to investigate the global effect of A238L on host macrophage gene transcription and also to carry out further investigation into the mechanism by which this protein functions. To determine the global effect of A238L on host macrophage gene transcription differential gene expression between porcine cells expressing A238L and control cells was examined using a porcine oligonucleotide microarray. These results demonstrated that A238L was a potent inhibitor of host macrophage gene expression. Functional characterisation of the annotated genes showed that a large proportion of A238L down-regulated genes are typically induced in response to cell stress. Significantly, genes regulated by the I kappa B kinase (IKK), mitogen-activated protein kinase (MAPK) and janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathways were all shown to be down regulated by A238L. Genes associated with the MAPK pathways were particularly enriched. The transcription of A238L-regulated genes is controlled by numerous different transcription factors, including NF-кB. All of the transcription factors identified interact with the transcription co-activator CBP/P300. This provides a common link between these factors, and indicates that A238L may target CBP/P300 to inhibit gene transcription. This observation supports recent work demonstrating that A238L interacts with and inhibits CBP/P300 function. To explore the potential mechanisms involved in the nuclear localisation of A238L, ASFV-infected Vero cells, expressing A238L under the control of its own promoter, were examined under a range of conditions using confocal microscopy. The results demonstrated that A238L was actively imported into the nucleus and exported by a CRM 1 mediated pathway, although a pool of A238L protein remained in the cytoplasm. Sequence analysis of A238L identified the presence of two putative nuclear localisation signals (NLS-1 and NLS-2). NLS-2 was located within A238L’s CaN docking motif. Mutation of these motifs indicated that both NLS-1 and NLS-2 are active and exhibit functional redundancy. Mutation of the CaN docking motif alone, in the presence of intact NLS-2, resulted in a dramatic increase in the nuclear localisation of A238L. These results are consistent with a model in which A238L functions within both the nucleus and the cytoplasm and suggest that binding of CaN to A238L masks NLS-2, contributing to the cytoplasmic retention of A238L.

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Kakita, Tsuyoshi. "p300 protein as a coactivator of GATA-5 in the transcription of cardiac-restricted atrial natriuretic factor gene." Kyoto University, 2001. http://hdl.handle.net/2433/150538.

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Michael, Bindhu. "Human T lymphotropic virus type 1 (HTLV-1) accessory protein p30(II) modulates cellular and viral gene expression." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1088784889.

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Thesis (Ph. D.)--Ohio State University, 2004.
Title from first page of PDF file. Document formatted into pages; contains xvii, 250 p.; also includes graphics (some col.) Includes bibliographical references (p. 207-250). Available online via OhioLINK's ETD Center

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Love, Ian M. "Critical and Independent Roles of the P/CAF Acetyltransferase in ARF-p53 Signaling: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/663.

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For 30 years, the tumor suppressor p53 has been a subject of intense research in nearly every discipline of scientific inquiry. While numerous surprising roles for p53 in health and disease are uncovered each year, the central role of its activation in preventing neoplastic transformation has been and will remain at the forefront of p53 research as investigators work to address an unexpectedly complex question—precisely how does p53 integrate upstream stress signals to coordinate activation of its target genes in response to stress? One manner in which to address this question is at the level of transcription initiation—after upstream signals converge on p53 and produce a number of pools of post-transcriptionally modified p53, how exactly are specific target promoters activated in such a sensitive, context-specific manner? The work presented herein aims to address the role of histone acetylation at the p21 promoter—a critical mediator of G1/S arrest—by the P/CAF acetyltransferase in response to a variety of p53-activating stresses. We show that depletion of P/CAF strongly inhibits p21 expression in response to a variety of stresses, despite normal stabilization of p53 and recruitment to target promoters. This defect in p21 expression correlates closely with abrogation of stress-induced cell-cycle arrest. Strikingly, a p53 allele lacking putative P/CAF acetylation sites was still able to direct p21 expression, which was still dependent upon P/CAF. We show further that histone acetylation at H3K14 at the p21 promoter following stress is dependent upon P/CAF. Rescue of p21 expression with wild-type P/CAF or a ∆HAT point mutant indicates that P/CAF requires an intact HAT domain, suggesting that histone acetylation at H3K14 is catalyzed by P/CAF HAT activity, not the molecular bridging of a heterologous HAT by P/CAF. Furthermore, RNA polymerase II (RNAP II) was present at the p21 proximal promoter under all basal and stress conditions, but elongation of RNAP II after stress required the presence of P/CAF. These data indicate that H3K14 acetylation by P/CAF closely correlates with the activation status of the p21 promoter, and may be necessary for activation of a larger subset of p53-responsive promoters. In addition to its critical role in p21 expression, we noted that p53 stabilization and cell-cycle arrest in response to p14ARF, but not other p53-stabilizing stresses, were also dependent on P/CAF. Cell-cycle arrest induced by p16INK4A was intact after P/CAF ablation, indicating a role for P/CAF in cell-cycle arrest specific to p14ARF-p53 signaling. Basal MDM2 levels were unaffected by P/CAF knockdown, as were p53- MDM2 and ARF-MDM2 complexes. A preliminary analysis of MDM2 localization was inconclusive, due to vastly different quantities of MDM2 in different conditions making analysis of subcellular localization difficult; however, the role of P/CAF in the relocalization of MDM2 to the nucleolus by p14ARF could potentially explain the defect in p53 stabilization, and should be explored further. These observations, underscored by recent reports that P/CAF undergoes loss of heterozygosity in several tumor types, suggest that P/CAF plays a critical role in p53-mediated cell-cycle arrest through multiple, independent mechanisms. Further study should clarify whether P/CAF is lost in tumors maintaining wild-type p53, and whether its reintroduction into these tumors confers any potential therapeutic benefit.

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Delboni, Thomaz Pileggi. "Investigação genético-clínica em pacientes com síndrome de Rubinstein-Taybi." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-19022010-163029/.

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INTRODUÇÃO: A Síndrome de Rubinstein-Taybi (RTS) é uma doença genética rara, caracterizada por dismorfismos craniofaciais típicos, polegares e háluces alargados, deficiência mental e baixa estatura. A incidência estimada é de 1: 125 000 a 1: 330000 nativivos. A SRT geralmente ocorre esporadicamente, mas pode ser herdada com um padrão de herança autossômico dominante. O diagnóstico da SRT é essencialmente clínico. OBJETIVOS: Realizar o estudo genético-clínico e citogenético em 30 pacientes brasileiros com SRT, e descrever de forma sistematizada a freqüência de dismorfismos faciais e malformações múltiplas encontradas. MÉTODOS: Neste estudo observacional retrospectivo e prospectivo, os pacientes foram seguidos no período de agosto de 2005 a junho de 2009. O cariótipo com bandeamento G foi realizado em todos os pacientes. RESULTADOS: A maioria dos pacientes avaliados foi do sexo feminino (60%). As seguintes características foram observadas em todos os pacientes da nossa casuística: atraso de desenvolvimento neuropsicomotor, ponta nasal voltada para baixo, columela proeminente, sorriso característico, dificuldades alimentares na infância, persistência dos coxins fetais, falanges distais dos polegares alargadas e pés planos. A baixa estatura e a microcefalia foi observada em 80% e 76% dos casos, respectivamente. As principais características craniofaciais observadas foram: fronte proeminente (86%), ponte nasal larga (60%), hipertelorismo (70%), sobrancelhas espessas e arqueadas (96%) cílios longos em 93%, prega epicântica (76%), fissura palpebral infra vertidas (76%), abertura bucal estreita (93%), retrognatismo (76 %), sorriso característico em 100%, palato alto e estreito (93%), anomalias dentárias (83%). Outras anomalias identificadas foram: estrabismo, erros de refração, obstrução do canal lacrimal, háluces e polegares alargados, angulação de polegares, anomalias do pavilhão auricular (rotação/posição/tamanho/forma), angulação do hálux, clinodactilia, sobreposição dos pododáctilos, falanges distais alargadas de outros dedos, marcha rígida, hipotonia, sopro cardíaco, cardiopatia congênita, criptoquidia, hemangioma plano e hipertricose. Uma paciente apresentou translocação recíproca de novo 46, XX, t (2; 16)(q36.3; p13.3). CONCLUSÕES: A raridade da SRT e o amplo espectro das manifestações clínicas pode atrasar o diagnóstico clínico. A média da idade ao diagnóstico dos nossos pacientes com SRT foi de três anos e oito meses. Todas as crianças devem receber avaliação por geneticista pediátrico, cardiologista, oftalmologista, neuropediatra, e odontopediatra
INTRODUCTION: Rubinstein-Taybi syndrome (RTS) is a rare genetic disorder characterized by distinctive craniofacial dysmorphisms, broad thumbs and toes and mental and statural deficiency. The prevalence of RTS has been estimated to be 1 in 125000 to 1: 330000 live births. RTS usually occurs sporadically although it can be inherited as an autosomal dominant disorder. The diagnosis of RTS is primarily based on clinical features. OBJECTIVES: We performed a clinical and cytogenetic assay in a group of 30 Brazilian RTS patients. We also decribed the frequencies of facial dysmorphisms and multiple malformations. METHODS: In this observational retrospective and prospective study, the patients were followed from August 2005 to June 2009. Chromosomal analysis was performed by G-banding karyotype. RESULTS: Most of the patients were female (60%).The following abnormalities were present in all of the patients: delayed psychomotor development, beaked nose, proeminent collumel, typical facies, broad thumbs and toes, flat feet, joint laxity, feeding problems during the childhood, and finger pads. Short stature was present in 80%, and microcephalia in 76% of the cases, respectively. Main craniofacial characteristics are frontal bossing (86%), wide nasal bridge (60%), ocular hyperthelorism (70%), high arched eyebrows (96%), long eyelashes (93%), epicathal folds (76%), downslanting palpebral fissures (76%), small opening of the mouth (93%), retrognathism (76%), grimacing smile (100%), high arched palate (93%), and dental anomalies (83%). Other findings were: strabism, refractive error, lacrimal obstruction, wide thumb and halux, angulated thumbs, external ears anomalies (rotation, implantation and morfology), angulated halux, clinodactyly, crowded toes, broad distal falanges of other fingers, stiff gait, hipotonia, cardiac murmur, congenital heart defect, undescendent testis, hypertrichosis, and hemangioma. One female patient has found to have a reciprocal de novo translocation t(2;16)(q36.3;p13.3) on G-banding karyotype CONCLUSIONS: The rarity of RTS and the wide spectrum of clinical manifestations, may delay the clinical diagnosis of RTS. The average age at the diagnosis of our patients was 3 years and 8 months. All children of RTS should receive an evaluation by a pediatric geneticist, cardiologist, ophthalmologist, pediatric neurologist, and pediatric dentist

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Book chapters on the topic "Protein P300"

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Koshlan, Tatiana, and Kirill Kulikov. "Mathematical Modelling of the Effect of Phosphorylation on the Stability of the Formation of Biological Complexes P53–Mdm2 and P53–P300." In Mathematical Modeling of Protein Complexes, 263–89. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-98304-2_6.

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Wang, Zhenyu, Xuehua Zhao, Mingzhe Li, Dongsun Cao, and Tong-Cun Zhang. "Cardiac Hypertrophy-Specific Genes are Synergistic Activated by Myocardin and CREB-binding protein (CBP) p300." In Proceedings of the 2012 International Conference on Applied Biotechnology (ICAB 2012), 789–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-37922-2_82.

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De Guzman, Roberto N., Maria A. Martinez-Yamout, H. Jane Dyson, and Peter E. Wright. "Structure and Function of the CBP/p300 TAZ Domains." In Zinc Finger Proteins, 114–20. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-27421-9_17.

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"p300/CBP-Interacting Protein." In Encyclopedia of Cancer, 3358. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_101748.

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"P300/CBP-Interacting Protein." In Encyclopedia of Cancer, 2747. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_4339.

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"CBP (CREB binding protein, p300)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 284–85. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_2449.

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"CREB-Binding Protein (CBP)/p300." In Encyclopedia of Cancer, 993. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1370.

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Fernández, Rosa, Karla Ramírez, Enrique Delgado-Zayas, Esther Gómez-Gil, Isabel Esteva, Antonio Guillamon, and Eduardo Pásaro. "An Analysis of the Implication of Estrogens and Steroid Receptor Coactivators in the Genetic Basis of Gender Incongruence." In Oxytocin and Health. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96668.

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In mammals, sex differences in the adult brain are established very early in development, when the brain is still very immature. In the case of having inherited the SRY gene, during embryogenesis, testosterone secreted by the testes enters the brain and is converted to estradiol by the aromatase. Then the estradiol acts by binding to intracellular estrogen receptors (ERs) located predominantly in neurons, masculinizing specific brain regions. But ERs are also transcription factors that, when they are exposed to their ligand, dimerize and form complexes with coactivator proteins and corepressors, modifying the transcription of multiple target genes in a cascade effect and ultimately neuronal function. Given the intimate relationship between steroids and brain dimorphism, and steroid coactivators and gene transcription, in the present work, we further explore the implication of ERs α and β, and steroid coactivators NCoA-1, NCoA-2, NCoA-3, NCoA-4, NCoA-5 and p300-CREBBP, in the genesis of brain dimorphism. Based on our data, we believe that the coactivators NCOA-1, NCOA-2 and p300-CREBBP could be considered as candidate genes for GI.

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Bekesi, Angela, Sara Abdellaoui, Natalie Holroyd, Wouter Van Delm, Els Pardon, Jarne Pauwels, Kris Gevaert, et al. "Challenges in the Structural–Functional Characterization of Multidomain, Partially Disordered Proteins CBP and p300: Preparing Native Proteins and Developing Nanobody Tools." In Methods in Enzymology, 607–75. Elsevier, 2018. http://dx.doi.org/10.1016/bs.mie.2018.09.032.

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Conference papers on the topic "Protein P300"

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Wang, Li-Ting, Shyh-Shin Chiou, and Shih-Hsien Hsu. "Abstract 1108: Intestine-specific homeobox recruits p300/CBP-associated factor and bromodomain-containing protein 4 to promote epithelial-mesenchymal transition." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1108.

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Wang, Li-Ting, Shyh-Shin Chiou, and Shih-Hsien Hsu. "Abstract 1108: Intestine-specific homeobox recruits p300/CBP-associated factor and bromodomain-containing protein 4 to promote epithelial-mesenchymal transition." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1108.

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Li, Mingzhe, Zhenyu Wang, Zhongyi Xie, Jing Luo, Dongsun Cao, and Tongcun Zhang. "CREB-binding Protein (CBP) p300 Enhanced the Expression of Cardiac Hypertrophy-Specific Genes Activated by Myocardin-Related Transcription Factor-A (MRTF-A)." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.118.

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Romano, Simona, Giovanna Nappo, Elena Cesaro, Antonio Candela, and Maria Fiammetta Romano. "Abstract 755: FK506 binding protein 51 (FKBP51) binds to p300 and acts as transcriptional co-regulator of ABCG2 gene expression in melanoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-755.

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Rio-Machin, Ana, Alba Maiques-Diaz, Sandra Rodriguez-Perales, Sara Alvarez, Rocio N. Salgado, Álvaro Eguileor, Raul Torres, Juan C. Ramirez, and Juan C. Cigudosa. "Abstract 472: Interactions of the fusion protein Nup98-Hoxa9 with Pbx3, p300 and HDAC1: widening the targeted therapy window in acute myeloid leukemia (AML)." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-472.

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Cheng, Jeffrey K., Victoria Le, Robert P. Mecham, and Jessica E. Wagenseil. "Mechanics and Modeling of Postnatal Arterial Development in Wild-Type and Elastin-Insufficient Mice." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53140.

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Large arteries in vertebrates serve as elastic reservoirs that store a portion of the blood volume with systole and discharge it during diastole. This function is made possible by the combination of extracellular matrix (ECM) proteins deposited by the smooth muscle cells (SMCs) in the arterial wall. Elastin and collagen expression in mice is first detectable around embryonic day 14 and peaks around postnatal day (P) 14, returning to baseline levels by P30. During this time, pressure and cardiac output increase significantly before leveling off ∼P30 [1]. Hence, the protein amounts and consequent mechanical properties of the arterial wall change simultaneously with the applied hemodynamic loads in a complicated and unknown feedback loop.

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Beck, George R., Roberta Carboni, Michael Van Scoy, Brad Zerler, and Elizabeth Moran. "GENE EXPRESSION IN pRB/p300-COMPROMISED MC3T3-E1 CELLS: OSTEOPONTIN." In 3rd International Conference on Osteopontin and SIBLING (Small Integrin-Binding Ligand, N-linked Glycoprotein) Proteins, 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.304.

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Chaikovskaya, L. A., V. V. Klyuchenko, M. I. Baranskaya, and O. L. Ovsienko. "Influence of microbial preparations and mineral fertilizers on the yield and quality of winter wheat grain." In CURRENT STATE, PROBLEMS AND PROSPECTS OF THE DEVELOPMENT OF AGRARIAN SCIENCE. Federal State Budget Scientific Institution “Research Institute of Agriculture of Crimea”, 2020. http://dx.doi.org/10.33952/2542-0720-2020-5-9-10-116.

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The use of biological products based on effective strains of microorganisms with a range of useful properties is one of the aspects of biological farming. The long-term field experiments were conducted in the soil and climatic conditions of the Crimea. А positive effect of the combined use of mineral fertilizers (NPK calculated at P30) and pre-sown inoculation of seeds (biopreparation based on L. nimipressuralis CCM 32-3) on the yield and quality of winter wheat grain was shown. The increase in grain productivity of winter wheat by 31 % compared to control (on average for 3 years) and grain quality indicators: protein and gluten – up to 12.5% and 28.0 % (in the control 9.9% and 19.2%, respectively) was revealed.

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Diskowski, L., K. Kubiak, M. Wiese, and CM Kramm. "The function of CBP/p300 and BET-proteins in dependence of H3.3K27M mutation in diffuse intrinsic pontine glioma (DIPG)." In 33. Jahrestagung der Kind-Philipp-Stiftung für pädiatr. onkolog. Forschung. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1709778.

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Stocklosa, Mirela, Raluca Vlad, Alexandra Moraru, Irina Dijmarescu, Ioana Oprescu, Cristina Becheanu, Daniela Pacurar, Dumitru Oraseanu, and Gabriela Lesanu. "P30 Why is cow’s milk protein allergy diagnosis so difficult in infants with gastrointestinal symptoms?" In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.118.

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