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1,249 results for “p53”
TMEM206 contributes to cancer hallmark functions in colorectal cancer cells and is regulated by p53 in a p21-dependent manner
<p><span>Acid-induced ion flux plays a role in pathologies where tissue acidification is prevalent, including cancer. In 2019, TMEM206 was identified as the molecular component of acid-induced chloride flux. Localizing to the plasma membrane, TMEM206 contributes to cellular processes like acid-induced cell death. Since over 50% of human cancers carry loss of function mutations in the p53 gene, we aimed to analyze how TMEM206 is regulated by p53 and its role in cancer hallmark function and acid-induced cell death in HCT116 colorectal cancer (CRC) cells. We generated p53-deficient HCT116 cells and assessed TMEM206-mediated Cl<sup>-</sup> currents and transcriptional regulation using the patch-clamp and a dual-luciferase reporter assay, respectively. To investigate the contribution of TMEM206 to cancer hallmark functions we performed migration and metabolic activity assays. The role of TMEM206 in p53-mediated acid-induced cell death has been assessed with cell death assays. TMEM206 mRNA level is significantly elevated in human primary CRC tumors. TMEM206 knockout increased acid-induced cell death and reduced proliferation and migration, indicating a role for TMEM206 in these cancer hallmark functions. Furthermore, we observed increased TMEM206 mRNA levels and currents in HCT116 p53 knockout cells. This phenotype can be rescued by transient overexpression of p53, but not by overexpression of dysfunctional p53. In addition, our data suggests that TMEM206 may mediate cancer hallmark functions within p53-associated pathways. TMEM206 promoter activity is not altered by p53 overexpression. Conversely, knockout of p21, a major target gene of p53, increased TMEM206-mediated currents suggesting expression control of TMEM206 by p21 downstream signaling. Our results show that in colorectal cancer cells, TMEM206 expression is elevated, contributes to cancer hallmark functions and its regulation is dependent on p53 through a p21-dependent mechanism.</span></p>
Data for Altered Glia-Neuron Communication in Alzheimer's Disease Affects WNT, p53, and NFkB Signaling Determined by snRNA-seq
<p><strong>data.tar.gz contains all files from the data directory associated with the 230313_TS_CCCinHumanAD GitHub project and includes the following:</strong></p><ul><li><strong>CellRangerCounts/</strong><ul><li><strong>GSE157827/</strong><ul><li><strong>post_soupX/ : </strong>contains 21 directories for 21 samples, which each contain 3 files obtained from ambient RNA removal with soupX. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN16100290_S01_AD/</strong><ul><li><strong>barcodes.tsv</strong></li><li><strong>genes.tsv</strong></li><li><strong>matrix.mtx</strong></li></ul></li></ul></li><li><strong>pre_soupX/ : </strong>contains 21 directories for 21 samples, which each contain 2 files obtained from Cell Ranger after aligning fastq files to the reference genome. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN16100290_S01_AD/</strong><ul><li><strong>filtered_feature_ bc_matrix.h5</strong></li><li><strong>Raw_feature_bc_matrix.h5</strong></li></ul></li></ul></li></ul></li><li><strong>GSE174367/ : </strong>contains 19 directories for 19 samples, which contain 3 files each from Cell Ranger alignment of fastq files to the reference genome. Below is a representative example, but this repo contains 1 directory per sample:<ul><li><strong>SAMN19128610_S1_CTRL/</strong><ul><li><strong>barcodes.tsv</strong></li><li><strong>genes.tsv</strong></li><li><strong>Matrix.mtx</strong></li></ul></li></ul></li></ul></li><li><strong>ccc/</strong><ul><li><strong>nichenet_grn/</strong><ul><li><strong>gr_network_human_21122021.rds : </strong>accessed in October 2023, gene regulation network – gene regulatory information from MultiNicheNet</li><li><strong>ligand_tf_matrix_nsga2r_final.rds: </strong>accessed in October 2023, ligand tf matrix for signaling path determination from MultiNicheNet</li><li><strong>signaling_network_human_21122021.rds : </strong>accessed in October 2023, signaling network – protein-protein interaction information from MultiNicheNet</li><li><strong>weighted_networks_nsga2r_final.rds : </strong>accessed in October 2023, networks weighted by literature evidence from MultiNicheNet</li></ul></li><li><strong>nichenet_prior/</strong><ul><li><strong>ligand_target_matrix.rds : </strong>accessed in April 2023, ligand to target matrix from NicheNet</li><li><strong>lr_network.rds : </strong>accessed in April 2023, ligand-receptor matrix from NicheNet</li></ul></li><li><strong>nichenet_v2_prior/</strong><ul><li><strong>ligand_target_matrix_nsga2r_final.rds : </strong>accessed in June 2023, ligand to target matrix from MultiNicheNet used to predict target genes.</li><li><strong>lr_network_human_21122021.rds : </strong>accessed in June 2023, ligand-receptor matrix from MultiNicheNet used to predict ligand-receptor pairs.</li></ul></li><li><strong>geo_multinichenet_output.rds </strong>: MultiNicheNet output for Morabito et al., 2021 data</li><li><strong>geo_signaling_igraph_objects.rds </strong>: list of igraph objects for 17 overlapping LRTs and their signaling mediators in the Morabito et al., 2021 dataset. </li><li><strong>gse_multinichenet_output.rds</strong> : MultiNicheNet output for Lau et al., 2020 data</li><li><strong>gse_signaling_igraph_objects.rds</strong> : list of igraph objects for 17 overlapping LRTs and their signaling mediators in the Lau et al., 2020 dataset </li></ul></li><li><strong>seurat_preprocessing/</strong><ul><li><strong>geo_filtered_seurat.rds : </strong>merged and filtered seurat object of Morabito et al., 2021 data</li><li><strong>geo_integrated_seurat.rds :</strong> seurat object integrated using harmony of Morabito et al., 2021 data</li><li><strong>geo_clustered_seurat.rds : </strong>clustered seurat object of Morabito et al., 2021 data</li><li><strong>geo_processed_seurat.rds : </strong>processed seurat object with final cell type assignments at specified resolution of Morabito et al., 2021 data</li><li><strong>gse_filtered_seurat.rds : </strong>merged and filtered seurat object of Lau et al., 2020 data</li><li><strong>gse_integrated_seurat.rds : </strong>seurat object integrated using harmony of Lau et al., 2020 data</li><li><strong>gse_clustered_seurat.rds :</strong> clustered seurat object of Lau et al., 2020 data</li><li><strong>gse_processed_seurat.rds : </strong>processed seurat object with final cell type assignments at specified resolution of Lau et al., 2020 data </li></ul></li></ul>
p53 alters intracellular Ca2+ signaling through regulation of TRPM4
<p>Altered expression of transient receptor potential channel melastatin 4 (TRPM4) contributes to several malignancies, including cardiac conduction diseases, immune diseases, and cancer. Yet the underlying mechanisms of TRPM4 expression changes remain elusive.In this study, we report that loss of tumor suppressor protein p53 or p63γ function or mutation of a putative p53 response element in the TRPM4 promoter region increase TRPM4 promoter activity in the colorectal cancer cell line HCT 116. In cells that lack p53 expression, we observed increased TRPM4 mRNA and protein levels and TRPM4-mediated Na<sup>+</sup> currents. This phenotype can be reversed by transient overexpression of p53. In the prostate cancer cell line LNCaP, which expresses p53 endogenously, p53 overexpression decreases TRPM4-mediated currents. As in other cancer cells, CRISPRcas9 mediated knockout of TRPM4 in p53 deficient HCT 116 cells results in increased store-operated Ca<sup>2+</sup>entry. The effect of the TRPM4 knockout is mimicked by p53 mediated suppression of TRPM4 in the parental cell line expressing TRPM4. In addition, a TRPM4 knockout-mediated shift in cell cycle is abolished upon loss of p53.Taken together, these findings indicate that p53 represses TRPM4 expression, thereby altering cellular Ca<sup>2+</sup> signaling and that TRPM4 adds to cell cycle shift dependent on p53 signaling.</p>
Characterization of p53 family homologs in evolutionary remote branches of Holozoa
<p>Supplementary materials to article: Characterization of p53 family homologs in evolutionary remote branches of Holozoa</p> <p>The p53 family of transcription factors plays key roles in development, genome stability, senescence and tumor development, and p53 is the most important tumor suppressor protein in humans. Although intensively investigated for many years, its initial evolutionary history is not yet fully elucidated. Using bioinformatic and structure prediction methods on current databases containing newly-sequenced genomes and transcriptomes, we present a detailed characterization of p53 family homologs in remote members of the Holozoa group, in the unicellular clades Filasterea, Ichthyosporea and Corallochytrea. Moreover, we show that these newly characterized homologous sequences contain domains that can form structures with high similarity to the human p53 family DNA-binding domain, and some also show similarities to the oligomerization and SAM domains. The presence of these remote homologs demonstrates an ancient origin of the p53 protein family.</p>
ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer
<p>The mechanisms underlying ETS-driven prostate cancer initiation and progression remain poorly understood due to a lack of model systems that recapitulate this phenotype. We generated a genetically engineered mouse with prostate-specific expression of the ETS factor, ETV4, at lower and higher protein dosages through mutation of its degron. Lower-level expression of ETV4 caused mild luminal cell expansion without histologic abnormalities and higher-level expression of stabilized ETV4 caused prostatic intraepithelial neoplasia (mPIN) with 100% penetrance within 1 week. Tumor progression was limited by p53-mediated senescence and Trp53 deletion cooperated with stabilized ETV4. The neoplastic cells expressed differentiation markers such as Nkx3.1 recapitulating luminal gene expression features of untreated human prostate cancer. Single-cell and bulk RNA-sequencing showed stabilized ETV4 induced a novel luminal-derived expression cluster with signatures of the cell cycle, senescence, and epithelial to mesenchymal transition. These data suggest that ETS overexpression alone, at sufficient dosage, can initiate prostate neoplasia.</p>
Rps19 R67∆ mutation creates a model of Diamond-Blackfan anemia and reveals downstream mediators of p53 pathway.
<p>Diamond-Blackfan anemia (DBA) is a rare bone marrow failure syndrome accompanied by cardiovascular, skeletal, and urogenital abnormalities. Most of the affected individuals carry mutations in ribosomal proteins, including S19 (Rps19), a part of the 40S ribosomal subunit. We developed a transgenic model harboring deletion of conserved Arg 67 in <em>RPS19</em>, which is the site of post-translational modification by protein-arginine methyl transferase family and could show that the defect in Rps19 causes phenotype in perfect overlap with the DBA including hematologic dysfunctions, hypotrophy, intrinsic anemia, severe craniofacial, skeletal, urogenital, cardiovascular, and cerebral abnormalities leading to premature lethality during the adolescence of the mouse. This DBA mouse model exhibited activation of the Trp53 signaling pathway in hematopoietic stem cells (HSCs) leading to reduced erythroid lineage development. Competitive transplantation assays using Rps19-deficient bone marrow cells confirmed that HSCs and their progeny lineages were affected while their differentiation was rescued after inactivation of the tumor suppressor Trp53 showing that the development of the DBA phenotype significantly involves non-canonical components of the p53 signaling pathway in the etiopathogenesis of DBA with the Rps19R67∆ mutation leading to the disrupted hematopoietic hierarchy starting at the stage of short-term repopulating stem cells. The activated p53 pathway was mediated by downstream molecules Zmat3, Phlda3, and Eda2r, whose overall function in the pathology of DBA involve erythroid differentiation blockade coupled with cell proliferation and survival disruption. To conclude, the new DBA model represents a powerful tool for exploring new therapeutic options for DBA.</p>
Nanomaterial genotoxicity evaluation using the high-throughput p53-binding protein 1 (53BP1) assay - data from the article published in PlosOne
<p>Data that have been used in the manuscript "Nanomaterial genotoxicity evaluation using the high-throughput p53-binding protein 1 (53BP1) assay" by M. Fontaine et al., published in PlosOne in 2023.</p>
ETV4 mediates dosage-dependent prostate tumor initiation and cooperates with p53 loss to generate prostate cancer
Open the record for dataset details and reuse information.
The Clinical Significance of Serum p53 Antibody Levels in Patients with Oral Squamous Cell Carcinoma in Japanese Clinical Practice
<p>Supplementary Figure S1. Serum anti-p53 antibody titers in each clinical stage.<br> Supplementary Table S1. The change of Ap53Ab titer in patients with OSCC after surgery.</p>
Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
<p>The investigation of the mechanisms behind p53 mutations in acute myeloid leukemia (AML) has been limited by the lack of suitable mouse models, which historically have resulted in lymphoma rather than leukemia. This study introduces two new AML mouse models. One model induces mutant p53 and <em>Mdm2</em> haploinsufficiency in early development, showing the role of Mdm2 in myeloid-biased hematopoiesis and AML predisposition, independent of p53. The second model mimics clonal hematopoiesis by inducing mutant p53 in adult hematopoietic stem cells, demonstrating that the timing of p53 mutation determines AML versus lymphoma development. In this context, age-related changes in hematopoietic stem cells (HSCs), collaborates with mutant p53 to predispose towards myeloid transformation rather than lymphoma development. Our study unveils new insights into the cooperative impact of HSC age, <em>Trp53</em> mutations and <em>Mdm2</em> haploinsufficiency on clonal hematopoiesis and the development of myeloid malignancies.</p>
The role of TAp63g and p53 point mutations in regulating DNA repair, mutational susceptibility and invasion of bladder cancer cell
<p>Raw data set for the manuscript submitted to e-Life (10-06-2021-RA-eLife-71184 ) for peer-review. </p>
Positive p53 expression is significantly found higher in luminal B HER-2 negative cases with primary endocrine therapy resistance: A multicenter retrospective cross-sectional study in Indonesia
<p><strong>Positive p53 expression is significantly found higher in luminal B HER-2 negative cases with primary endocrine therapy resistance: A multicenter retrospective cross-sectional study in Indonesia</strong></p>
Contaminated sediment in the Detroit River selects for evolved CYP1A and p53 responses in wild brown bullhead (Ameiurus nebulosus) populations
<div> <div> <p><span>In a previous study, adaptive responses to a single polycyclic aromatic hydrocarbon (PAH), benzo[a]pyrene (BaP), were identified in brown bullhead (</span><span><em>Ameiurus nebulosu</em>s</span><span>) captured from contaminated sites across the Great Lakes. The tumor suppressor p53 and phase I toxin metabolizing CYP1A genes showed a protective and refractory response, respectively, up to the F1 generation (Williams and Hubberstey, 2014). As an extension to the first study, bullhead were exposed to sediment collected from sites along the Detroit River to see if these adaptive responses are attainable when fish from a contaminated site are exposed to a mixture of contaminants, instead of a single compound. p53 and CYP1A proteins were measured in both studies with the addition of phase II glutathione-s-transferase (GST) activity in the second. Three treatment groups were measured: acute (treated immediately), cleared (depurated for three months and subsequent treatment), and farm raised F1 offspring. All three treatment groups were exposed to clean and contaminated sediment for 24 and 96 hours. </span><span>Acute fish from contaminated sites exposed to contaminated sediment revealed an initial elevated p53 response that was not reached in cleared fish exposed to contaminated sediment. Instead, cleared and F1 bullhead from clean and contaminated sites had overlapping p53 expression patterns in response to contaminated sediment by 96 hours. Acute fish from contaminated sites exposed to contaminated sediment revealed refractory CYP1A expression, which disappeared in cleared fish and whose F1 refractory response overlapped with clean site F1 offspring. Decreasing GST activity was evident in both clean and contaminated fish over time, with clean site fish responding to contaminated sediment more deliberately. By 96 hours, the response patterns of F1 offspring from clean and contaminated sites to clean and contaminated sediment exposures were similar. </span><span> </span></p> </div> <div> <p><span>Because p53, CYP1A and GST activity responses to contaminated sediment dosing overlapped in clean and contaminated farm-raised F1 offspring, these results suggest that contaminated fish have acclimated to the contaminants present in their environments by reaching a tolerance threshold and no evidence of adaptation was detected in these biomarkers. </span></p> </div> </div>
P53 Mutational Status and cf HPV DNA for the Management of HPV-associated OPSCC
ClinicalTrials.gov study NCT03077243. IPD Sharing: NO. Countries: 1. Publications: 1.
p53 Activation in Platinum-Resistant High Grade Serous Ovarian Cancer, a Study of PLD With APR-246
ClinicalTrials.gov study NCT03268382. IPD Sharing: Not stated. Countries: 3. Publications: 2.
p53 Suppressor Activation in Recurrent High Grade Serous Ovarian Cancer, a Phase Ib/II Study of Systemic Carboplatin Combination Chemotherapy With or Without APR-246
ClinicalTrials.gov study NCT02098343. IPD Sharing: Not stated. Countries: 8. Publications: 2.
Phase II Study of Metastatic Cancer That Overexpresses P53 Using Lymphodepleting Conditioning Followed by Infusion of Anti-P53 TCR-Gene Engineered Lymphocytes
ClinicalTrials.gov study NCT00393029. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Data from: PITAR, a DNA damage-inducible Cancer/Testis long noncoding RNA, inactivates p53 by binding and stabilizing TRIM28 mRNA
Open the record for dataset details and reuse information.
Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
Open the record for dataset details and reuse information.
Data from: Ovarian BDNF promotes survival, migration, and attachment of tumor precursors originated from p53 mutant fallopian tube epithelial cells
<p class="CxSpFirst"><span>High-grade serous ovarian carcinoma (HGSOC) is the most lethal gynecological malignancy. New evidence supports a hypothesis that HGSOC can originate from fallopian tube epithelium (FTE). It is unclear how genetic alterations and pathophysiological processes drive the progression of FTE tumor precursors into widespread HGSOCs. In this study, we uncovered that brain-derived neurotrophic factor (BDNF) in the follicular fluid stimulates the tropomyosin receptor kinase B (TrkB)-expressing FTE cells to promote their survival, migration, and attachment. Using <i>in vitro</i> and <i>in vivo</i> models, we further identified that the acquisition of common TP53 gain-of-function (GOF) mutations in FTE cells led to enhanced BDNF/TrkB signaling comparing to that of FTE cells with <i>TP53</i> loss-of-function (LOF) mutations. Different mutant p53 proteins can either increase TrkB transcription or enhance TrkB endocytic recycling. Our findings have demonstrated possible interplays between genetic alterations in FTE tumor precursors (i.e., p53 gain-of-function mutations) and pathophysiological processes (i.e., the release of follicular fluid upon ovulation) during the initiation of HGSOC from the fallopian tube. Our data revealed molecular events underlying the link between HGSOC tumorigenesis and ovulation, a physiological process that has been associated with risk factors of HGSOC. </span></p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.