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https://www.readbyqxmd.com/read/28645193/irf6-regulates-alternative-activation-by-suppressing-ppar%C3%AE-in-male-murine-macrophages
#1
Chuan Li, Wei Ying, Zheping Huang, Tyler Brehm, Andrew Morin, Anthony T Vella, Beiyan Zhou
Aberrant pro-inflammatory and suppressed anti-inflammatory (alternative) macrophage activation underlies the chronic inflammation associated with obesity and other metabolic disorders. This study demonstrates a novel role for Interferon Regulatory Factor 6 (IRF6) in regulating macrophage alternative activation (M2) by suppressing peroxisome proliferator-activated receptor-γ (PPARγ) expression, a critical regulator of alternative macrophage polarization. The data demonstrate suppression of IRF6 in both M2 macrophages and obese adipose tissue macrophages (ATMs)...
June 22, 2017: Endocrinology
https://www.readbyqxmd.com/read/28643015/the-role-of-screening-mri-in-the-era-of-next-generation-sequencing-and-moderate-risk-genetic-mutations
#2
REVIEW
Sarah Macklin, Jennifer Gass, Ghada Mitri, Paldeep S Atwal, Stephanie Hines
With the advent of next-generation sequencing, the ability to rapidly analyze numerous genes simultaneously has led to the creation of large cancer gene panels. Some of these genes, like BRCA1 and BRCA2, have been heavily researched and have well-established management guidelines. Other more newly established genes, like ATM, CHEK2, and PALB2, have previously had less robust research surrounding them which has limited the ability to create accurate risk estimates. With their inclusion on gene panels, there has been more pressure to produce management guidelines for patients discovered to carry pathogenic variants in these genes...
June 22, 2017: Familial Cancer
https://www.readbyqxmd.com/read/28642860/ataxia-telangiectasia-mutated-atm-polymorphisms-and-risk-of-lung-cancer-in-a-chinese-population
#3
Ajay A Myneni, Shen-Chih Chang, Rungui Niu, Li Liu, Baoxing Zhao, Jianping Shi, Xiaoyou Han, Jiawei Li, Jia Su, Shunzhang Yu, Zuo-Feng Zhang, Lina Mu
BACKGROUND: The ataxia telangiectasia-mutated (ATM) gene has a key role in DNA repair including activation and stabilization of p53, which implicates the importance of ATM polymorphisms in the development of cancer. This study aims to investigate the association of two ATM single-nucleotide polymorphisms (SNPs) with lung cancer, as well as their potential interaction with p53 gene and other known risk factors of lung cancer. METHODS: A population-based case-control study was conducted in Taiyuan city, China with 399 cases and 466 controls matched on the distribution of age and sex of cases...
2017: Frontiers in Public Health
https://www.readbyqxmd.com/read/28642277/adipose-tissue-macrophages-develop-from-bone-marrow-independent-progenitors-in-xenopus-laevis-and-mouse
#4
Syed F Hassnain Waqas, Anna Noble, Anh C Hoang, Grace Ampem, Manuela Popp, Sarah Strauß, Matthew Guille, Tamás Röszer
ATMs have a metabolic impact in mammals as they contribute to metabolically harmful AT inflammation. The control of the ATM number may have therapeutic potential; however, information on ATM ontogeny is scarce. Whereas it is thought that ATMs develop from circulating monocytes, various tissue-resident Mϕs are capable of self-renewal and develop from BM-independent progenitors without a monocyte intermediate. Here, we show that amphibian AT contains self-renewing ATMs that populate the AT before the establishment of BM hematopoiesis...
June 22, 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28638267/synergistic-antitumor-effect-of-sorafenib-in-combination-with-atm-inhibitor-in-hepatocellular-carcinoma-cells
#5
Jianhua Liu, Yahui Liu, Lingyu Meng, Bai Ji, Daqing Yang
Background: Currently, sorafenib is the only systemic chemotherapy drug for advanced stage Hepatocellular carcinoma (HCC). However, emerging data from some clinical HCC patients indicate that sorafenib alone has only moderate antitumor efficacy, and could not inhibit disease metastasis and progression. KU-55933 is a specific ATM inhibitor, which has pro-apoptotic effect on tumor cells. In this study, we analyzed the synergistic effect of sorafenib and KU-55933 on the proliferation of HCC cell lines. Methods: Three HCC cell lines were treated with sorafenib and KU-55933 alone or combination in vitro to investigate inhibitory effect by MTT and wound healing assay...
2017: International Journal of Medical Sciences
https://www.readbyqxmd.com/read/28636366/oxygenation-via-c-h-c-c-bond-activation-with-molecular-oxygen
#6
Yu-Feng Liang, Ning Jiao
The selective oxidation of organic molecules is a fundamentally important component of modern synthetic chemistry. In the past decades, direct oxidative C-H and C-C bond functionalization has proved to be one of the most efficient and straightforward methods to synthesize complex products from simple and readily available starting materials. Among these oxidative processes, the use of molecular oxygen as a green and sustainable oxidant has attracted considerable attention because of its highly atom-economical, abundant, and environmentally friendly characteristics...
June 21, 2017: Accounts of Chemical Research
https://www.readbyqxmd.com/read/28635423/inner-retinal-dystrophy-in-a-patient-with-biallelic-sequence-variants-in-brat1
#7
Julius T Oatts, Jacque L Duncan, Creig S Hoyt, Anne M Slavotinek, Anthony T Moore
BACKGROUND: Mutations in the BRCA1-associated protein required for the ataxia telangiectasia mutated (ATM) activation-1 (BRAT1) gene cause lethal neonatal rigidity and multifocal seizure syndrome characterized by rigidity and intractable seizures and a milder phenotype with intellectual disability, seizures, nonprogressive cerebellar ataxia or dyspraxia, and cerebellar atrophy. To date, nystagmus, cortical visual impairment, impairment of central vision, optic nerve hypoplasia, and optic atrophy have been described in this condition...
March 2, 2017: Ophthalmic Genetics
https://www.readbyqxmd.com/read/28634159/a-role-for-the-nonsense-mediated-mrna-decay-pathway-in-maintaining-genome-stability-in-caenorhabditis-elegans
#8
Víctor González-Huici, Bin Wang, Anton Gartner
Ionizing radiation (IR) is commonly used in cancer therapy and is a main source of DNA double-strand-breaks (DSBs), one of the most toxic forms of DNA damage. We have used Caenorhabditis elegans as an invertebrate model to identify novel factors required for repair of DNA damage inflicted by IR. We have performed an unbiased genetic screen, finding that smg-1 mutations confer strong hypersensitivity to IR. SMG-1 is a phosphoinositide-3 kinase (PI3K) kinase involved in mediating nonsense-mediated mRNA decay (NMD) of transcripts containing premature stop codons and related to the ATM and ATR kinases which are at the apex of DNA damage signalling pathways...
June 20, 2017: Genetics
https://www.readbyqxmd.com/read/28631426/hsp90%C3%AE-regulates-atm-and-nbn-functions-in-sensing-and-repair-of-dna-double-strand-breaks
#9
Rosa Pennisi, Antonio Antoccia, Stefano Leone, Paolo Ascenzi, Alessandra di Masi
The molecular chaperone heat shock protein 90 (Hsp90α) regulates cells proteostasis and mitigates the harmful effects of endogenous and exogenous stressors on the proteome. Indeed, the inhibition of Hsp90α ATPase activity affects the cellular response to ionizing radiation (IR). Although the interplay between Hsp90α and several DNA damage response (DDR) proteins has been reported, its role in the DDR is still unclear. Here, we show that ATM and NBN, but not 53BP1, RAD50, and MRE11, are Hsp90α clients as the Hsp90α inhibitor 17-(allylamino)-17-demethoxygeldanamycin (17-AAG) induces ATM and NBN polyubiquitination and proteosomal degradation in normal fibroblasts and lymphoblastoid cells lines...
June 20, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28630191/ceftazidime-avibactam-and-aztreonam-an-interesting-strategy-to-overcome-%C3%AE-lactam-resistance-conferred-by-metallo-%C3%AE-lactamases-in-enterobacteriaceae-and-pseudomonas-aeruginosa
#10
Benjamin Davido, Lesly Fellous, Christine Lawrence, Virginie Maxime, Martin Rottman, Aurélien Dinh
We have read with great interest Marshal S. et al. regarding the efficacy of the ceftazidime-avibactam (CAZ-AVI) and aztreonam (ATM) combination on metallo- β -lactamases producing Enterobacteriaceae (1).….
June 19, 2017: Antimicrobial Agents and Chemotherapy
https://www.readbyqxmd.com/read/28628639/small-molecule-inhibitors-uncover-synthetic-genetic-interactions-of-human-flap-endonuclease-1-fen1-with-dna-damage-response-genes
#11
Thomas A Ward, Peter J McHugh, Stephen T Durant
Flap endonuclease 1 (FEN1) is a structure selective endonuclease required for proficient DNA replication and the repair of DNA damage. Cellularly active inhibitors of this enzyme have previously been shown to induce a DNA damage response and, ultimately, cell death. High-throughput screens of human cancer cell-lines identify colorectal and gastric cell-lines with microsatellite instability (MSI) as enriched for cellular sensitivity to N-hydroxyurea series inhibitors of FEN1, but not the PARP inhibitor olaparib or other inhibitors of the DNA damage response...
2017: PloS One
https://www.readbyqxmd.com/read/28628186/knockdown-of-homeobox-containing-1-increases-the-radiosensitivity-of-cervical-cancer-cells-through-telomere-shortening
#12
Shuliang Zhou, Youde Xiao, Yafei Zhuang, Yinyin Liu, Hong Zhao, Hui Yang, Conghua Xie, Fuxiang Zhou, Yunfeng Zhou
Homeobox containing 1 (HMBOX1) modulates telomere length in various types of tumor cells by binding to double‑stranded telomeric DNA. There is a negative correlation between telomere length and radiosensitivity in tumor cells. In the present study, we aimed to investigate the relationship among HMBOX1, telomere and radiosensitivity in cervical cancer cells. Lentivirus-based shRNAs were used to establish stable transfected cell lines in which protein and mRNA levels of HMBOX1 were notably decreased. Knockdown of HMBOX1 increased the radiosensitivity of HeLa and C33A cells...
July 2017: Oncology Reports
https://www.readbyqxmd.com/read/28627265/atm-radiation-and-the-risk-of-second-primary-breast-cancer
#13
Jonine L Bernstein, Patrick Concannon
PURPOSE: It was first suggested more than 40 years ago that heterozygous carriers for the human autosomal recessive disorder Ataxia-Telangiectasia (A-T) might also be at increased risk for cancer. Subsequent studies have identified the responsible gene, Ataxia-Telangiectasia Mutated (ATM), characterized genetic variation at this locus in A-T and a variety of different cancers, and described the functions of the ATM protein with respect to cellular DNA damage responses. However, an overall model of how ATM contributes to cancer risk, and in particular, the role of DNA damage in this process, remains lacking...
June 19, 2017: International Journal of Radiation Biology
https://www.readbyqxmd.com/read/28627173/ternary-gold-hydrides-routes-to-stable-and-potentially-superconducting-compounds
#14
Martin Rahm, Roald Hoffmann, N W Ashcroft
In a search for gold hydrides, an initial discouraging result of no theoretical stability in any binary AuHn at P < 300 GPa was overcome by introducing alkali atoms as reductants. A set of AAuH2 compounds, A = Li, Na, K, Rb, and Cs, is examined; of these, certain K, Rb, and Cs compounds are predicted to be thermodynamically stable. All contain AuH2(-) molecular units and are semiconducting at P = 1 atm, and some form metallic and superconducting symmetrically bonded AuHAu sheets under compression. To induce metallicity by bringing the Au atoms closer together under ambient conditions, we examined alkaline earth ion substitution for two A, i...
June 19, 2017: Journal of the American Chemical Society
https://www.readbyqxmd.com/read/28624372/taming-tricky-dsbs-atm-on-duty
#15
REVIEW
Thomas Clouaire, Aline Marnef, Gaëlle Legube
Ataxia Telangiectasia Mutated (ATM) has been known for decades as the main kinase mediating the DNA Double-Strand Break Response (DDR). Extensive studies have revealed its dual role in locally promoting detection and repair of DSBs as well as in activating global DNA damage checkpoints. However, recent studies pinpoint additional unanticipated functions for ATM in modifying both the local chromatin landscape and the global chromosome organization, more particularly at persistent breaks. Given the emergence of a novel and unexpected class of DSBs prevalently arising in transcriptionally active genes and intrinsically difficult to repair, a specific role of ATM at refractory DSBs could be an important and so far overlooked feature of Ataxia Telangiectasia (A-T) a severe disorder associated with ATM mutations...
June 9, 2017: DNA Repair
https://www.readbyqxmd.com/read/28623072/commentary-on-integrative-clinical-genomics-of-advanced-prostate-cancer-robinson-d-van-allen-em-wu-ym-schultz-n-lonigro-rj-mosquera-jm-montgomery-b-taplin-me-pritchard-cc-attard-g-beltran-h-abida-w-bradley-rk-vinson-j-cao-x-vats-p-kunju-lp-hussain-m-feng-fy
#16
Stephen J Freedland, William J Aronson
Toward development of a precision medicine framework for metastatic, castration-resistant prostate cancer (mCRPC), we established a multi-institutional clinical sequencing infrastructure to conduct prospective whole-exome and transcriptome sequencing of bone or soft tissue tumor biopsies from a cohort of 150 mCRPC affected individuals. Aberrations of AR, ETS genes, TP53, and PTEN were frequent (40%-60% of cases), with TP53 and AR alterations enriched in mCRPC compared to primary prostate cancer. We identified new genomic alterations in PIK3CA/B, R-spondin, BRAF/RAF1, APC, β-catenin, and ZBTB16/PLZF...
June 13, 2017: Urologic Oncology
https://www.readbyqxmd.com/read/28623070/commentary-on-inherited-dna-repair-gene-mutations-in-men-with-metastatic-prostate-cancer-pritchard-cc-mateo-j-walsh-mf-de-sarkar-n-abida-w-beltran-h-garofalo-a-gulati-r-carreira-s-eeles-r-elemento-o-rubin-ma-robinson-d-lonigro-r-hussain-m-chinnaiyan-a-vinson
#17
Stephen J Freedland, William J Aronson
BACKGROUND: Inherited mutations in DNA-repair genes such as BRCA2 are associated with increased risks of lethal prostate cancer. Although the prevalence of germline mutations in DNA-repair genes among men with localized prostate cancer who are unselected for family predisposition is insufficient to warrant routine testing, the frequency of such mutations in patients with metastatic prostate cancer has not been established. METHODS: We recruited 692 men with documented metastatic prostate cancer who were unselected for family history of cancer or age at diagnosis...
June 13, 2017: Urologic Oncology
https://www.readbyqxmd.com/read/28622525/atm-atr-and-dna-pk-the-trinity-at-the-heart-of-the-dna-damage-response
#18
REVIEW
Andrew N Blackford, Stephen P Jackson
In vertebrate cells, the DNA damage response is controlled by three related kinases: ATM, ATR, and DNA-PK. It has been 20 years since the cloning of ATR, the last of the three to be identified. During this time, our understanding of how these kinases regulate DNA repair and associated events has grown profoundly, although major questions remain unanswered. Here, we provide a historical perspective of their discovery and discuss their established functions in sensing and responding to genotoxic stress. We also highlight what is known regarding their structural similarities and common mechanisms of regulation, as well as emerging non-canonical roles and how our knowledge of ATM, ATR, and DNA-PK is being translated to benefit human health...
June 15, 2017: Molecular Cell
https://www.readbyqxmd.com/read/28620865/involvement-of-atm-and-trp53-in-neural-cell-loss-due-to-terf2-inactivation-during-mouse-brain-development
#19
Jusik Kim, Inseo Choi, Youngsoo Lee
Maintenance of genomic integrity is one of the critical features for proper neurodevelopment and inhibition of neurological diseases. The signals from both ATM and ATR to TP53 are well-known mechanisms to remove neural cells with DNA damage during neurogenesis. Here we examined the involvement of Atm and Atr in genomic instability due to Terf2 inactivation during mouse brain development. Selective inactivation of Terf2 in neural progenitors induced apoptosis, resulting in a complete loss of the brain structure...
June 15, 2017: Histochemistry and Cell Biology
https://www.readbyqxmd.com/read/28619709/loss-of-fam46c-promotes-cell-survival-in-myeloma
#20
Yuan Xiao Zhu, Chang-Xin Shi, Laura A Bruins, Patrick Jedlowski, Xuewei Wang, K Martin Kortüm, Moulun Luo, Jonathan Ahmann, Esteban Braggio, A Keith Stewart
FAM46C is one of the most recurrently mutated genes in multiple myeloma (MM), however its role in disease pathogenesis has not been determined. Here we demonstrate that wild type (WT) FAM46C overexpression induces substantial cytotoxicity in MM cells. In contrast, FAM46C mutations found in MM patients abrogate this cytotoxicity, indicating a survival advantage conferred by the FAM46C mutant phenotype. WT FAM46C overexpression downregulated IRF4, CEBPB, and MYC and upregulated immunoglobulin (Ig) light chain and HSPA5/BIP Furthermore, pathway analysis suggests that enforced FAM46C expression activated the unfolded protein response (UPR) pathway and induced mitochondrial dysfunction...
June 15, 2017: Cancer Research
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