China
Africa
Explore chapters and articles related to this topic
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
Effects of HRG and TP73 gene variations on ovarian response
Published in Gynecological Endocrinology, 2022
Kadir Bakay, Ulas Coban, Mehmet Alper Arslan, Davut Guven, Sengul Tural
The purpose of the study is to examine the effects of HRG and TP73 variants on the IVF treatment and particularly on the response to gonadotropin treatment. In light of the recent extensive epidemiological and molecular analyses, it can be stated that p73 plays a critical role in responses to drug therapies and the presence of TP73-dependent polymorphisms, in particular, have impact on the clinical response in drug therapies. In addition, mutations in this gene also have impact on the responses to chemotherapeutic treatments applied in some malignant diseases [8–10]. Due to the reasons mentioned above, through this study, we have aimed at examining the impact of HRG and TP73 gene variations on the gonadotropin treatments administered for ovulation induction, particularly in IVF.
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
Since p73 has been reported to play a crucial role in inducing apoptosis in a p53-independent manner in cancer [29–31], we examined if p73 is involved in pladienolide B -induced apoptosis in human cervical carcinoma cells. Western blot and immunofluorescence were described in our previous published papers [29,30] and applied to analyse the protein expression, respectively. As shown in Figure 4(A), the p73 gene possesses an extrinsic P1 promoter and an intrinsic P2 promoter, resulting in TAp73 and DNp73 isoforms, respectively. We examined the levels of Tap73 and ΔNp73 proteins by western blot analysis, using β-Actin as a control. Levels of Tap73 were strongly increased in HeLa cells at 24 h after different concentration of pladienolide B treatment compared with control group. In contrast, levels of ΔNp73 were slowly decreased. Obviously, pladienolide B induced an increase in the Tap73/ΔNp73 ratio (Figure 4(C)). To verify the expression of Tap73 and ΔNp73 proteins and examine the subcellular localization of these proteins, we next performed immunofluorescent staining. As shown in Figure 4(D), weak fluorescence of Tap73 was detected in the nucleus and cytoplasm, but strong fluorescence of ΔNp73 was detected in the cytoplasm. Consistent with the western blot analysis, Tap73 expression was obviously up-regulated in HeLa cells treated with pladienolide B compared with untreated HeLa cells while ΔNp73 expression was significantly decreased. Thus, inhibition of SF3b1 by pladienolide B up-regulated Tap73 and down-regulated ΔNp73, indicating activation of p53 responsive apoptosis genes.
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.