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https://www.readbyqxmd.com/read/28613983/azithromycin-attenuates-myofibroblast-differentiation-and-lung-fibrosis-development-through-proteasomal-degradation-of-nox4
#1
Kazuya Tsubouchi, Jun Araya, Shunsuke Minagawa, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Nahoko Sato, Masahiro Yoshida, Yusuke Kurita, Kenji Kobayashi, Saburo Ito, Yu Fujita, Hirofumi Utsumi, Haruhiko Yanagisawa, Mitsuo Hashimoto, Hiroshi Wakui, Yutaka Yoshii, Takeo Ishikawa, Takanori Numata, Yumi Kaneko, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Yoichi Nakanishi, Kazuyoshi Kuwano
Accumulation of profibrotic myofibroblasts is involved in the process of fibrosis development during idiopathic pulmonary fibrosis (IPF) pathogenesis. TGFB (transforming growth factor beta) is one of the major profibrotic cytokines for myofibroblast differentiation and NOX4 (NADPH oxidase 4) has an essential role in TGFB-mediated cell signaling. Azithromycin (AZM), a second-generation antibacterial macrolide, has a pleiotropic effect on cellular processes including proteostasis. Hence, we hypothesized that AZM may regulate NOX4 levels by modulating proteostasis machineries, resulting in inhibition of TGFB-associated lung fibrosis development...
June 14, 2017: Autophagy
https://www.readbyqxmd.com/read/28592083/-correlation-between-mir-1178-expression-and-clinicopathological-significance-in-human-pancreatic-cancer
#2
Z Cao, S L Zheng, G Yang, M Y Feng, L F Zheng, T P Zhang, Y P Zhao
Objective: To test the expression of miR-1178 in pancreatic cancer and study its clinicopathological significance and mechanism. Methods: The expression of miR-1178 in 87 paired paraffin pancreatic ductal adenocarcinoma specimens and adjacent non- cancerous pancreatic tissue diagnosed by Pathology Department of Peking Union Medical College Hospital was detected by hybridization in situ. The relationship between the expression of miR-1178 and clinicopathological characters was analyzed.miR-1178 mimics and inhibitor were used to further detect the close relationship among miR-1178 and cancer invasion...
June 1, 2017: Zhonghua Wai Ke za Zhi [Chinese Journal of Surgery]
https://www.readbyqxmd.com/read/28536267/the-ubiquitin-ligase-stub1-regulates-stability-and-activity-of-runx1-and-runx1-runx1t1
#3
Taishi Yonezawa, Hirotaka Takahashi, Shiori Shikata, Xiaoxiao Liu, Moe Tamura, Shuhei Asada, Tsuyoshi Fukushima, Tomofusa Fukuyama, Yosuke Tanaka, Tatsuya Sawasaki, Toshio Kitamura, Susumu Goyama
RUNX1 is a member of RUNX transcription factors and plays important roles in hematopoiesis. Disruption of RUNX1 activity has been implicated in the development of hematopoietic neoplasms. Chromosomal translocations involving the RUNX1 gene are associated with several types of leukemia, including acute myeloid leukemia driven by a leukemogenic fusion protein RUNX1-RUNX1T1. Previous studies have shown that RUNX1 is an unstable protein and is subjected to proteolytic degradation mediated by the ubiquitin-proteasome pathway...
May 23, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28536143/aurora-kinase-a-promotes-ar-degradation-via-the-e3-ligase-chip
#4
Sukumar Sarkar, David L Brautigan, James M Larner
Reducing the levels of the androgen receptor (AR) is one of the most viable approaches to combat castration-resistant prostate cancer (CRPC). Previously, we observed that proteasomal-dependent degradation of AR in response to 2-methoxyestradiol (2-ME) depends primarily on the E3 ligase C-terminus of HSP70-interacting protein (STUB1/CHIP). Here, 2-ME stimulation activates CHIP by phosphorylation via Aurora kinase A (AURKA). Aurora A kinase inhibitors and RNAi knockdown of Aurora A transcript selectively blocked CHIP phosphorylation and AR degradation...
May 23, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28444220/a-panel-study-on-patients-with-dominant-cerebellar-ataxia-highlights-the-frequency-of-channelopathies
#5
Marie Coutelier, Giulia Coarelli, Marie-Lorraine Monin, Juliette Konop, Claire-Sophie Davoine, Christelle Tesson, Rémi Valter, Mathieu Anheim, Anthony Behin, Giovanni Castelnovo, Perrine Charles, Albert David, Claire Ewenczyk, Mélanie Fradin, Cyril Goizet, Didier Hannequin, Pierre Labauge, Florence Riant, Pierre Sarda, Yves Sznajer, François Tison, Urielle Ullmann, Lionel Van Maldergem, Fanny Mochel, Alexis Brice, Giovanni Stevanin, Alexandra Durr
Autosomal dominant cerebellar ataxias have a marked heterogeneous genetic background, with mutations in 34 genes identified so far. This large amount of implicated genes accounts for heterogeneous clinical presentations, making genotype-phenotype correlations a major challenge in the field. While polyglutamine ataxias, linked to CAG repeat expansions in genes such as ATXN1, ATXN2, ATXN3, ATXN7, CACNA1A and TBP, have been extensively characterized in large cohorts, there is a need for comprehensive assessment of frequency and phenotype of more 'conventional' ataxias...
June 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28396517/in-vitro-characterization-of-six-stub1-variants-in-spinocerebellar-ataxia-16-reveals-altered-structural-properties-for-the-encoded-chip-proteins
#6
Yasaman Pakdaman, Monica Sanchez-Guixé, Rune Kleppe, Sigrid Erdal, Helene J Bustad, Lise Bjørkhaug, Kristoffer Haugarvoll, Charalampos Tzoulis, Ketil Heimdal, Per M Knappskog, Stefan Johansson, Ingvild Aukrust
Spinocerebellar ataxia, autosomal recessive 16 (SCAR16) is caused by biallelic mutations in the STIP1 homology and U-box containing protein 1 (STUB1) gene encoding the ubiquitin E3 ligase and dimeric co-chaperone C-terminus of Hsc70-interacting protein (CHIP). It has been proposed that the disease mechanism is related to CHIP's impaired E3 ubiquitin ligase properties and/or interaction with its chaperones. However, there is limited knowledge on how these mutations affect the stability, folding, and protein structure of CHIP itself...
April 30, 2017: Bioscience Reports
https://www.readbyqxmd.com/read/28346425/chip-stub1-regulates-the-warburg-effect-by-promoting-degradation-of-pkm2-in-ovarian-carcinoma
#7
Y Shang, J He, Y Wang, Q Feng, Y Zhang, J Guo, J Li, S Li, Y Wang, G Yan, F Ren, Y Shi, J Xu, N Zeps, Y Zhai, D He, Z Chang
Tumor cells preferentially adopt aerobic glycolysis for their energy supply, a phenomenon known as the Warburg effect. It remains a matter of debate as to how the Warburg effect is regulated during tumor progression. Here, we show that CHIP (carboxyl terminus of Hsc70-interacting protein), a U-box E3 ligase, suppresses tumor progression in ovarian carcinomas by inhibiting aerobic glycolysis. While CHIP is downregulated in ovarian carcinoma, induced expression of CHIP results in significant inhibition of the tumor growth examined by in vitro and in vivo experiments...
March 27, 2017: Oncogene
https://www.readbyqxmd.com/read/28338815/enhanced-tenogenic-differentiation-and-tendon-like-tissue-formation-by-chip-overexpression-in-tendon-derived-stem-cells
#8
Weifeng Han, Lei Chen, Junpeng Liu, Ai Guo
The carboxyl terminus of Hsc70-interacting protein (CHIP, also known as STUB1) plays critical roles in the proliferation and differentiation of many types of cells. The potential function of CHIP in tendon-derived stem cells (TDSCs) remains largely unknown at present. Here, we investigated the effects of CHIP on tenogenic differentiation of TDSCs via lentivirus-mediated overexpression. Forced expression of CHIP induced morphological changes and significantly enhanced cell proliferation, as well as tendon differentiation in vitro...
February 22, 2017: Acta Biochimica et Biophysica Sinica
https://www.readbyqxmd.com/read/28193273/stub1-chip-mutations-cause-gordon-holmes-syndrome-as-part-of-a-widespread-multisystemic-neurodegeneration-evidence-from-four-novel-mutations
#9
Stefanie Nicole Hayer, Tine Deconinck, Benjamin Bender, Katrien Smets, Stephan Züchner, Selina Reich, Ludger Schöls, Rebecca Schüle, Peter De Jonghe, Jonathan Baets, Matthis Synofzik
BACKGROUND: CHIP, the protein encoded by STUB1, is a central component of cellular protein homeostasis and interacts with several key proteins involved in the pathogenesis of manifold neurodegenerative diseases. This gives rise to the hypothesis that mutations in STUB1 might cause a far more multisystemic neurodegenerative phenotype than the previously reported cerebellar ataxia syndrome. METHODS: Whole exome sequencing data-sets from n = 87 index subjects of two ataxia cohorts were screened for individuals with STUB1 mutations...
February 13, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28143869/stabilization-of-notch1-by-the-hsp90-chaperon-is-crucial-for-t-cell-leukemogenesis
#10
Zhaojing Wang, Yufeng Hu, Daibiao Xiao, Jingchao Wang, Chuntao Liu, Yisheng Xu, Xiaomeng Shi, Peng Jiang, Liang Huang, Peng Li, Hudan Liu, Guoliang Qing
PURPOSE: Notch1 deregulation is assuming a focal role in T-cell acute lymphoblastic leukemia (T-ALL). Despite tremendous advances in our understanding of Notch1 transcriptional programs, the mechanisms by which Notch1 stability and turnover are regulated remain obscure. The goal of the present study is to identify intracellular Notch1 (ICN1, the activated form of Notch1) binding partner(s) regulating its stability and activity. EXPERIMENTAL DESIGN: We employed immunoaffinity purification to identify ICN1-associating partner and used co-immunoprecipitation to verify the endogenous protein interaction...
January 31, 2017: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/28042827/bag2-interferes-with-chip-mediated-ubiquitination-of-hsp72
#11
Bianca Schönbühler, Verena Schmitt, Heike Huesmann, Andreas Kern, Martin Gamerdinger, Christian Behl
The maintenance of cellular proteostasis is dependent on molecular chaperones and protein degradation pathways. Chaperones facilitate protein folding, maturation, and degradation, and the particular fate of a misfolded protein is determined by the interaction of chaperones with co-chaperones. The co-factor CHIP (C-terminus of HSP70-inteacting protein, STUB1) ubiquitinates chaperone substrates and directs proteins to the cellular degradation systems. The activity of CHIP is regulated by two co-chaperones, BAG2 and HSPBP1, which are potent inhibitors of the E3 ubiquitin ligase activity...
December 30, 2016: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/27811304/the-cerebellum-and-embodied-semantics-evidence-from-a-case-of-genetic-ataxia-due-to-stub1-mutations
#12
Adolfo M García, Sofía Abrevaya, Giselle Kozono, Indira García Cordero, Marta Córdoba, Marcelo Andrés Kauffman, Ricardo Pautassi, Edinson Muñoz, Lucas Sedeño, Agustín Ibáñez
No abstract text is available yet for this article.
February 2017: Journal of Medical Genetics
https://www.readbyqxmd.com/read/27616566/metformin-pharmacogenomics-a-genome-wide-association-study-to-identify-genetic-and-epigenetic-biomarkers-involved-in-metformin-anticancer-response-using-human-lymphoblastoid-cell-lines
#13
Nifang Niu, Tongzheng Liu, Junmei Cairns, Reynold C Ly, Xianglin Tan, Min Deng, Brooke L Fridley, Krishna R Kalari, Ryan P Abo, Gregory Jenkins, Anthony Batzler, Erin E Carlson, Poulami Barman, Sebastian Moran, Holger Heyn, Manel Esteller, Liewei Wang
Metformin is currently considered as a promising anticancer agent in addition to its anti-diabetic effect. To better individualize metformin therapy and explore novel molecular mechanisms in cancer treatment, we conducted a pharmacogenomic study using 266 lymphoblastoid cell lines (LCLs). Metformin cytotoxicity assay was performed using the MTS assay. Genome-wide association (GWA) analyses were performed in LCLs using 1.3 million SNPs, 485k DNA methylation probes, 54k mRNA expression probe sets, and metformin cytotoxicity (IC50s)...
September 11, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27451077/common-and-differentially-expressed-long-noncoding-rnas-for-the-characterization-of-high-and-low-grade-bladder-cancer
#14
Miao Wang, Xingyuan Xiao, Fuqing Zeng, Fei Xie, Yebin Fan, Chao Huang, Guosong Jiang, Liang Wang
Our study aimed to explore long non-coding RNAs (lncRNAs) contributing to the development of bladder cancer, as well as to identify more critical DEGs and lncRNAs that would characterize low- and high-grade bladder cancer. The microarray data of GSE55433 was downloaded from Gene Expression Omnibus database, including 57 urothelial cancer samples (23 low-grade NMI, 14 high-grade NMI and 20 invasive tumors) and 26 normal controls. The differentially expressed genes (DEGs) and differentially expressed lncRNAs were identified in 3 groups (low-grade NMI vs...
October 30, 2016: Gene
https://www.readbyqxmd.com/read/27325702/amyloid-precursor-protein-app-may-act-as-a-substrate-and-a-recognition-unit-for-crl4crbn-and-stub1-e3-ligases-facilitating-ubiquitination-of-proteins-involved-in-presynaptic-functions-and-neurodegeneration
#15
Dolores Del Prete, Richard C Rice, Anjali M Rajadhyaksha, Luciano D'Adamio
The amyloid precursor protein (APP), whose mutations cause Alzheimer disease, plays an important in vivo role and facilitates transmitter release. Because the APP cytosolic region (ACR) is essential for these functions, we have characterized its brain interactome. We found that the ACR interacts with proteins that regulate the ubiquitin-proteasome system, predominantly with the E3 ubiquitin-protein ligases Stub1, which binds the NH2 terminus of the ACR, and CRL4(CRBN), which is formed by Cul4a/b, Ddb1, and Crbn, and interacts with the COOH terminus of the ACR via Crbn...
August 12, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27324694/cimetidine-down-regulates-stability-of-foxp3-protein-via-stub1-in-treg-cells
#16
Yizhi Zhang, Zhoujia Chen, Xuerui Luo, Bin Wu, Bin Li, Bin Wang
Foxp3-expressing Treg cells have been well documented to provide immune regulation by promoting immune tolerance and suppressing immune over-reaction. Cimetidine (CIM), used to inhibit stomach acid secretion, has been reported to promote immune responses and suppress Treg cell function in several studies. However, the underlying mechanism is unknown. To investigate CIM effects on the suppressive function of Treg and Foxp3, here we used CIM to stimulate human CD4(+)CD25(+) Treg cells and Jurkat T cells and evaluated changes of Foxp3 expression and stability...
October 2, 2016: Human Vaccines & Immunotherapeutics
https://www.readbyqxmd.com/read/27283392/transcription-factor-rfx1-is-ubiquitinated-by-e3-ligase-stub1-in-systemic-lupus-erythematosus
#17
Yu Guo, Ming Zhao, Qianjin Lu
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease caused by complex interactions between genes and the environment. The expression level of transcription factor regulatory factor X 1 (RFX1) is reduced in T cells from SLE patients. RFX1 can regulate epigenetic modifications of CD70 and CD11a and plays an important role in the development of SLE. However, the mechanisms that mediate reduction of RFX1 in SLE are unclear. Here, we demonstrate that RFX1 protein expression can be tightly regulated by polyubiquitination-mediated proteosomal degradation via STIP1 homology and U-box containing protein 1 (STUB1)...
August 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/27199454/comprehensive-database-of-human-e3-ubiquitin-ligases-application-to-aquaporin-2-regulation
#18
Barbara Medvar, Viswanathan Raghuram, Trairak Pisitkun, Abhijit Sarkar, Mark A Knepper
Aquaporin-2 (AQP2) is regulated in part via vasopressin-mediated changes in protein half-life that are in turn dependent on AQP2 ubiquitination. Here we addressed the question, "What E3 ubiquitin ligase is most likely to be responsible for AQP2 ubiquitination?" using large-scale data integration based on Bayes' rule. The first step was to bioinformatically identify all E3 ligase genes coded by the human genome. The 377 E3 ubiquitin ligases identified in the human genome, consisting predominant of HECT, RING, and U-box proteins, have been used to create a publically accessible and downloadable online database (https://hpcwebapps...
July 1, 2016: Physiological Genomics
https://www.readbyqxmd.com/read/27178152/chip-mediates-down-regulation-of-nucleobindin-1-in-preosteoblast-cell-line-models
#19
Fuying Xue, Yanping Wu, Xinghui Zhao, Taoran Zhao, Ying Meng, Zhanzhong Zhao, Junwei Guo, Wei Chen
Nucleobindin-1 (NUCB1), also known as Calnuc, is a highly conserved, multifunctional protein widely expressed in tissues and cells. It contains two EF-hand motifs which have been shown to play a crucial role in binding Ca(2+) ions. In this study, we applied comparative two-dimensional gel electrophoresis to characterize differentially expressed proteins in HA-CHIP over-expressed and endogenous CHIP depleted MC3T3-E1 stable cell lines, identifying NUCB1 as a novel CHIP/Stub1 targeted protein. NUCB1 interacts with and is down-regulated by CHIP by both proteasomal dependent and independent pathways, suggesting that CHIP-mediated down-regulation of nucleobindin-1 might play a role in osteoblast differentiation...
2016: Cellular Signalling
https://www.readbyqxmd.com/read/27163177/an-integrative-proteomic-approach-identifies-novel-cellular-smyd2-substrates
#20
Hazem Ahmed, Shili Duan, Cheryl H Arrowsmith, Dalia Barsyte-Lovejoy, Matthieu Schapira
Protein methylation is a post-translational modification with important roles in transcriptional regulation and other biological processes, but the enzyme-substrate relationship between the 68 known human protein methyltransferases and the thousands of reported methylation sites is poorly understood. Here, we propose a bioinformatic approach that integrates structural, biochemical, cellular, and proteomic data to identify novel cellular substrates of the lysine methyltransferase SMYD2. Of the 14 novel putative SMYD2 substrates identified by our approach, six were confirmed in cells by immunoprecipitation: MAPT, CCAR2, EEF2, NCOA3, STUB1, and UTP14A...
June 3, 2016: Journal of Proteome Research
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