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#33639194   2021/02/24 To Up

Research progress in use of traditional Chinese medicine monomer for treatment of non-alcoholic fatty liver disease.

With the improvement of people's living standards and the change of eating habits, non-alcoholic fatty liver disease (NAFLD) has gradually become one of the most common chronic liver diseases in the world. However, there are no effective drugs for the treatment of NAFLD. Therefore, it is urgent to find safe, efficient, and economical anti-NAFLD drugs. Compared with western medicines that possess fast lipid-lowering effect, traditional Chinese medicines (TCM) have attracted increasing attention for the treatment of NAFLD due to their unique advantages such as multi-targets and multi-channel mechanisms of action. TCM monomers have been proved to treat NAFLD through regulating various pathways, including inflammation, lipid production, insulin sensitivity, mitochondrial dysfunction, autophagy, and intestinal microbiota. In particular, peroxisome proliferator-activated receptor α (PPAR-α), sterol regulatory element-binding protein 1c (SREBP-1c), nuclear transcription factor kappa (NF-κB), phosphoinositide 3-kinase (PI3K), sirtuin1 (SIRT1), AMP-activated protein kinase (AMPK), p53 and nuclear factor erythroid 2-related factor 2 (Nrf2) are considered as important molecular targets for ameliorating NAFLD by TCM monomers. Therefore, by searching PubMed, Web of Science and SciFinder databases, this paper updates and summarizes the experimental and clinical evidence of TCM monomers for the treatment of NAFLD in the past six years (2015-2020), thus providing thoughts and prospects for further exploring the pathogenesis of NAFLD and TCM monomer therapies.
Honglin Zhou, Cheng Ma, Cheng Wang, Lihong Gong, Yafang Zhang, Yunxia Li

2032 related Products with: Research progress in use of traditional Chinese medicine monomer for treatment of non-alcoholic fatty liver disease.

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#33638942   2021/02/01 To Up

Cancer clocks in tumourigenesis: the p53 pathway and beyond.

Circadian rhythms regulate a vast array of physiological and cellular processes, as well as the hormonal milieu, to keep our cells synchronised to the light-dark cycle. Epidemiologic studies have implicated circadian disruption in the development of breast and other cancers, and numerous clock genes are dysregulated in human tumours. Here we review the evidence that circadian rhythms, when altered at the molecular level, influence cancer growth. We also note some common pitfalls in circadian-cancer research and how they might be avoided to maximise comparable results and minimise misleading data. Studies of circadian gene mutant mice, and human cancer models in vitro and in vivo, demonstrate that clock genes can impact tumourigenesis. Clock genes influence important cancer related pathways, ranging from p53-mediated apoptosis to cell cycle progression. Confusingly, clock dysfunction can be both pro- or anti- tumourigenic in a model and cell type specific manner. Due to this duality, there is no canonical mechanism for clock interaction with tumourigenic pathways. To understand the role of the circadian clock in patients' tumours requires analysis of the molecular clock status compared to healthy tissue. Novel mathematical approaches are under development, but this remains largely aspirational, and is hampered by a lack of temporal information in publicly available datasets. Current evidence broadly supports the notion that the circadian clock is important for cancer biology. More work is necessary to develop an overarching model of this connection. Future studies would do well to analyse the clock network in addition to alterations in single clock genes.
Ewan Michael Stephenson, Laura Emma Jane Usselmann, Vinay Tergaonkar, David Virshup, Robert Dallmann

2562 related Products with: Cancer clocks in tumourigenesis: the p53 pathway and beyond.

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#33638320   2021/02/08 To Up

Voluntary exercise improves sperm parameters in high fat diet receiving rats through alteration in testicular oxidative stress, mir-34a/SIRT1/p53 and apoptosis.

High fat diet can lead to testicular structural and functional disturbances, spermatogenesis disorders as well as infertility. So, the present investigation was proposed to clarify whether voluntary exercise could prevent high fat diet induced reproductive complications in rats through testicular stress oxidative and apoptosis.
Hamed Heydari, Rafighe Ghiasi, Gholamreza Hamidian, Saber Ghaderpour, Rana Keyhanmanesh

1679 related Products with: Voluntary exercise improves sperm parameters in high fat diet receiving rats through alteration in testicular oxidative stress, mir-34a/SIRT1/p53 and apoptosis.

4 Arrays/Slide2 Pieces/Box2 Pieces/Box2 Pieces/Box4 Membranes/Box4 Arrays/Slide96 wells (1 kit)4 Membranes/Box2 Pieces/Box4 Membranes/Box2 Pieces/Box100ul

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#33638205   2021/02/26 To Up

The foggy world(s) of p63 isoform regulation in normal cells and cancer.

The p53-family member, p63, exists as two major protein variants (TAp63 and ΔNp63) with distinct expression patterns and functional properties. Whilst downstream target genes of p63 have been studied intensively, how p63 variants are themselves controlled has been relatively neglected. Here, we review advances in understanding ΔNp63 and TAp63 regulation, highlighting their distinct pathways. TAp63 has roles in senescence and metabolism, and in germ cell genome maintenance, where it is activated post-transcriptionally by phosphorylation cascades after DNA damage. The function and regulation of TAp63 in mesenchymal and haematopoietic cells is less clear but may involve epigenetic control through DNA methylation. ΔNp63 functions to maintain stem/progenitor cells in various epithelia and is overexpressed in squamous and certain other cancers. ΔNp63 is transcriptionally regulated through multiple enhancers in concert with chromatin modifying proteins. Many signalling pathways including growth factors, morphogens, inflammation and the extracellular matrix influence ΔNp63 levels, with inconsistent results reported. There is also evidence for reciprocal regulation, including ΔNp63 activating its own transcription. ΔNp63 is downregulated during cell differentiation through transcriptional regulation, while post-transcriptional events cause proteasomal degradation. Throughout the review, we identify knowledge gaps and highlight discordances, providing potential explanations including cell-context and cell-matrix interactions. Identifying individual p63 variants has roles in differential diagnosis and prognosis, and understanding their regulation suggests clinically approved agents for targeting p63 that may be useful combination therapies for selected cancer patients. This article is protected by copyright. All rights reserved.
Zuzana Pokorná, Jan Vysloužil, Václav Hrabal, Bořivoj Vojtěšek, Philip J Coates

2141 related Products with: The foggy world(s) of p63 isoform regulation in normal cells and cancer.



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#33637564   2021/02/26 To Up

The Common Germline TP53-R337H Mutation is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model.

The TP53-R337H founder mutation exists at a high frequency throughout southern Brazil and represents one of the most common germline TP53 mutations reported to date. It was identified in pediatric adrenocortical tumors in families with a low incidence of cancer. The R337H mutation has since been found in association with early-onset breast cancers and Li-Fraumeni syndrome (LFS). To study this variability in tumor susceptibility, we generated a knockin mutant p53 mouse model (R334H). Endogenous murine p53-R334H protein was naturally expressed at high levels in multiple tissues and was functionally compromised in a tissue- and stress-specific manner. Mutant p53-R334H mice developed tumors with long latency and incomplete penetrance, consistent with many human carriers being at a low but elevated risk for cancer. These findings suggest the involvement of additional cooperating genetic alterations when TP53-R337H occurs in the context of LFS, which has important implications for genetic counseling and long-term clinical follow up.
John R Jeffers, Emilia M Pinto, Jerold E Rehg, Michael R Clay, Jinling Wang, Geoffrey Neale, Richard J Heath, Guillermina Lozano, Enzo Lalli, Bonald C Figueiredo, Alberto S Pappo, Carlos Rodriguez-Galindo, Wenan Chen, Stanley Pounds, Raul C Ribeiro, Gerard P Zambetti

1321 related Products with: The Common Germline TP53-R337H Mutation is Hypomorphic and Confers Incomplete Penetrance and Late Tumor Onset in a Mouse Model.

50 ul100 ug0.1ml (1mg/ml)100ug Lyophilized100 ul100ug Lyophilized100ug Lyophilized0.1ml100ug Lyophilized

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#33636337   2021/02/23 To Up

Oxidative stress induces downregulation of TP53INP2 and suppresses osteogenic differentiation of BMSCs during osteoporosis through the autophagy degradation pathway.

Oxidative stress plays an important role in the pathogenesis of osteoporosis and impaired bone formation. However, the mechanisms behind which oxidative stress represses bone formation remains unclear. TP53INP2, a target of the tumor suppressor p53, is ubiquitously expressed in various cell types including BMSCs and contributes to autophagosome formation by recruiting ubiquitinated substrates to autophagosomes for degradation. However, little is known about its function in BMSCs and its relation to osteoporosis. In this study, first, we verified that the expression of TP53INP2 was persistently decreased in BMSCs derived from osteoporosis patients and OVX mice, and that the antioxidant N-acetylcysteine could ameliorate this decreased TP53INP2 level in vitro. Second, we identified that the mRNA and protein levels of TP53INP2 decreased in BMSCs under HO induced oxidative stress in a dose-dependent manner, with resultant co-location of LC3 and TP53INP2. Additionally, the autophagy-lysosome system was involved in the degradation process of TP53INP2 and applying autophagy inhibitors (Baf-A1) could significantly increase the TP53INP2 levels in murine and human BMSCs under oxidative stress. Third, gain- and loss-of-function assays revealed that knockdown of TP53INP2 inhibited osteogenic differentiation of BMSCs, while overexpression of TP53INP2 promoted osteogenic differentiation of BMSCs in vitro. Further analysis demonstrated that TP53INP2 promoted osteogenic differentiation of BMSCs by activating Wnt/β-cantenin signaling. DKK1, an inhibitor of Wnt signaling, resulted in osteogenic defects of BMSCs that had over-expressed TP53INP2. Lithium, a Wnt/β-catenin activator, improved the mineralization ability in TP53INP2-knockdown BMSCs. Moreover, restoring TP53INP2 levels recovered OVX-derived BMSCs osteogenic differentiation and attenuated bone loss in OVX mice. Taken together, our study indicated that oxidative stress-induced downregulation of TP53INP2 suppressed osteogenic differentiation of BMSCs during osteoporosis and was mediated by the autophagy degradation pathway. These findings may introduce a novel therapeutic target for osteoporosis.
Yuehua Yang, Yuan Sun, Wei-Wei Mao, Haonan Zhang, Binbin Ni, Leisheng Jiang

1907 related Products with: Oxidative stress induces downregulation of TP53INP2 and suppresses osteogenic differentiation of BMSCs during osteoporosis through the autophagy degradation pathway.

24 wells16 5 G100ug Lyophilized50 mg1200 2 Pieces/Box25 mg1mg

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#33635505   2021/02/26 To Up

(+)-Usnic acid modulates the Nrf2-ARE pathway in FaDu hypopharyngeal carcinoma cells.

Naturally occurring phytochemicals of different origin and structure, arctigenin, bergenin, usnic acid and xanthohumol, were shown to affect Nrf2 pathway in the context of various diseases, but their effect on this pathway in cancer cells was not extensively investigated. This study aimed to evaluate the effect of these compounds on Nrf2 expression and activation in hypopharyngeal FaDu squamous cell carcinoma cells. FaDu cells were treated with 2 or 10 μM arctigenin, bergenin, (+)-usnic acid or xanthohumol for 24 h. While arctigenin, bergenin, and xanthohumol did not affect either Nrf2 expression or activation, (+)-usnic acid treatment increased its transcript level and increased the nuclear/cytosol Nrf2 protein ratio-the measure of Nrf2 pathway activation. Consequently, (+)-usnic acid enhanced the transcription and translation of Nrf2 target genes: NQO1, SOD, and to a lesser extent, GSTP. The treatment of FaDu cells with (+)-usnic acid decreased both GSK-3β transcript and protein level, indicating its possible involvement in Nrf2 activation. All the tested compounds decreased Bax mRNA but did not change the level of Bax protein. (+)-Usnic acid tended to increase the percentage of early apoptotic cells and LC3 protein, autophagy marker. Significant induction of p53 also was observed after treatment with (+)-usnic acid. In summary, the results of this study indicate that low concentrations of (+)-usnic acid activate Nrf2 transcription factor, most probably as a result of ROS accumulation, but do not lead to FaDu hypopharyngeal carcinoma cells death.
Violetta Krajka-Kuźniak, Jarosław Paluszczak, Robert Kleszcz, Wanda Baer-Dubowska

1758 related Products with: (+)-Usnic acid modulates the Nrf2-ARE pathway in FaDu hypopharyngeal carcinoma cells.

100 µg1.5x10(6) cells500 MG100ug Lyophilized2 Pieces/Box 1 G2 Pieces/Box100 μg

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