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Food Interactions, Sirtuins, Genes, Homeostasis, and General Discussion
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
In 1997, two other proteins, p63 and p73, were identified beside p53 protein (124, 130). The p53 family consists of three proteins – p53, p63, and p73 – that are homologous at the amino acid level in the three primary domains of p53: transactivation domain, DNA-binding domain, and C-terminal oligomerization domain (124). p53, p63, and p73 have their own unique functions (130).
Black Cumin: A Review of Phytochemistry, Antioxidant Potential, Extraction Techniques, and Therapeutic Perspectives
Published in Megh R. Goyal, Durgesh Nandini Chauhan, Plant- and Marine-Based Phytochemicals for Human Health, 2018
Muhammad Jawad Iqbal, Masood Sadiq Butt, Hafiz Ansar Rasul Suleria
Besides, TQ treatment has proved efficient to check various cancer cells. It performs the antiproliferative action due to its ability to induce apoptosis, arrests the cells in G1 phase, and reduces metastasis and angiogenesis. Moreover, it modulates the activity of various expressions such as p53, p73, PTEN, STAT3, PPAR-G, and activates the caspases 3, 6, and 8 for apoptosis induction.
Transport of mRNA into the Cytoplasm
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
Werner E. G. Müller, Paul S. Agutter, Heinz C. Schröder
The hnRNA is bound to a specific set of proteins to form hnRNP particles with sedimentation coefficients of 200 to 300 S.105 The poly(A) sequence is also protected against attack by endoribonuclease IV through specific poly(A)-binding proteins.106–111 By selective radiolabeling of the protein components in the polysomal poly(A)-RNP from L5l78y mouse lymphoma cells with [3H]dansyl chloride, two protein species of Mr. 77,000 (p77) and 54,000 (p54) have been identified by Bernd et al.109 A quantitative analysis revealed that the poly(A)-RNP complex is composed of 3.7 molecules of p54 and 1.9 molecules of p77 per 155 AMP residues. Digestion experiments with ribonuclease A indicated that p54 covers 15 to 20 AMP residues and p77 a sequence of 40 to 45 nucleotides on the poly(A)155 stretch of L5l78y cell poly(A)-RNP. Using different approaches. Adams et al.107 reported that a 45-nucleotide tract is covered by the poly(A)-associated proteins, while Baer and Kornberg112 found fragments of 22 AMP units. Van Eekelen et al.114 demonstrated that p73 was associated with poly(A) in HeLa cell cytoplasm, but not in the nucleus. It was shown that a different protein, p63, is the major poly(A)-associated protein in the nucleus.114
Association of TP73-AS1 gene polymorphisms with the risk and survival of gastric cancer in a Chinese Han Population
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Wangwang Chen, Jian Xiao, Liang Shi, Linling Lin, Mingkun Jiang, Yugang Ge, Zengliang Li, Hao Fan, Li Yang, Zekuan Xu
SPSS (Version 22.0, IBM, Armonk, NY, USA) was performed to analyze the data. Student’s t-tests and χ2 tests were applied to identify differences in demographic variables between the case and control groups. The goodness-of-χ2 test was used to analyze the Hardy-Weinberg equilibrium among control subjects. The relations of alleles/genotypes with GC susceptibility were evaluated by odds ratio (OR) and 95% confidence interval (CI) by using the methods of the unconditional univariate analysis. Adopting 2−ΔCT algorithm, we calculated the relative expression levels of TP73-AS1 in 80 GC tissues. ANOVA was applied to identify the relations of the TP73-AS1 polymorphism with the expression levels of TP73-AS1. Survival curves were calculated by the Kaplan–Meier method, and differences between curves were analyzed by the log-rank test. Mean survival time (MST) was provided because the median survival time could not be figured out. The relation between the SNP and the OS of GC patients was estimated by calculating the hazard ratio (HR) with 95%CI in univariate analyses and adjusted HR with 95%CI in multivariate analyses. P values <.05 was considered to be statistically significant.
Tumor suppression by the EGR1, DMP1, ARF, p53, and PTEN Network
Published in Cancer Investigation, 2018
Kazushi Inoue, Elizabeth A. Fry
The 2nd p73 promoter regulates the expression of a set of isoforms are known as ΔNp73; they lack the same transactivating domain, and, therefore generates effects distinct from those of p53 (99–101, 105). Consistently, many of the roles of ΔNp73 are oncogenic, having distinct set of target genes that can be transcriptionally regulated. Of note, ΔNp73 in not induced by Egr1 (98). Kartasheva et al. (105) examined whether ΔNp73α might modulate cellular transcription in the absence of p53. ΔNp73α increased the expression of EGR1 and CDC6, whereas it decreased the mRNA levels of c-MYC, Cyclin A2, NFκB1, ODC1, and RET finger protein. They concluded that the impact of ΔNp73α on gene expression was not limited to p53-responsive genes. Although the p63 family of gene products that are related to p53 may play a role in tumor suppression, they appear not to be regulated by Egr1. Both the p63 and p73 genes are infrequently mutated in cancers (100) although p53 is mutated in half of human cancers (106). In summary, TAp73 and TAp63 could act in place of p53 in p53-deficient cancer cells when an apoptosis response is required to remove damaged cells.
Inhibition of SF3b1 by pladienolide B evokes cycle arrest, apoptosis induction and p73 splicing in human cervical carcinoma cells
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Qianjing Zhang, Cuixia Di, Junfang Yan, Fang Wang, Tao Qu, Yupei Wang, Yuhong Chen, Xuetian Zhang, Yang Liu, Hongying Yang, Hong Zhang
One striking finding is that SF3b1 knockdown led to activation of p53 pathway [37]. p73 is homologue of the tumour suppressor p53, which functions as a transcriptional factor [38]. The p73 locus encodes two types of transcription factors: full-length pro-apoptotic isoforms (TAp73), and N-terminally truncated anti-apoptotic proteins (ΔNp73) [31]. Christine et al. showed that Tap73 could, at least when overproduced, activate the transcription of p53-responsive genes and inhibit cell growth in a p53-like manner by inducing apoptosis (programmed cell death) [39]. However, ΔNp73 are able to bind to DNA and to form dimers with TAp73, thereby behaving as dominant negative, anti-apoptotic factors [40]. Indeed, many in vitro and in vivo evidences demonstrated that the Tap73 was a pro-apoptotic isoform and ΔNp73 was an anti-apoptotic isoform. Recently, some studies showed that the ratio between Tap73 and ΔNp73 determined the fate of the cell-survive or die [41]. Our previous study showed that carbon beams unregulated the ratio of Tap73/np73, and the combination of the radiation and diallyl disulphide induced higher ratio of Tap73/ΔNp73 in HeLa cells [30]. Interestingly, administration with diallyl disulphide in mouse testis prevented radiation-induced Tap73/ΔNp73 expression and consequently down regulated p53 responsive genes [29]. Although there is ample evident that the p73 is associated with apoptosis, the ratio between Tap73 and ΔNp73 involved in SF3b1-induced apoptosis in human cervical carcinoma cells remains unclear. In the study, our results showed that pladienolide B treatment obviously induced increase in the Tap73/ΔNp73 ratio, indicating that administration with pladienolide B induced apoptosis in p73 dependent manner.