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P73 protein

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https://www.readbyqxmd.com/read/29662640/potential-therapeutic-targets-of-tp53-gene-in-the-context-of-its-classically-canonical-functions-and-its-latest-non-canonical-functions-in-human-cancer
#1
REVIEW
Toshimichi Tanaka, Masahiko Watanabe, Keishi Yamashita
In normal tissue, p53 protein has a wide range of functions involving cell homeostasis; its mutation, however, permits a carcinogenic acquisition of function. TP53 gene mutation is a major genomic aberration in various human cancers and is a critical event in the multi-step carcinogenesis process. TP53 mutation is clinically relevant for the molecular classification of carcinogenesis, as most recently described rigorously by the Cancer Genome Atlas Research Network. TP53 gene mutation has been considered to work as a tumor suppressor gene through the loss of its transcriptional activity, which is designated as a canonical function...
March 23, 2018: Oncotarget
https://www.readbyqxmd.com/read/29628507/%C3%AE-np73-enhances-hif-1%C3%AE-protein-stability-through-repression-of-the-ecv-complex
#2
Marina Stantic, Johanna Wolfsberger, Habib A M Sakil, Margareta T Wilhelm
Cellular responses to low oxygen conditions are mainly regulated by the Hypoxia-inducible factors (HIFs). Induction of HIF-1α in tumor cells activates the angiogenic switch and allows for metabolic adaptations. HIF-1α protein levels are tightly regulated through ubiquitin-mediated proteosomal degradation; however, high levels of HIF-1α is a common feature in many solid tumors and is thought to enhance cancer cell proliferation, migration, and survival. Here, we report that the oncogenic p73 isoform, ∆Np73, increases HIF-1α protein stability...
April 9, 2018: Oncogene
https://www.readbyqxmd.com/read/29620203/inhibition-of-dna%C3%A2-pk-activity-sensitizes-a549-cells-to-x%C3%A2-ray-irradiation-by-inducing-the-atm%C3%A2-dependent-dna-damage-response
#3
Lina Yang, Xinrui Yang, Yiwei Tang, Defu Zhang, Lijie Zhu, Shengnan Wang, Bo Wang, Tao Ma
Non‑small cell lung cancer (NSCLC) is radioresistant to X‑rays due to powerful cellular DNA damage repair mechanisms. DNA‑dependent protein kinase (DNA‑PK) is a key enzyme involved in DNA damage repair and the phenomenon and molecular mechanism of NSCLC radionsensitivity were investigated following inhibition of DNA‑PK activity. In the present study A549 cells were treated with the DNA‑PK inhibitor NU7026 and/or siRNA directed against ataxia telangiectasia mutated (ATM), followed by exposure to 4 Gy X‑ray irradiation...
March 29, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29615516/mutant-and-wild-type-p53-form-complexes-with-p73-upon-phosphorylation-by-the-kinase-jnk
#4
Eric R Wolf, Ciarán P McAtarsney, Kristin E Bredhold, Amber M Kline, Lindsey D Mayo
The transcription factors p53 and p73 are critical to the induction of apoptotic cell death, particularly in response to cell stress that activates c-Jun N-terminal kinase (JNK). Mutations in the DNA-binding domain of p53, which are commonly seen in cancers, result in conformational changes that enable p53 to interact with and inhibit p73, thereby suppressing apoptosis. In contrast, wild-type p53 reportedly does not interact with p73. We found that JNK-mediated phosphorylation of Thr81 in the proline-rich domain (PRD) of p53 enabled wild-type p53, as well as mutant p53, to form a complex with p73...
April 3, 2018: Science Signaling
https://www.readbyqxmd.com/read/29562599/epstein-barr-virus-gene-barf1-expression-is-regulated-by-the-epithelial-differentiation-factor-%C3%AE-np63%C3%AE-in-undifferentiated-nasopharyngeal-carcinoma
#5
Eveline Hoebe, Coral Wille, Stacy Hagemeier, Shannon Kenney, Astrid Greijer, Jaap Middeldorp
Epstein-Barr Virus (EBV) BamHI-A rightward frame 1 (BARF1) protein is considered a viral oncogene in epithelial cells and has immune-modulating properties. During viral lytic replication BARF1 is expressed as an early gene, regulated by the immediate early EBV protein R. However, in viral latency BARF1 is exclusively expressed in epithelial tumors such as nasopharyngeal (NPC) and gastric carcinoma (GC) but not in lymphomas, indicating that activation of the BARF1 promoter is cell type specific. Undifferentiated NPC is characterized by high expression of ΔNp63 isoforms of the epithelial differentiation marker p63, a member of the p53 family of transcription factors...
March 17, 2018: Cancers
https://www.readbyqxmd.com/read/29534752/teriflunomide-promotes-oligodendroglial-differentiation-and-myelination
#6
Peter Göttle, Anastasia Manousi, David Kremer, Laura Reiche, Hans-Peter Hartung, Patrick Küry
BACKGROUND: Multiple sclerosis (MS) is a neuroinflammatory autoimmune disease of the central nervous system (CNS) which in most cases initially presents with episodes of transient functional deficits (relapsing-remitting MS; RRMS) and eventually develops into a secondary progressive form (SPMS). Aside from neuroimmunological activities, MS is also characterized by neurodegenerative and regenerative processes. The latter involve the restoration of myelin sheaths-electrically insulating structures which are the primary targets of autoimmune attacks...
March 13, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29518025/emerging-roles-of-p53-family-members-in-glucose-metabolism
#7
REVIEW
Yoko Itahana, Koji Itahana
Glucose is the key source for most organisms to provide energy, as well as the key source for metabolites to generate building blocks in cells. The deregulation of glucose homeostasis occurs in various diseases, including the enhanced aerobic glycolysis that is observed in cancers, and insulin resistance in diabetes. Although p53 is thought to suppress tumorigenesis primarily by inducing cell cycle arrest, apoptosis, and senescence in response to stress, the non-canonical functions of p53 in cellular energy homeostasis and metabolism are also emerging as critical factors for tumor suppression...
March 8, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29511339/p73-coordinates-with-%C3%AE-133p53-to-promote-dna-double-strand-break-repair
#8
Hongjian Gong, Yuxi Zhang, Kunpeng Jiang, Shengfan Ye, Shuming Chen, Qinghe Zhang, Jinrong Peng, Jun Chen
Tumour repressor p53 isoform Δ133p53 is a target gene of p53 and an antagonist of p53-mediated apoptotic activity. We recently demonstrated that Δ133p53 promotes DNA double-strand break (DSB) repair by upregulating transcription of the repair genes RAD51, LIG4 and RAD52 in a p53-independent manner. However, Δ133p53 lacks the transactivation domain of full-length p53, and the mechanism by which it exerts transcriptional activity independently of full-length p53 remains unclear. In this report, we describe the accumulation of high levels of both Δ133p53 and p73 (a p53 family member) at 24 h post γ-irradiation (hpi)...
March 6, 2018: Cell Death and Differentiation
https://www.readbyqxmd.com/read/29497314/mir-1180-5p-regulates-apoptosis-of-wilms-tumor-by-targeting-p73
#9
Xiuyun Jiang, Huaicheng Li
Introduction: Wilms' tumor (WT), the most common childhood tumor, occurs in sporadic or familial forms. Recent findings reported that abnormal expression in microRNA (miRNA) suggests an important role of miRNAs during WT progress. MiRNAs are endogenous short-chain noncoding RNAs, which have been reported as key biomarkers for detecting tumor onset and progression. However, the functional role of miR-1180 in WT has remained unknown. Materials and methods: MTT and clonogenic survival assays were used to detect WT cell proliferation...
2018: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29458146/enhanced-anticancer-effects-of-scutellaria-barbata-d-don-in-combination-with-traditional-chinese-medicine-components-on-non-small-cell-lung-cancer-cells
#10
Qian Wang, Narayan Acharya, Zhongwei Liu, Xianmei Zhou, Meghan Cromie, Jia Zhu, Weimin Gao
ETHNOPHARMACOLOGICAL RELEVANCE: Experience-based herbal medicine as a complementary to modern western medicine has triggered an array of studies in quest of novel anticancer drugs. Scutellaria barbata D. Don (SB) is commonly used to treat different types of cancers, but its molecular mechanism of action is not clearly understood. In this study, we attempted to elucidate the mode of action of a traditional Chinese medicine prescription with a total of 14 components, named Lian-Jia-San-Jie-Fang (LJSJF, in Chinese), where SB works as the "principle" against non-small cell lung cancer (NSCLC) cells...
February 16, 2018: Journal of Ethnopharmacology
https://www.readbyqxmd.com/read/29452959/differential-expressions-of-mdm2-and-tap73-in-cancer-and-cancer-adjacent-tissues-in-patients-with-non-small-cell-lung-carcinoma
#11
B Wang, X Liu, H Liu, J Guo, T Zhang, N Zhou, Y Ma, H Yu, L Chen, Z Ren, K Fan, X Tian
AIM: To investigate the differences in mRNA and protein expressions of MDM2 (mouse double minute 2 homolog) and P73 in cancer and cancer-adjacent tissues in patients with non-small-cell lung carcinoma (NSCLC). MATERIALS AND METHODS: We compared the protein expressions of MDM2 and P73 in lung cancer and cancer-adjacent tissues in NSCLC patients by IHC (immunohistochemistry) and WB (Western blot). We divided the NSCLC patients into two subgroups, adenocarcinoma and squamous carcinoma...
February 13, 2018: Revista Portuguesa de Pneumologia
https://www.readbyqxmd.com/read/29434772/transcription-activated-p73-modulated-cyclin-d1-expression-leads-to-doxorubicin-resistance-in-gastric-cancer
#12
Zhi-Peng Ji, Ling Qiang, Jian-Liang Zhang
Gastric cancer (GC) is one of the leading types of cancer in terms of mortality cases worldwide. Doxorubicin (Dox), a common chemotherapy drug, is frequently used to treat GC; however, acquired resistance to Dox hinders the chemotherapeutic outcome and causes shorter survival in GC patients. Several Dox-resistant GC cell lines, including SGC7901, SNU-1 and SNU-5 were generated to investigate the mechanism of Dox resistance in GC. Various methods were used to test the response of Dox-resistant GC cells and parental cells, including flow cytometry, Cell Counting kit-8 assay, reverse transcription polymerase chain reaction and western blot analysis...
February 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29412778/the-long-noncoding-rna-tp73-as1-interacted-with-mir-124-to-modulate-glioma-growth-by-targeting-inhibitor-of-apoptosis-stimulating-protein-of-p53
#13
Shuai Xiao, Rensheng Wang, Xiangwei Wu, Wen Liu, Shanshan Ma
P73 antisense RNA 1T (non-protein coding), known as TP73-AS1 or PDAM, is a long noncoding RNA (lncRNA), which may regulate apoptosis by regulation of p53-dependent antiapoptotic genes. An abnormal change of TP73-AS1 expression was noticed in cancers. The effects of TP73-AS1 in brain glioma growth and the underlying mechanism remain unclear so far. In this study, the effect of TP73-AS1 in human brain glioma cell lines and clinical tumor samples was detected so as to reveal its role and function. In this study, TP73-AS1 was specifically upregulated in brain glioma cell lines and promoted glioma cell growth through targeting miR-124...
February 2018: DNA and Cell Biology
https://www.readbyqxmd.com/read/29366442/dna-binding-partners-of-yap-taz
#14
Min-Kyu Kim, Ju-Won Jang, Suk-Chul Bae
Hippo signaling plays critical roles in regulation of tissue homeostasis, organ size, and tumorigenesis by inhibiting YES-associated protein (YAP) and PDZ-binding protein TAZ through MST1/2 and LATS1/2 pathway. It is also engaged in cross-talk with various other signaling pathways, including WNT, BMPs, Notch, GPCRs, and Hedgehog to further modulate activities of YAP/TAZ. Because YAP and TAZ are transcriptional coactivators that lack DNA-binding activity, both proteins must interact with DNA-binding transcription factors to regulate target gene's expression...
January 25, 2018: BMB Reports
https://www.readbyqxmd.com/read/29339502/protein-aggregation-of-the-p63-transcription-factor-underlies-severe-skin-fragility-in-aec-syndrome
#15
Claudia Russo, Christian Osterburg, Anna Sirico, Dario Antonini, Raffaele Ambrosio, Julia Maren Würz, Jörg Rinnenthal, Marco Ferniani, Sebastian Kehrloesser, Birgit Schäfer, Peter Güntert, Satrajit Sinha, Volker Dötsch, Caterina Missero
The p63 gene encodes a master regulator of epidermal commitment, development, and differentiation. Heterozygous mutations in the C-terminal domain of the p63 gene can cause ankyloblepharon-ectodermal defects-cleft lip/palate (AEC) syndrome, a life-threatening disorder characterized by skin fragility and severe, long-lasting skin erosions. Despite deep knowledge of p63 functions, little is known about mechanisms underlying disease pathology and possible treatments. Here, we show that multiple AEC-associated p63 mutations, but not those causative of other diseases, lead to thermodynamic protein destabilization, misfolding, and aggregation, similar to the known p53 gain-of-function mutants found in cancer...
January 30, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29307398/p53-and-reproduction
#16
REVIEW
Hey-Joo Kang, Zev Rosenwaks
Tumor protein 53 (TP53) and its related family of p63 and p73 are tumor suppressor genes that regulate cellular activity to enhance longevity. p53 binds to specific response elements in DNA, modulating the transcription of genes that govern the major defenses against tumor growth. Additional members of the p53 family are involved with male and female germ cell survival. Although the majority of studies have focused on p53 as a tumor suppressor gene, little is known about its function in normal cellular processes...
January 2018: Fertility and Sterility
https://www.readbyqxmd.com/read/29295500/decitabine-and-melphalan-fail-to-reactivate-p73-in-p53-deficient-myeloma-cells
#17
Pierre-Samuel Gillardin, Géraldine Descamps, Sophie Maiga, Benoit Tessoulin, Hanane Djamai, Benedetta Lucani, David Chiron, Philippe Moreau, Steven Le Gouill, Martine Amiot, Catherine Pellat-Deceunynck, Agnès Moreau-Aubry
(1) Background: TP53 deficiency remains a major adverse event in Multiple Myeloma (MM) despite therapeutic progresses. As it is not possible to target TP53 deficiency with pharmacological agents, we explored the possibility of activating another p53 family member, p73, which has not been well studied in myeloma. (2) Methods: Using human myeloma cell lines (HMCLs) with normal or abnormal TP53 status, we assessed TP73 methylation and expression. (3) Results: Using microarray data, we reported that TP73 is weakly expressed in 47 HMCLs and mostly in TP53 wild type ( TP53wt ) HMCLs ( p = 0...
December 23, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29274472/protein-phosphatase-2ac%C3%AE-gene-knock-out-results-in-cortical-atrophy-through-activating-hippo-cascade-in-neuronal-progenitor-cells
#18
Bo Liu, Li-Hua Sun, Yan-Fei Huang, Li-Jun Guo, Li-Shu Luo
Protein phosphatase 2ACα (PP2ACα), a vital member of the protein phosphatase family, has been studied primarily as a regulator for the development, growth and protein synthesis of a lot of cell types. Dysfunction of PP2ACα protein results in neurodegenerative disease; however, this finding has not been directly confirmed in the mouse model with PP2ACα gene knock-out. Therefore, in this study presented here, we generated the PP2ACα gene knock-out mouse model by the Cre-loxP targeting gene system, with the purpose to directly observe the regulatory role of PP2ACα gene in the development of mouse's cerebral cortex...
February 2018: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/29260852/targeting-the-prion-like-aggregation-of-mutant-p53-to-combat-cancer
#19
Jerson L Silva, Elio A Cino, Iaci N Soares, Vitor F Ferreira, Guilherme A P de Oliveira
Prion-like behavior of several amyloidogenic proteins has been demonstrated in recent years. Despite having functional roles in some cases, irregular aggregation can have devastating consequences. The most commonly known amyloid diseases are Alzheimer's, Parkinson's, and Transmissible Spongiform Encephalopathies (TSEs). The pathophysiology of prion-like diseases involves the structural transformation of wild-type (wt) proteins to transmissible forms that can convert healthy proteins, generating aggregates. The mutant form of tumor suppressor protein, p53, has recently been shown to exhibit prion-like properties...
January 16, 2018: Accounts of Chemical Research
https://www.readbyqxmd.com/read/29228353/the-roles-of-p53-and-its-family-proteins-p63-and-p73-in-the-dna-damage-stress-response-in-organogenesis-stage-mouse-embryos
#20
Nazem El Husseini, Barbara F Hales
Members of the P53 transcription factor family, P53, P63 and P73, play important roles in normal development and in regulating the expression of genes that control apoptosis and cell cycle progression in response to genotoxic stress. P53 is involved in the DNA damage response pathway that is activated by hydroxyurea in organogenesis-stage murine embryos. The extent to which P63 and P73 contribute to this stress response is not known. To address this question, we examined the roles of P53, P63 and P73 in mediating the response of Trp53-positive and Trp53-deficient murine embryos to a single dose of hydroxyurea (400 mg/kg) on gestational day 9...
December 7, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
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