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https://www.readbyqxmd.com/read/28324645/three-dimensional-analysis-of-somatic-mitochondrial-dynamics-in-fission-deficient-injured-motor-neurons-using-fib-sem
#1
Hiromi Tamada, Sumiko Kiryu-Seo, Hiroki Hosokawa, Keisuke Ohta, Naotada Ishihara, Masatoshi Nomura, Katsuyoshi Mihara, Kei-Ichiro Nakamura, Hiroshi Kiyama
Mitochondria undergo morphological changes through fusion and fission for their quality control, which are vital for neuronal function. In this study, we examined three-dimensional morphologies of mitochondria in motor neurons under normal, nerve injured, and nerve injured plus fission-impaired conditions using the focused ion beam/scanning electron microscopy (FIB/SEM), because the FIB/SEM technology is a powerful tool to demonstrate both 3D images of whole organelle and the intra-organellar structure simultaneously...
March 21, 2017: Journal of Comparative Neurology
https://www.readbyqxmd.com/read/28281638/mir-34a-5p-promotes-multi-chemoresistance-of-osteosarcoma-through-down-regulation-of-the-dll1-gene
#2
Youguang Pu, Fangfang Zhao, Haiyan Wang, Shanbao Cai
MiR-34a-5p has been implicated in the tumorigenesis and progression of several types of cancer. However, the role of miR-34a-5p in osteosarcoma (OS) remains largely unknown. This study was performed in two multi-chemosensitive (G-292 and MG63.2) and two resistant (SJSA-1 and MNNG/HOS) OS cell lines. MiR-34a-5p promotes OS multi-chemoresistance via its repression of the Delta-like ligand 1 (DLL1) gene, the ligand of the Notch pathway, and thus negatively correlates with OS chemoresistance. The siRNA-mediated repression of the DLL1 gene suppressed cell apoptosis and de-sensitized G-292 and MG63...
March 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28275095/bap1-inhibits-the-er-stress-gene-regulatory-network-and-modulates-metabolic-stress-response
#3
Fangyan Dai, Hyemin Lee, Yilei Zhang, Li Zhuang, Hui Yao, Yuanxin Xi, Zhen-Dong Xiao, M James You, Wei Li, Xiaoping Su, Boyi Gan
The endoplasmic reticulum (ER) is classically linked to metabolic homeostasis via the activation of unfolded protein response (UPR), which is instructed by multiple transcriptional regulatory cascades. BRCA1 associated protein 1 (BAP1) is a tumor suppressor with de-ubiquitinating enzyme activity and has been implicated in chromatin regulation of gene expression. Here we show that BAP1 inhibits cell death induced by unresolved metabolic stress. This prosurvival role of BAP1 depends on its de-ubiquitinating activity and correlates with its ability to dampen the metabolic stress-induced UPR transcriptional network...
March 21, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28272390/atf3-acts-as-a-rheostat-to-control-jnk-signalling-during-intestinal-regeneration
#4
Jun Zhou, Bruce A Edgar, Michael Boutros
Epithelial barrier function is maintained by coordination of cell proliferation and cell loss, whereas barrier dysfunction can lead to disease and organismal death. JNK signalling is a conserved stress signalling pathway activated by bacterial infection and tissue damage, often leading to apoptotic cell death and compensatory cell proliferation. Here we show that the stress inducible transcription factor ATF3 restricts JNK activity in the Drosophila midgut. ATF3 regulates JNK-dependent apoptosis and regeneration through the transcriptional regulation of the JNK antagonist, Raw...
March 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28253359/csb-ablation-induced-apoptosis-is-mediated-by-increased-endoplasmic-reticulum-stress-response
#5
Manuela Caputo, Alessio Balzerano, Ivan Arisi, Mara D'Onofrio, Rossella Brandi, Silvia Bongiorni, Stefano Brancorsini, Mattia Frontini, Luca Proietti-De-Santis
The DNA repair protein Cockayne syndrome group B (CSB) has been recently identified as a promising anticancer target. Suppression, by antisense technology, of this protein causes devastating effects on tumor cells viability, through a massive induction of apoptosis, while being non-toxic to non-transformed cells. To gain insights into the mechanisms underlying the pro-apoptotic effects observed after CSB ablation, global gene expression patterns were determined, to identify genes that were significantly differentially regulated as a function of CSB expression...
2017: PloS One
https://www.readbyqxmd.com/read/28250971/atf3-reduces-migration-capacity-by-regulation-of-matrix-metalloproteinases-via-nf%C3%AE%C2%BAb-and-stat3-inhibition-in-glioblastoma
#6
Jessica Guenzle, Louisa J Wolf, Nicklas W C Garrelfs, Jonathan M Goeldner, Nadja Osterberg, Cora R Schindler, Joseph E Saavedra, Astrid Weyerbrock
Glioblastoma is associated with poor survival and a high recurrence rate in patients due to inevitable uncontrolled infiltrative tumor growth. The elucidation of the molecular mechanisms may offer opportunities to prevent relapses. In this study we investigated the role of the activating transcription factor 3 (ATF3) in migration of GBM cells in vitro. RNA microarray revealed that gene expression of ATF3 is induced by a variety of chemotherapeutics and experimental agents such as the nitric oxide donor JS-K (O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl)piperazin-1-yl]diazen-1-ium-1,2-diolate)...
2017: Cell Death Discovery
https://www.readbyqxmd.com/read/28250112/editorial-binge-drinking-lessons-from-atf3-and-hdac1-collaboration
#7
EDITORIAL
Banishree Saha
No abstract text is available yet for this article.
March 2017: Journal of Leukocyte Biology
https://www.readbyqxmd.com/read/28249877/cardiac-fibroblast-specific-activating-transcription-factor-3-protects-against-heart-failure-by-suppressing-map2k3-p38-signaling
#8
Yulin Li, Zhenya Li, Congcong Zhang, Ping Li, Yina Wu, Chunxiao Wang, Wayne Bond Lau, Xin-Liang Ma, Jie Du
Background -Hypertensive ventricular remodeling is a common cause of heart failure. However, the molecular mechanisms regulating ventricular remodeling remain poorly understood. Methods -We used a discovery-driven/nonbiased approach to indentify increased ATF3 expression in hypertensive heart. We employed loss/gain of function approaches to understand the role of ATF3 in heart failure. We also examine the mechanisms through transcriptome, CHIP-seq analysis and in vivo and vitro experiments. Results -ATF3 expression increased in murine hypertensive heart and human hypertrophic heart...
March 1, 2017: Circulation
https://www.readbyqxmd.com/read/28239957/activating-transcription-factor-3-promotes-malignance-of-lung-cancer-cells-in-vitro
#9
Xuebing Li, Xuexia Zhou, Yongwen Li, Lingling Zu, Hongli Pan, Boning Liu, Wang Shen, Yaguang Fan, Qinghua Zhou
BACKGROUND: Lung cancer remains the most common cause of cancer-related death, with high rates of recurrence and poor outcomes. An abnormally high expression of activating transcription factor 3 (ATF3) in various cancers suggests an oncogenic role; however, its function in lung cancer is largely unknown. METHODS: Sixty-four pairs of lung cancer tissues were collected for ATF3 expression analysis by quantitative real-time PCR, immunoblotting, and immunohistochemistry staining...
February 27, 2017: Thoracic Cancer
https://www.readbyqxmd.com/read/28210955/the-effects-of-igf-1-on-tnf-%C3%AE-treated-drg-neurons-by-modulating-atf3-and-gap-43-expression-via-pi3k-akt-s6k-signaling-pathway
#10
Lei Zhang, Yaping Yue, Meishuo Ouyang, Huaxiang Liu, Zhenzhong Li
Upregulation of the pro-inflammatory cytokine tumor necrosis factor α (TNF-α) is involved in the development and progression of numerous neurological disorders. Recent reports have challenged the concept that TNF-α exhibits only deleterious effects of pro-inflammatory destruction, and have raised the awareness that it may play a beneficial role in neuronal growth and function in particular conditions, which prompts us to further investigate the role of this cytokine. Insulin-like growth factor-1 (IGF-1) is a cytokine possessing powerful neuroprotective effects in promoting neuronal survival, neuronal differentiation, neurite elongation, and neurite regeneration...
February 16, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28205069/transcriptomic-analysis-of-thp-1-macrophages-exposed-to-lipoprotein-hydrolysis-products-generated-by-lipoprotein-lipase
#11
Narmadaa Thyagarajan, Jenika D Marshall, Arthur T Pickett, Clemens Schumacher, Yanbo Yang, Sherri L Christian, Robert J Brown
Macrophage lipoprotein lipase (LPL) induces lipid accumulation and promotes atherosclerosis. However, the effects of lipoprotein hydrolysis products generated by LPL on macrophage-derived foam cell formation are not clearly understood. Thus, we analyzed the transcriptomic response to hydrolysis products via microarray analyses on RNA isolated from human THP-1 macrophages incubated with total lipoprotein hydrolysis products generated by LPL. The expression of 183 transcripts was significantly upregulated and 133 transcripts were significantly downregulated...
March 2017: Lipids
https://www.readbyqxmd.com/read/28193539/dimeric-but-not-monomeric-%C3%AE-lactalbumin-potentiates-apoptosis-by-up-regulation-of-atf3-and-reduction-of-histone-deacetylase-activity-in-primary-and-immortalised-cells
#12
Julie A Sharp, Amelia J Brennan, Galina Polekhina, David B Ascher, Christophe Lefevre, Kevin R Nicholas
α-lactalbumin is a protein of dual function found in milk of most mammals. α-lactalbumin binds β-1,4-galactosyltransferase to form the regulatory subunit for lactose synthesis and has also been shown to cause cell death. This study shows, for the first time, that α-lactalbumin isolated in a rare 28kDa dimeric form induces cell death, while 14kDa monomeric α-lactalbumin is inactive. In contrast to the casein derived and chemically induced α-lactalbumin variants, MAL and HAMLET/BAMLET, the effects of 28kDa α-lactalbumin are calcium independent and, unlike MAL and HAMLET, 28kDa α-lactalbumin dimer causes cell death of primary mammary cells and a variety of immortalised cell lines, which are committed to cell death pathways within 1-4h of exposure...
February 11, 2017: Cellular Signalling
https://www.readbyqxmd.com/read/28186491/combinatorial-bzip-dimers-display-complex-dna-binding-specificity-landscapes
#13
José A Rodríguez-Martínez, Aaron W Reinke, Devesh Bhimsaria, Amy E Keating, Aseem Z Ansari
How transcription factor dimerization impacts DNA-binding specificity is poorly understood. Guided by protein dimerization properties, we examined DNA binding specificities of 270 human bZIP pairs. DNA interactomes of 80 heterodimers and 22 homodimers revealed that 72% of heterodimer motifs correspond to conjoined half-sites preferred by partnering monomers. Remarkably, the remaining motifs are composed of variably-spaced half-sites (12%) or 'emergent' sites (16%) that cannot be readily inferred from half-site preferences of partnering monomers...
February 10, 2017: ELife
https://www.readbyqxmd.com/read/28185985/activating-transcription-factor-3-represses-cigarette-smoke-induced-il6-and-il8-expression-via-suppressing-nf-%C3%AE%C2%BAb-activation
#14
Yan-Ping Wu, Chao Cao, Yin-Fang Wu, Miao Li, Tian-Wen Lai, Chen Zhu, Yong Wang, Song-Min Ying, Zhi-Hua Chen, Hua-Hao Shen, Wen Li
Airway and lung inflammation is a fundamental hallmark of chronic obstructive pulmonary disease (COPD). Activating transcription factor 3 (ATF3) has been reported to negatively regulate many pro-inflammatory cytokines and chemokines. However, little is known about the impact of ATF3 on the inflammatory response of COPD. Since cigarette smoke (CS) is considered to be the most important risk factor in the etiology of COPD, we attempted to investigate the effects and molecular mechanisms of ATF3 in CS-induced inflammation...
March 15, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28177121/activating-transcription-factor-3-atf3-protects-against-lipopolysaccharide-induced-acute-lung-injury-via-inhibiting-the-expression-of-tl1a
#15
Lanlan Qian, Yunfeng Zhao, Liang Guo, Shaoying Li, Xueling Wu
Excessive inflammatory responses are critical in the pathogenesis of acute lung injury (ALI). Activating transcription factor 3 (ATF3) is a stress-induced transcriptional regulator that is a negative regulator of inflammatory responses. Therefore, we investigated the role and signaling pathways of ATF3 in lipopolysaccharide (LPS)-induced ALI in mice. The mouse macrophage RAW264.7 cells were cultured on HTS 24-Transwell filter plates in presence of ATF3 siRNA before exposure to LPS. ATF3 knock-out (KO) and wild type (WT) mice were challenged by intra-peritoneal injection of LPS (15mg/kg)...
February 8, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28165887/a-small-molecule-activator-induces-ulk1-modulating-autophagy-associated-cell-death-in-triple-negative-breast-cancer
#16
Liang Ouyang, Lan Zhang, Leilei Fu, Bo Liu
ULK1 (unc-51 like autophagy activating kinase 1) is well known to be required to initiate the macroautophagy/autophagy process, and thus activation of ULK1-modulating autophagy/autophagy-associated cell death (ACD) may be a possible therapeutic strategy in triple negative breast cancer (TNBC). Here, our integrated The Cancer Genome Atlas (TCGA) dataset, tissue microarray-based analyses and multiple biological evaluations together demonstrate a new small-molecule activator of ULK1 for better understanding of how ULK1, the mammalian homolog of yeast Atg1, as a potential drug target can regulate ACD by the ULK complex (ULK1-ATG13-RB1CC1/FIP200-ATG101), as well as other possible ULK1 interactors, including ATF3, RAD21 and CASP3/caspase3 in TNBC...
February 6, 2017: Autophagy
https://www.readbyqxmd.com/read/28134810/acidosis-activates-endoplasmic-reticulum-stress-pathways-through-gpr4-in-human-vascular-endothelial-cells
#17
Lixue Dong, Elizabeth A Krewson, Li V Yang
Acidosis commonly exists in the tissue microenvironment of various pathophysiological conditions such as tumors, inflammation, ischemia, metabolic disease, and respiratory disease. For instance, the tumor microenvironment is characterized by acidosis and hypoxia due to tumor heterogeneity, aerobic glycolysis (the "Warburg effect"), and the defective vasculature that cannot efficiently deliver oxygen and nutrients or remove metabolic acid byproduct. How the acidic microenvironment affects the function of blood vessels, however, is not well defined...
January 27, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28120235/identifying-key-genes-associated-with-hirschsprung-s-disease-based-on-bioinformatics-analysis-of-rna-sequencing-data
#18
Wei-Kang Pan, Ya-Fei Zhang, Hui Yu, Ya Gao, Bai-Jun Zheng, Peng Li, Chong Xie, Xin Ge
BACKGROUND: Hirschsprung's disease (HSCR) is a type of megacolon induced by deficiency or dysfunction of ganglion cells in the distal intestine and is associated with developmental disorders of the enteric nervous system. To explore the mechanisms of HSCR, we analyzed the RNA-sequencing data of the expansion and the narrow segments of colon tissues separated from children with HSCR. METHODS: RNA-sequencing of the expansion segments and the narrow segments of colon tissues isolated from children with HSCR was performed...
January 25, 2017: World Journal of Pediatrics: WJP
https://www.readbyqxmd.com/read/28095324/formalin-injection-produces-long-lasting-hypersensitivity-with-characteristics-of-neuropathic-pain
#19
Ana Belen Salinas-Abarca, Sabino Hazael Avila-Rojas, Paulino Barragán-Iglesias, Jorge Baruch Pineda-Farias, Vinicio Granados-Soto
The purpose of this study was to investigate whether 1%, 2% or 5% formalin injection produce hypersensitivity with characteristics of the neuropathic pain induced by spinal nerve injury. Formalin injection (1%, 2% and 5%) produced concentration-dependent long-lasting (at least 14 days) mechanical allodynia and hyperalgesia in both paws. Likewise, L5/L6 spinal nerve ligation induced allodynia and hyperalgesia in both paws. The intensity of hypersensitivity was greater in the ipsilateral than in the contralateral paw in all models...
January 14, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28093456/effect-of-lipid-bound-apolipoprotein-a-i-cysteine-mutant-on-atf3-in-raw264-7-cells
#20
Yunlong Wang, Yanhui Wang, Shaoyou Jia, Qingzhe Dong, Yuanbin Chen, Shulai Lu, Lin Hou
Activating transcription factor 3 (ATF3) is a TLR-induced repressor that plays an important role in the inhibition of specific inflammatory signals. We previously constructed recombinant high density lipoproteins (rHDL) (including rHDLWT, rHDLM, rHDL228 and rHDL74) and found that rHDL74 had a strong anti-inflammatory ability. In the present study, we investigate the roles of recombinant apolipoprotein A-I (ApoA-I) (rHDLWT) and its cysteine mutant HDLs (rHDLM, rHDL228 and rHDL74) on ATF3 function in RAW264.7 cells stimulated by lipopolysaccharide...
February 28, 2017: Bioscience Reports
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