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P73 protein

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https://www.readbyqxmd.com/read/27889317/the-p53-family-coordinates-wnt-and-nodal-inputs-in-mesendodermal-differentiation-of-embryonic-stem-cells
#1
Qiong Wang, Yilong Zou, Sonja Nowotschin, Sang Yong Kim, Qing V Li, Chew-Li Soh, Jie Su, Chao Zhang, Weiping Shu, Qiaoran Xi, Danwei Huangfu, Anna-Katerina Hadjantonakis, Joan Massagué
In this study, we outline a regulatory network that involves the p53 tumor suppressor family and the Wnt pathway acting together with the TGF-β pathway in mesendodermal differentiation of mouse and human embryonic stem cells. Knockout of all three members, p53, p63, and p73, shows that the p53 family is essential for mesendoderm specification during exit from pluripotency in embryos and in culture. Wnt3 and its receptor Fzd1 are direct p53 family target genes in this context, and induction of Wnt signaling by p53 is critical for activation of mesendodermal differentiation genes...
November 9, 2016: Cell Stem Cell
https://www.readbyqxmd.com/read/27878984/sulforaphane-induced-apoptosis-in-xuanwei-lung-adenocarcinoma-cell-line-xwlc-05
#2
Lan Zhou, Qian Yao, Yan Li, Yun-Chao Huang, Hua Jiang, Chuan-Qiong Wang, Lei Fan
BACKGROUND: Xuanwei district in Yunnan Province has the highest incidence of lung cancer in China, especially among non-smoking women. Cruciferous vegetables can reduce lung cancer risk by prompting a protective mechanism against respiratory tract inflammation caused by air pollution, and are rich in sulforaphane, which can induce changes in gene expression. We investigated the effect of sulforaphane-induced apoptosis in Xuanwei lung adenocarcinoma cell line (XWCL-05) to explore the value of sulforaphane in lung cancer prevention and treatment...
November 23, 2016: Thoracic Cancer
https://www.readbyqxmd.com/read/27866875/p53-and-p73-regulate-apoptosis-but-not-cell-cycle-progression-in-mouse-embryonic-stem-cells-upon-dna-damage-and-differentiation
#3
Hanbing He, Cheng Wang, Qian Dai, Fengtian Li, Johann Bergholz, Zhonghan Li, Qintong Li, Zhi-Xiong Xiao
Embryonic stem cells (ESCs) are fast proliferating cells capable of differentiating into all somatic cell types. In somatic cells, it is well documented that p53 is rapidly activated upon DNA damage to arrest the cell cycle and induce apoptosis. In mouse ESCs, p53 can also be functionally activated, but the precise biological consequences are not well characterized. Here, we demonstrated that doxorubicin treatment initially led to cell-cycle arrest at G2/M in ESCs, followed by the occurrence of massive apoptosis...
November 16, 2016: Stem Cell Reports
https://www.readbyqxmd.com/read/27865929/g2-m-cell-cycle-arrest-on-ht-29-cancer-cells-and-toxicity-assessment-of-triphenylphosphanegold-i-carbonimidothioates-ph3pau-sc-or-nph-r-me-et-and-ipr-during-zebrafish-development
#4
Kah Kooi Ooi, Chien Ing Yeo, Theventhiran Mahandaran, Kok Pian Ang, Abdah Md Akim, Yoke-Kqueen Cheah, Hoi-Ling Seng, Edward R T Tiekink
Phosphanegold(I) thiolates, Ph3PAu[SC(OR)=NPh], R=Me (1), Et (2) and iPr (3), were previously shown to be significantly cytotoxic toward HT-29 cancer cells and to induce cell death by both intrinsic and extrinsic apoptotic pathways whereby 1 activated the p73 gene, and each of 2 and 3 activated p53; 2 also caused apoptotic cell death via the c-Jun N-terminal kinase/mitogen-activated protein kinase pathway. Apoptosis pathways have been further evaluated by mitochondrial cytochrome c measurements and annexin V screening, confirming apoptotic pathways of cell death...
November 4, 2016: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/27832139/a-subpopulation-of-the-k562-cells-are-killed-by-curcumin-treatment-after-g2-m-arrest-and-mitotic-catastrophe
#5
Macario Martinez-Castillo, Raul Bonilla-Moreno, Leticia Aleman-Lazarini, Marco Antonio Meraz-Rios, Lorena Orozco, Leticia Cedillo-Barron, Emilio J Cordova, Nicolas Villegas-Sepulveda
Curcumin is extensively investigated as a good chemo-preventive agent in the development of many cancers and particularly in leukemia, including treatment of chronic myelogenous leukemia and it has been proposed as an adjuvant for leukemia therapies. Human chronic myeloid leukemia cells (K562), were treated with 20 μM of curcumin, and we found that a subpopulation of these cells were arrested and accumulate in the G2/M phase of the cell cycle. Characterization of this cell subpopulation showed that the arrested cells presented nuclear morphology changes resembling those described for mitotic catastrophe...
2016: PloS One
https://www.readbyqxmd.com/read/27825141/p73-expression-is-regulated-by-ribosomal-protein-rpl26-through-mrna-translation-and-protein-stability
#6
Min Zhang, Jin Zhang, Wensheng Yan, Xinbin Chen
p73, a p53 family tumor suppressor, is regulated by multiple mechanisms, including transcription and mRNA and protein stability. However, whether p73 expression is regulated via mRNA translation has not been explored. To test this, we examined whether ribosomal protein 26 (RPL26) plays a role in p73 expression. Here, we showed that p73 expression is controlled by RPL26 via protein stability and mRNA translation. To examine whether MDM2 mediates RPL26 to regulate p73 protein stability, we generated multiple MDM2-knockout cell lines by CRISPR-cas9...
November 4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27807512/lipopolysaccharide-induces-human-pulmonary-micro-vascular-endothelial-apoptosis-via-the-yap-signaling-pathway
#7
Lei Yi, Xiaoqin Huang, Feng Guo, Zengding Zhou, Mengling Chang, Jiajun Tang, Jingning Huan
Gram-negative bacterial lipopolysaccharide (LPS) induces a pathologic increase in lung vascular leakage under septic conditions. LPS-induced human pulmonary micro-vascular endothelial cell (HPMEC) apoptosis launches and aggravates micro-vascular hyper-permeability and acute lung injury (ALI). Previous studies show that the activation of intrinsic apoptotic pathway is vital for LPS-induced EC apoptosis. Yes-associated protein (YAP) has been reported to positively regulate intrinsic apoptotic pathway in tumor cells apoptosis...
2016: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/27716744/mechanism-of-tap73-inhibition-by-%C3%AE-np63-and-structural-basis-of-p63-p73-hetero-tetramerization
#8
Jakob Gebel, Laura M Luh, Daniel Coutandin, Christian Osterburg, Frank Löhr, Birgit Schäfer, Ann-Sophie Frombach, Manuela Sumyk, Lena Buchner, Tobias Krojer, Eidarus Salah, Sebastian Mathea, Peter Güntert, Stefan Knapp, Volker Dötsch
Members of the p53 tumor-suppressor family are expressed as multiple isoforms. Isoforms with an N-terminal transactivation domain are transcriptionally active, while those ones lacking this domain often inhibit the transcriptional activity of other family members. In squamous cell carcinomas, the high expression level of ΔNp63α inhibits the tumor-suppressor function of TAp73β. This can in principle be due to blocking of the promoter or by direct interaction between both proteins. p63 and p73 can hetero-oligomerize through their tetramerization domains and a hetero-tetramer consisting of two p63 and two p73 molecules is thermodynamically more stable than both homo-tetramers...
December 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27622714/crocetin-exploits-p53-induced-death-domain-pidd-and-fas-associated-death-domain-fadd-proteins-to-induce-apoptosis-in-colorectal-cancer
#9
Pallab Ray, Deblina Guha, Juni Chakraborty, Shuvomoy Banerjee, Arghya Adhikary, Samik Chakraborty, Tanya Das, Gaurisankar Sa
Tumor suppressor p53 preserves the genomic integrity by restricting anomaly at the gene level. The hotspots for mutation in half of all colon cancers reside in p53. Hence, in a p53-mutated cellular milieu targeting cancer cells may be achievable by targeting the paralogue(s) of p53. Here we have shown the effectiveness of crocetin, a dietary component, in inducing apoptosis of colon cancer cells with varying p53 status. In wild-type p53-expressing cancer cells, p53 in one hand transactivates BAX and in parallel up-regulates p53-induced death domain protein (PIDD) that in turn cleaves and activates BID through caspase-2...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27600721/aggregation-tendencies-in-the-p53-family-are-modulated-by-backbone-hydrogen-bonds
#10
Elio A Cino, Iaci N Soares, Murilo M Pedrote, Guilherme A P de Oliveira, Jerson L Silva
The p53 family of proteins is comprised of p53, p63 and p73. Because the p53 DNA binding domain (DBD) is naturally unstable and possesses an amyloidogenic sequence, it is prone to form amyloid fibrils, causing loss of functions. To develop p53 therapies, it is necessary to understand the molecular basis of p53 instability and aggregation. Light scattering, thioflavin T (ThT) and high hydrostatic pressure (HHP) assays showed that p53 DBD aggregates faster and to a greater extent than p63 and p73 DBDs, and was more susceptible to denaturation...
2016: Scientific Reports
https://www.readbyqxmd.com/read/27599791/sh003-selectively-induces-p73%C3%A2-dependent-apoptosis-in-triple%C3%A2-negative-breast-cancer-cells
#11
Eun Kyoung Choi, Seung-Mi Kim, Seung-Woo Hong, Jai-Hee Moon, Jae-Sik Shin, Jeong Hee Kim, Ih-Yeon Hwang, Soo-A Jung, Dae-Hee Lee, Eun Young Lee, Seul Lee, Hyunwoo Kim, Daejin Kim, Yeong Seok Kim, Youn Kyung Choi, Hyo In Kim, Hyeong Sim Choi, Sung-Gook Cho, Jeong Eun Kim, Kyu Pyo Kim, Yong Sang Hong, Won Keun Lee, Jung Shin Lee, Tae Won Kim, Seong-Gyu Ko, Dong-Hoon Jin
Triple-negative breast cancer (TNBC) is a breast cancer subtype that has an aggressive phenotype, is highly metastatic, has limited treatment options and is associated with a poor prognosis. In addition, metastatic TNBC has no preferred standard chemotherapy due to resistance to anthracyclines and taxanes. The present study demonstrated that a herbal extract, SH003, reduced cell viability and induced apoptosis in TNBC without cell cytotoxicity. Cell viability was examined using trypan blue exclusion and colony formation assays, which revealed a decrease in the cell viability...
October 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27588182/dna-methylation-and-leukemia-susceptibility-in-china-evidence-from-an-updated-meta-analysis
#12
Danjie Jiang, Yirun Li, Qingxiao Hong, Yusheng Shen, Chunjing Xu, Yan Xu, Huangkai Zhu, Dongjun Dai, Guifang Ouyang, Shiwei Duan
Mounting evidence supports a role for DNA methylation in the pathogenesis of leukemia; however, there no overview of these results in the Chinese population. The present study performed a comprehensive meta-analysis to establish candidate genes with an altered methylation status in Chinese leukemia patients. Eligible studies were identified through searching the National Center of Biotechnology Information PubMed and Wanfang databases. Studies were pooled and overall odds ratios with corresponding confidence intervals were calculated...
September 2016: Molecular and Clinical Oncology
https://www.readbyqxmd.com/read/27549118/aggregation-and-prion-like-properties-of-misfolded-tumor-suppressors-is-cancer-a-prion-disease
#13
Danielly C F Costa, Guilherme A P de Oliveira, Elio A Cino, Iaci N Soares, Luciana P Rangel, Jerson L Silva
Prion diseases are disorders that share several characteristics that are typical of many neurodegenerative diseases. Recently, several studies have extended the prion concept to pathological aggregation in malignant tumors involving misfolded p53, a tumor-suppressor protein. The aggregation of p53 and its coaggregation with p53 family members, p63 and p73, have been shown. Certain p53 mutants exert a dominant-negative regulatory effect on wild-type (WT) p53. The basis for this dominant-negative effect is that amyloid-like mutant p53 converts WT p53 into an aggregated species, leading to a gain-of-function (GoF) phenotype and the loss of its tumor-suppressor function...
October 3, 2016: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/27533450/prima-1-targets-the-vulnerability-of-multiple-myeloma-of-deregulated-protein-homeostasis-through-the-perturbation-of-er-stress-via-p73-demethylation
#14
Phaik Ju Teoh, Chonglei Bi, Chirackal Sintosebastian, Liang Seah Tay, Rafael Fonseca, Wee Joo Chng
Despite therapeutic advancement, multiple myeloma (MM) remains incurable with drug resistance being one of the main challenges in the clinic. Myeloma cells possess high protein secretory load, leading to increased intracellular endoplasmic reticulum (ER) stress. Hence, they are vulnerable to further perturbation to its protein homeostasis. In studying the therapeutic mechanism of PRIMA-1 (mutant-p53-reactivating-agent), we uncovered its novel p53-independent-mechanism that can be exploited for myeloma. Despite its inability in restoring the wild type-p53 protein conformation and transcriptional function in the mutant-p53-human-myeloma-cells, PRIMA-1 was efficacious against myeloma cells with differential p53 genotypes...
August 12, 2016: Oncotarget
https://www.readbyqxmd.com/read/27486986/mirna-193a-5p-repression-of-p73-controls-cisplatin-chemoresistance-in-primary-bone-tumors
#15
Camille Jacques, Lidia Rodriguez Calleja, Marc Baud'huin, Thibaut Quillard, Dominique Heymann, François Lamoureux, Benjamin Ory
Osteosarcoma and Ewing Sarcoma are the two most common types of Bone Sarcomas, principally localized at the long bones of the extremities and mainly affecting adolescents and young adults. Cisplatin is one of the current options in the therapeutic arsenal of drugs available to cure these aggressive cancers. Unfortunately, chemoresistance against this agent is still a major cause of patient relapse. Thus, a better understanding of the molecular pathways by which these drugs induce cancer cell death, together with a better delineation of the origins of chemoresistance are required to improve the success rate of current treatments...
July 29, 2016: Oncotarget
https://www.readbyqxmd.com/read/27359056/post-translational-deregulation-of-yap1-is-genetically-controlled-in-rat-liver-cancer-and-determines-the-fate-and-stem-like-behavior-of-the-human-disease
#16
Maria M Simile, Gavinella Latte, Maria I Demartis, Stefania Brozzetti, Diego F Calvisi, Alberto Porcu, Claudio F Feo, Maria A Seddaiu, Lucia Daino, Carmen Berasain, Maria L Tomasi, Matias A Avila, Francesco Feo, Rosa M Pascale
Previous studies showed that YAP1 is over-expressed in hepatocellular carcinoma (HCC). Here we observed higher expression of Yap1/Ctgf axis in dysplastic nodules and HCC chemically-induced in F344 rats, genetically susceptible to hepatocarcinogenesis, than in lesions induced in resistant BN rats. In BN rats, highest increase in Yap1-tyr357, p73 phosphorylation and Caspase 3 cleavage occurred. In human HCCs with poorer prognosis (< 3 years survival after partial liver resection, HCCP), levels of YAP1, CTGF, 14-3-3, and TEAD proteins, and YAP1-14-3-3 and YAP1-TEAD complexes were higher than in HCCs with better outcome (> 3 years survival; HCCB)...
June 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/27349281/rip-kinase-mediated-ros-production-triggers-xaf1-expression-through-activation-of-tap73-in-casticin-treated-bladder-cancer-cells
#17
Yoon Hee Chung, Daejin Kim
The p53 family protein p73 plays an important role in apoptosis induced by chemotherapeutic drugs. Transcriptionally active (TA) p73 (TAp73) substitutes for p53 in the response to stress. XIAP associated factor 1 (XAF1) is a novel predictive and prognostic factor in patients with bladder cancer, but the association between TAp73 and XAF1 expression in bladder cancer cells is poorly understood. Here, we investigated the status of TAp73 and XAF1 in T24 bladder cancer cells to identify molecular mechanisms in casticin‑exposed T24 cells...
August 2016: Oncology Reports
https://www.readbyqxmd.com/read/27228340/microrna-1301-mediated-rangap1-downregulation-induces-bcr-abl-nuclear-entrapment-to-enhance-imatinib-efficacy-in-chronic-myeloid-leukemia-cells
#18
Tsung-Yao Lin, Ku-Chung Chen, Hsing-Jin Eugene Liu, Ann-Jeng Liu, Kun-Li Wang, Chwen-Ming Shih
Chronic myeloid leukemia (CML) is a myeloproliferative disease. Imatinib (IM), the first line treatment for CML, is excessively expensive and induces various side effects in CML patients. Therefore, it is essential to investigate a new strategy for improving CML therapy. Our immunoblot data revealed that RanGTPase activating protein 1 (RanGAP1) protein levels increased by approximately 30-fold in K562 cells compared with those in normal cells. RanGAP1 is one of the important components of RanGTPase system, which regulates the export of nuclear protein...
2016: PloS One
https://www.readbyqxmd.com/read/27208086/editor-s-highlight-hydroxyurea-exposure-activates-the-p53-signaling-pathway-in-murine-organogenesis-stage-embryos
#19
Nazem El Husseini, Ava E Schlisser, Barbara F Hales
Hydroxyurea, an anticancer agent and potent teratogen, induces oxidative stress and activates a DNA damage response pathway in the gestation day (GD) 9 mouse embryo. To delineate the stress response pathways activated by this drug, we investigated the effect of hydroxyurea exposure on the transcriptome of GD 9 embryos. Timed pregnant CD-1 mice were treated with saline or hydroxyurea (400 mg/kg or 600 mg/kg) on GD 9; embryonic gene and protein expression were examined 3 h later. Microarray analysis revealed that the expression of 1346 probe sets changed significantly in embryos exposed to hydroxyurea compared with controls; the P53 signaling pathway was highly affected...
August 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/27181203/p27t187a-knockin-identifies-skp2-cks1-pocket-inhibitors-for-advanced-prostate-cancer
#20
H Zhao, Z Lu, F Bauzon, H Fu, J Cui, J Locker, L Zhu
SCF(Skp2/Cks1) ubiquitinates Thr187-phosphorylated p27 for degradation. Overexpression of Skp2 coupled with underexpression of p27 are frequent characteristics of cancer cells. When the role of SCF(Skp2/Cks1)-mediated p27 ubiquitination in cancer was specifically tested by p27 Thr187-to-Ala knockin (p27T187A KI), it was found dispensable for Kras(G12D)-induced lung tumorigenesis but essential for Rb1-deficient pituitary tumorigenesis. Here we identify pRb and p53 doubly deficient (DKO) prostate tumorigenesis as a context in which p27 ubiquitination by SCF(Skp2/Cks1) is required for p27 downregulation...
May 16, 2016: Oncogene
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