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Operations on Genomic Intervals and Genome Arithmetic
Published in Altuna Akalin, Computational Genomics with R, 2020
Download P300 ChIP-seq peaks data from the UCSC browser. The peaks are locations where P300 binds. The P300 binding marks enhancer regions in the genome. (HINT: group: “regulation”, track: “Txn Factor ChIP”, table:“wgEncodeRegTfbsClusteredV3”, you need to filter the rows for “EP300” name.) Check enrichment of H3K4me3, H3K27ac and DNase-seq (H1.ESC.dnase.chr20.bw) experiments on chr20 on and arounf the P300 binding-sites, use data from compGenomRData package. Make multi-heatmaps and metaplots. What is different from the TSS profiles? [Difficulty: Advanced]
Rubinstein−Taybi Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
The EP300 gene on chromosome 22q13.2 consists of 31 exons in a stretch of 87.75 kb and encodes p300 that contains 3 cysteine- and histidine-rich regions, including the carboxyterminal region interacting specifically with E1A, and a centrally located bromodomain representing a hallmark of certain transcriptional coactivators. As a homolog to CREBBP, p300 shares >70% and 63% homology with CREBBP at nucleotide and amino acid levels, respectively, and demonstrates HAT activity. Strongly expressed in human cerebellum as well as in other brain regions, p300 functions as transcriptional coactivator in the regulation of gene expression via chromatin remodeling and plays an important role in the processes of cell proliferation and differentiation. CREBBP/p300 may also modulate with p53 pathway through P53 acetylation, and loss of CREBBP/p300 could disrupt p53 activation, stability, and transactivation of target genes. It has been shown that p300 knockdown by hammerhead ribozymes inhibits apoptosis, probably by disrupting the p53-mediated response to DNA damage [1].
Neurophysiological changes associated with dementia in Down syndrome
Published in Vee P. Prasher, Down Syndrome and Alzheimer’s Disease, 2018
Frank E. Visser, Satnam Kunar, Vee P. Prasher
Goodin and colleagues59 reported the findings of a study in which they presented subjects with a series of auditory tones and recorded the resulting evoked potentials. A total of 53 individuals were tested, consisting of 27 patients with dementia and 26 patients with normal mental function but with some other neurological disease (e.g. multiple sclerosis). Dementia was diagnosed using the MMSE.40 Evoked potentials were compared with data previously collected from 40 normal controls aged 15–76 years. The researchers found that impaired mental functioning in dementia was highly correlated with changes in the latency and amplitude of the P300 component of the AEP. The P300 was delayed in patients with dementia compared with controls, and the P300 abnormalities were not due to neurological disease per se but to dementia.50
Presence of endolymphatic hydrops on listening difficulties in patients with normal hearing level
Published in Acta Oto-Laryngologica, 2023
Tadao Yoshida, Masumi Kobayashi, Satofumi Sugimoto, Yukari Fukunaga, Daisuke Hara, Shinji Naganawa, Michihiko Sone
Mismatch negativity and P300 are known as event-related potentials associated with hearing. Mismatch negativity is a negative potential detected at a latency of 100–200 ms after a sound stimulus [5]. P300 is a positive wave that is recognized at a latency of about 300 ms after a sound stimulus. Event-related potentials are considered to reflect higher-order functions and are used to assess the effects of treatments for psychological, physiological, psychiatric, and neurological disorders. Mismatch negativity is expected to be applied to the study of auditory memory, such as attention testing for infants who cannot understand tasks, and for the temporal integration of auditory information. P300 is considered useful as an objective method for evaluating attention function in people with attention deficit hyperactivity disorder in terms of temporal changes and treatment effects and as an objective method to evaluate APD. P300 is also expected to be a neurophysiological biomarker for the objective assessment of APD.
Taking the road less traveled – the therapeutic potential of CBP/β-catenin antagonists
Published in Expert Opinion on Therapeutic Targets, 2021
Global genomic and proteomic analyses in p300 knock-down, N-terminal p300 edited [164], p300 S89A edited cell lines and also p300 S89A knockin mice [81], have all demonstrated that differential N-terminal Kat3 coactivator usage provides a highly evolutionarily conserved mechanism to transcriptionally couple metabolism and energy production, to cellular state and function [81]. p300 Serine 89 (S89) has previously been shown to be a substrate for a number of kinase cascades including, PKC [165,166], AMPK [167], and SIK2167, associated with metabolic regulation of insulin/glucagon signaling [168] and carbohydrate-responsive element-binding protein (ChREBP) control of glycolysis and lipogenesis [169]. Phosphorylation of p300 S89 also critically regulates the differentiation of mouse ES cells [63] and adult progenitor cells [65]. Clearly, an array of post-translational modifications (kinases and phosphatases) of this single highly evolutionary conserved residue in the amino terminus of p300 can integrate multiple signaling cascade inputs to coordinate and regulate cellular and metabolic states.
Role of visual P300 in cognitive assessment of subacute stroke patients: a longitudinal study
Published in International Journal of Neuroscience, 2020
Simona De Salvo, Viviana Lo Buono, Lilla Bonanno, Katia Micchia, Emanuele Cartella, Laura Romeo, Francesca Arcadi, Francesco Corallo, Fabrizia Caminiti, Alessia Bramanti, Roberto Giorgianni, Silvia Marino
The P300 (ERPs’s main wave) is generated by cognitive tasks which stimulate the attention of subjects after an unexpected stimulus [5]. It represents a non-invasive tool to assess cortical signal processing [6, 7] and brain functional state. It can be also elicited by visual, auditory, somatosensory, or olfactory stimuli in different experimental settings. The P300 is involved in cognitive processes resulting from cortical and subcortical areas, especially auditory cortex, hippocampus, and amygdala thalamic structures [8]. Recent studies have confirmed the role of ERPs as prognostic markers in patients with severe brain acquired lesions [9, 10]. P300 seems to be susceptible to stimuli recognition and the presence of this wave is an important prognostic marker for functional recovery in patients with global aphasia [11, 12]. In addition, the increase of P300 latency is associated to post-stroke depression [13].