Visualization and Analysis of Tumor Protein P53 by VMD

2018 ◽  
Vol 13 (2) ◽  
pp. 30-38
Author(s):  
Mohammed I. Jameel ◽  
Arshed H. Yaseen ◽  
Marwan Q. Al-Samarraie
Keyword(s):  
Protein P53 ◽  
Tumor Protein P53

scholarly journals Upregulation of ULK1 expression in PC-3 cells following tumor protein P53 transfection by sonoporation

2015 ◽  
Vol 11 (1) ◽  
pp. 699-704 ◽  
Author(s):  
YU WANG ◽  
YI-NI CHEN ◽  
WEI ZHANG ◽  
YU YANG ◽  
WEN-KUN BAI ◽  
...  
Keyword(s):  
Protein P53 ◽  
Tumor Protein P53

scholarly journals Tumor Protein p53 (TP53) Testing and Li-Fraumeni Syndrome

2013 ◽  
Vol 17 (1) ◽  
pp. 31-47 ◽  
Author(s):  
April D. Sorrell ◽  
Carin R. Espenschied ◽  
Julie O. Culver ◽  
Jeffrey N. Weitzel
Keyword(s):  
Li Fraumeni Syndrome ◽  
Protein P53 ◽  
Tumor Protein P53 ◽  
Li Fraumeni

scholarly journals Significance of tumor protein p53 mutation in cellular process and drug selection in brain lower grade (WHO grades II and III) glioma

2020 ◽  
Vol 14 (12) ◽  
pp. 1139-1150
Author(s):  
Chang-feng Guo ◽  
Yugang Zhuang ◽  
Yuanzhuo Chen ◽  
Sheng Chen ◽  
Hu Peng ◽  
...  
Keyword(s):  
Differentially Expressed Genes ◽  
Tp53 Mutation ◽  
The Cancer Genome Atlas ◽  
Functional Enrichment ◽  
Differentially Expressed ◽  
World Health ◽  
Outcome Analysis ◽  
Lower Grade ◽  
Protein P53 ◽  
Tumor Protein P53

Aim: Tumor protein p53 ( TP53) mutant is one of the most frequently mutated genes in glioma. Results: The Cancer Genome Atlas data has shown that TP53 mutation is present in 49% of lower grade (World Health Organization [WHO] grades II and III) glioma patients. Data from The Genomics of Drug Sensitivity in Cancer database showed that three drugs: (5Z)-7-oxozeaenol, dabrafenib and nutlin-3a (−), have shown more resistance in patients with TP53 mutation. We identified 1100 differentially expressed genes. Functional enrichment analysis showed that the differentially expressed genes are mainly concentrated in the transport of ionic and cancer-related pathways. The top ten hub genes were identified and an outcome analysis revealed the most critical genes related to prognosis. Conclusion: Our results identified the key genes and pathways that might provide the basic proof to improve individualized treatment in patients with glioma.

scholarly journals Assignment of tumor protein p53 induced nuclear protein 1 (TP53INP1) gene to human chromosome band 8q22 by in situ hybridization

2002 ◽  
Vol 97 (1-2) ◽  
pp. 140E-140E ◽  
Author(s):  
J. Nowak ◽  
R. Tomasini ◽  
M.-G. Mattei ◽  
L.A. Azizi Samir ◽  
J.-C. Dagorn ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Human Chromosome ◽  
Nuclear Protein ◽  
Chromosome Band ◽  
Protein P53 ◽  
Tumor Protein P53 ◽  
Human Chromosome Band

scholarly journals The inhibition of tumor protein p53 by microRNA-151a-3p induced cell proliferation, migration and invasion in nasopharyngeal carcinoma

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Haibin Liu ◽  
Yin Cheng ◽  
Yaping Xu ◽  
He Xu ◽  
Zheng Lin ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Nasopharyngeal Carcinoma ◽  
B Cell Lymphoma ◽  
Cell Counting ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Signal Pathways ◽  
P53 Expression ◽  
Protein P53 ◽  
Tumor Protein P53

Abstract A close relation between microRNA-151a-3p (miR-151a-3p) and nasopharyngeal carcinoma (NPC) has been reported, however, the molecular mechanism is still unclear. The aim of the present study was to explore the mechanism in the promotion of miR-151a-3p to NPC progression. The levels of miR-151-3p in several NPC cell lines were detected in order to screen an experimental cell line. MiR-151a-3p mimic and inhibitor were constructed and transfected into 5-8F cells and cell proliferation were detected by Cell Counting Kit-8 (CCK-8). The apoptosis rate, cell migration and invasion were determined by flow cytometry, wound healing and Transwell assays. The predicted target was further verified by luciferase reporter assay. Real-time quantification-PCR and Western blot were carried out for mRNA and protein level analysis. Tumor protein p53 was co-transfected to verify the functions of miR-151a-3p. The miR-151a-3p level in NPC tissues was much higher than that in adjacent tissues. After transfecting cells with miR-151a-3p mimic, the cell proliferation and patients’ survival rate were much increased, and this was accompanied by the increase in B-cell lymphoma 2 (Bcl-2) and decreases in Bax and cleaved caspase-3 (P<0.01). Moreover, the migration rate and number of invaded cells were also remarkably increased, however, the miR-151a-3p inhibitor had opposite effects on the 5-8F cells. Noticeably, p53 was revealed as a potential target of miR-151a-3p. Co-transfection of P53 could partially reverse the promotive effects of miR-151a-3p on NPC cell progression. Our data indicated that blocking p53 expression and mediated signal pathways contribute to the positive effects of miR-151a-3p on NPC cell proliferation, migration and invasion.

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