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https://www.readbyqxmd.com/read/27651363/high-risk-human-papillomavirus-e7-proteins-target-ptpn14-for-degradation
#1
Elizabeth A White, Karl Münger, Peter M Howley
UNLABELLED: The major transformation activity of the high-risk human papillomaviruses (HPV) is associated with the E7 oncoprotein. The interaction of HPV E7 with retinoblastoma family proteins is important for several E7 activities; however, this interaction does not fully account for the high-risk E7-specific cellular immortalization and transformation activities. We have determined that the cellular non-receptor protein tyrosine phosphatase PTPN14 interacts with HPV E7 from many genus alpha and beta HPV types...
September 20, 2016: MBio
https://www.readbyqxmd.com/read/27552662/the-deubiquitinase-usp47-stabilizes-mapk-by-counteracting-the-function-of-the-n-end-rule-ligase-poe-ubr4-in-drosophila
#2
Dariel Ashton-Beaucage, Caroline Lemieux, Christian M Udell, Malha Sahmi, Samuel Rochette, Marc Therrien
RAS-induced MAPK signaling is a central driver of the cell proliferation apparatus. Disruption of this pathway is widely observed in cancer and other pathologies. Consequently, considerable effort has been devoted to understanding the mechanistic aspects of RAS-MAPK signal transmission and regulation. While much information has been garnered on the steps leading up to the activation and inactivation of core pathway components, comparatively little is known on the mechanisms controlling their expression and turnover...
August 2016: PLoS Biology
https://www.readbyqxmd.com/read/27212660/zika-virus-targets-human-stat2-to-inhibit-type-i-interferon-signaling
#3
Alesha Grant, Sanket S Ponia, Shashank Tripathi, Vinod Balasubramaniam, Lisa Miorin, Marion Sourisseau, Megan C Schwarz, Mari Paz Sánchez-Seco, Matthew J Evans, Sonja M Best, Adolfo García-Sastre
The ongoing epidemic of Zika virus (ZIKV) illustrates the importance of flaviviruses as emerging human pathogens. All vector-borne flaviviruses studied thus far have to overcome type I interferon (IFN) to replicate and cause disease in vertebrates. The mechanism(s) by which ZIKV antagonizes IFN signaling is unknown. Here, we report that the nonstructural protein NS5 of ZIKV and other flaviviruses examined could suppress IFN signaling, but through different mechanisms. ZIKV NS5 expression resulted in proteasomal degradation of the IFN-regulated transcriptional activator STAT2 from humans, but not mice, which may explain the requirement for IFN deficiency to observe ZIKV-induced disease in mice...
June 8, 2016: Cell Host & Microbe
https://www.readbyqxmd.com/read/26792178/the-ubiquitin-ligase-ubr4-controls-stability-of-podocin-mec-2-supercomplexes
#4
Markus M Rinschen, Puneet Bharill, Xiongwu Wu, Priyanka Kohli, Matthäus J Reinert, Oliver Kretz, Isabel Saez, Bernhard Schermer, Martin Höhne, Malte P Bartram, Sriram Aravamudhan, Bernard R Brooks, David Vilchez, Tobias B Huber, Roman-Ulrich Müller, Marcus Krüger, Thomas Benzing
The PHB-domain protein podocin maintains the renal filtration barrier and its mutation is an important cause of hereditary nephrotic syndrome. Podocin and its Caenorhabditis elegans orthologue MEC-2 have emerged as key components of mechanosensitive membrane protein signalling complexes. Whereas podocin resides at a specialized cell junction at the podocyte slit diaphragm, MEC-2 is found in neurons required for touch sensitivity. Here, we show that the ubiquitin ligase Ubr4 is a key component of the podocin interactome purified both from cultured podocytes and native glomeruli...
April 1, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/26664787/molecular-neuropathology-of-the-synapse-in-sheep-with-cln5-batten-disease
#5
Inês S Amorim, Nadia L Mitchell, David N Palmer, Stephen J Sawiak, Roger Mason, Thomas M Wishart, Thomas H Gillingwater
AIMS: Synapses represent a major pathological target across a broad range of neurodegenerative conditions. Recent studies addressing molecular mechanisms regulating synaptic vulnerability and degeneration have relied heavily on invertebrate and mouse models. Whether similar molecular neuropathological changes underpin synaptic breakdown in large animal models and in human patients with neurodegenerative disease remains unclear. We therefore investigated whether molecular regulators of synaptic pathophysiology, previously identified in Drosophila and mouse models, are similarly present and modified in the brain of sheep with CLN5 Batten disease...
November 2015: Brain and Behavior
https://www.readbyqxmd.com/read/26651948/meta-and-orthogonal-integration-of-influenza-omics-data-defines-a-role-for-ubr4-in-virus-budding
#6
Shashank Tripathi, Marie O Pohl, Yingyao Zhou, Ariel Rodriguez-Frandsen, Guojun Wang, David A Stein, Hong M Moulton, Paul DeJesus, Jianwei Che, Lubbertus C F Mulder, Emilio Yángüez, Dario Andenmatten, Lars Pache, Balaji Manicassamy, Randy A Albrecht, Maria G Gonzalez, Quy Nguyen, Abraham Brass, Stephen Elledge, Michael White, Sagi Shapira, Nir Hacohen, Alexander Karlas, Thomas F Meyer, Michael Shales, Andre Gatorano, Jeffrey R Johnson, Gwen Jang, Tasha Johnson, Erik Verschueren, Doug Sanders, Nevan Krogan, Megan Shaw, Renate König, Silke Stertz, Adolfo García-Sastre, Sumit K Chanda
Several systems-level datasets designed to dissect host-pathogen interactions during influenza A infection have been reported. However, apparent discordance among these data has hampered their full utility toward advancing mechanistic and therapeutic knowledge. To collectively reconcile these datasets, we performed a meta-analysis of data from eight published RNAi screens and integrated these data with three protein interaction datasets, including one generated within the context of this study. Further integration of these data with global virus-host interaction analyses revealed a functionally validated biochemical landscape of the influenza-host interface, which can be queried through a simplified and customizable web portal (http://www...
December 9, 2015: Cell Host & Microbe
https://www.readbyqxmd.com/read/25720193/identification-of-gene-fragments-related-to-nitrogen-deficiency-in-eichhornia-crassipes-pontederiaceae
#7
Minghui Fu, Lihua Jiang, Yuanmei Li, Guohua Yan, Lijun Zheng, Peng Jinping
Eichhornia crassipes is an aquatic plant native to the Amazon River Basin. It has become a serious weed in freshwater habitats in rivers, lakes and reservoirs both in tropical and warm temperate areas worldwide. Some research has stated that it can be used for water phytoremediation, due to its strong assimilation of nitrogen and phosphorus, and the accumulation of heavy metals, and its growth and spread may play an important role in environmental ecology. In order to explore the molecular mechanism of E. crassipes to responses to nitrogen deficiency, we constructed forward and reversed subtracted cDNA libraries for E...
December 2014: Revista de Biología Tropical
https://www.readbyqxmd.com/read/25582440/kcmf1-potassium-channel-modulatory-factor-1-links-rad6-to-ubr4-ubiquitin-n-recognin-domain-containing-e3-ligase-4-and-lysosome-mediated-degradation
#8
Jenny H Hong, Lilia Kaustov, Etienne Coyaud, Tharan Srikumar, Janet Wan, Cheryl Arrowsmith, Brian Raught
RAD6 is a ubiquitin E2 protein with roles in a number of different biological processes. Here, using affinity purification coupled with mass spectrometry, we identify a number of new RAD6 binding partners, including the poorly characterized ubiquitin E3 ligases KCMF1 (potassium channel modulatory factor 1) and UBR4 (ubiquitin N-recognin domain-containing E3 ligase 4), a protein that can bind N-end rule substrates, and which was recently linked to lysosome-mediated degradation and autophagy. NMR, combined with in vivo and in vitro interaction mapping, demonstrate that the KCMF1 C terminus binds directly to RAD6, whereas N-terminal domains interact with UBR4 and other intracellular vesicle- and mitochondria-associated proteins...
March 2015: Molecular & Cellular Proteomics: MCP
https://www.readbyqxmd.com/read/25424645/p600-ubr4-in-the-central-nervous-system
#9
REVIEW
Kari Parsons, Yoshihiro Nakatani, Minh Dang Nguyen
A decade ago, the large 600 kDa mammalian protein p600 (also known as UBR4) was discovered as a multifunctional protein with roles in anoikis, viral transformation and protein degradation. Recently, p600 has emerged as a critical protein in the mammalian brain with roles in neurogenesis, neuronal migration, neuronal signaling and survival. How p600 integrates these apparently unrelated functions to maintain tissue homeostasis and murine survival remains unclear. The common molecular basis underlying many of the actions of p600 suggests, however, certain conservation and transposition of these functions across systems...
March 2015: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/25084275/time-of-day-and-light-dependent-expression-of-ubiquitin-protein-ligase-e3-component-n-recognin-4-ubr4-in-the-suprachiasmatic-nucleus-circadian-clock
#10
Harrod H Ling, Christian Beaulé, Cheng-Kang Chiang, Ruijun Tian, Daniel Figeys, Hai-Ying M Cheng
Circadian rhythms of behavior and physiology are driven by the biological clock that operates endogenously but can also be entrained to the light-dark cycle of the environment. In mammals, the master circadian pacemaker is located in the suprachiasmatic nucleus (SCN), which is composed of individual cellular oscillators that are driven by a set of core clock genes interacting in transcriptional/translational feedback loops. Light signals can trigger molecular events in the SCN that ultimately impact on the phase of expression of core clock genes to reset the master pacemaker...
2014: PloS One
https://www.readbyqxmd.com/read/25034033/p600-stabilizes-microtubules-to-prevent-the-aggregation-of-camkii%C3%AE-during-photoconductive-stimulation
#11
Camille Belzil, Tim Ramos, Kamon Sanada, Michael A Colicos, Minh Dang Nguyen
The large microtubule-associated/Ca(2+)-signalling protein p600 (also known as UBR4) is required for hippocampal neuronal survival upon Ca(2+) dyshomeostasis induced by glutamate treatment. During this process, p600 prevents aggregation of the Ca(2+)/calmodulin-dependent kinase IIα (CaMKIIα), a proxy of neuronal death, via direct binding to calmodulin in a microtubuleindependent manner. Using photoconductive stimulation coupled with live imaging of single neurons, we identified a distinct mechanism of prevention of CaMKIIα aggregation by p600...
September 2014: Cellular & Molecular Biology Letters
https://www.readbyqxmd.com/read/24121706/pink1-is-degraded-through-the-n-end-rule-pathway
#12
Koji Yamano, Richard J Youle
PINK1, a mitochondrial serine/threonine kinase, is the product of a gene mutated in an autosomal recessive form of Parkinson disease. PINK1 is constitutively degraded by an unknown mechanism and stabilized selectively on damaged mitochondria where it can recruit the E3 ligase PARK2/PARKIN to induce mitophagy. Here, we show that, under steady-state conditions, endogenous PINK1 is constitutively and rapidly degraded by E3 ubiquitin ligases UBR1, UBR2 and UBR4 through the N-end rule pathway. Following precursor import into mitochondria, PINK1 is cleaved in the transmembrane segment by a mitochondrial intramembrane protease PARL generating an N-terminal destabilizing amino acid and then retrotranslocates from mitochondria to the cytosol for N-end recognition and proteasomal degradation...
November 1, 2013: Autophagy
https://www.readbyqxmd.com/read/23982692/a-novel-locus-for-episodic-ataxia-ubr4-the-likely-candidate
#13
Judith Conroy, Paul McGettigan, Raymond Murphy, David Webb, Sinéad M Murphy, Blathnaid McCoy, Christine Albertyn, Dara McCreary, Cara McDonagh, Orla Walsh, Sallyann Lynch, Sean Ennis
Episodic ataxias (EAs) are rare neurological channelopathies that are characterized by spells of imbalance and a lack of co-ordination. There are seven clinically recognized EAs and multiple isolated cases. Five disease-causing genes have been identified to date. We describe a novel form of autosomal dominant EA in a large three-generation Irish family. This form of EA presents in early childhood with periods of unsteadiness generalized weakness and slurred speech during an attack, which may be triggered by physical tiredness or stress...
April 2014: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/23861403/a-ca2-dependent-mechanism-of-neuronal-survival-mediated-by-the-microtubule-associated-protein-p600
#14
Camille Belzil, Gernot Neumayer, Alex P Vassilev, Kyoko L Yap, Hiroaki Konishi, Serge Rivest, Kamon Sanada, Mitsuhiko Ikura, Yoshihiro Nakatani, Minh Dang Nguyen
In acute and chronic neurodegeneration, Ca(2+) mishandling and disruption of the cytoskeleton compromise neuronal integrity, yet abnormalities in the signaling roles of cytoskeletal proteins remain largely unexplored. We now report that the microtubule-associated protein p600 (also known as UBR4) promotes neuronal survival. Following depletion of p600, glutamate-induced Ca(2+) influx through NMDA receptors, but not AMPA receptors, initiates a degenerative process characterized by endoplasmic reticulum fragmentation and endoplasmic reticulum Ca(2+) release via inositol 1,4,5-trisphosphate receptors...
August 23, 2013: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/23849394/the-n-end-rule-and-retroviral-infection-no-effect-on-integrase
#15
Guney Boso, Takafumi Tasaki, Yong Tae Kwon, Nikunj V Somia
BACKGROUND: Integration of double stranded viral DNA is a key step in the retroviral life cycle. Virally encoded enzyme, integrase, plays a central role in this reaction. Mature forms of integrase of several retroviruses (i.e. HIV-1 and MLV) bear conserved destabilizing N-terminal residues of the N-end rule pathway - a ubiquitin dependent proteolytic system in which the N-terminal residue of a protein determines its half life. Substrates of the N-end rule pathway are recognized by E3 ubiquitin ligases called N-recognins...
July 13, 2013: Virology Journal
https://www.readbyqxmd.com/read/23747339/post-translational-loss-of-renal-trpv5-calcium-channel-expression-ca-2-wasting-and-bone-loss-in-experimental-colitis
#16
Vijayababu M Radhakrishnan, Rajalakshmy Ramalingam, Claire B Larmonier, Robert D Thurston, Daniel Laubitz, Monica T Midura-Kiela, Rita-Marie T McFadden, Makoto Kuro-O, Pawel R Kiela, Fayez K Ghishan
BACKGROUND & AIMS: Dysregulated Ca(2+) homeostasis likely contributes to the etiology of inflammatory bowel disease-associated loss of bone mineral density. Experimental colitis leads to decreased expression of Klotho, a protein that supports renal Ca(2+) reabsorption by stabilizing the transient receptor potential vanilloid 5 (TRPV5) channel on the apical membrane of distal tubule epithelial cells. METHODS: Colitis was induced in mice via administration of 2,4,6-trinitrobenzenesulfonic acid (TNBS) or transfer of CD4(+)interleukin-10(-/-) and CD4(+), CD45RB(hi) T cells...
September 2013: Gastroenterology
https://www.readbyqxmd.com/read/23628846/the-n-end-rule-proteolytic-system-in-autophagy
#17
Sung Tae Kim, Takafumi Tasaki, Adriana Zakrzewska, Young Dong Yoo, Ki Sa Sung, Su-Hyeon Kim, Hyunjoo Cha-Molstad, Joonsung Hwang, Kyoung A Kim, Bo Yeon Kim, Yong Tae Kwon
The N-end rule pathway is a cellular proteolytic system that utilizes specific N-terminal residues as degradation determinants, called N-degrons. N-degrons are recognized and bound by specific recognition components (N-recognins) that mediate polyubiquitination of low-abundance regulators and selective proteolysis through the proteasome. Our earlier work identified UBR4/p600 as one of the N-recognins that promotes N-degron-dependent proteasomal degradation. In this study, we show that UBR4 is associated with cellular cargoes destined to autophagic vacuoles and is degraded by the lysosome...
July 2013: Autophagy
https://www.readbyqxmd.com/read/23555265/dengue-virus-co-opts-ubr4-to-degrade-stat2-and-antagonize-type-i-interferon-signaling
#18
Juliet Morrison, Maudry Laurent-Rolle, Ana M Maestre, Ricardo Rajsbaum, Giuseppe Pisanelli, Viviana Simon, Lubbertus C F Mulder, Ana Fernandez-Sesma, Adolfo García-Sastre
An estimated 50 million dengue virus (DENV) infections occur annually and more than forty percent of the human population is currently at risk of developing dengue fever (DF) or dengue hemorrhagic fever (DHF). Despite the prevalence and potential severity of DF and DHF, there are no approved vaccines or antiviral therapeutics available. An improved understanding of DENV immune evasion is pivotal for the rational development of anti-DENV therapeutics. Antagonism of type I interferon (IFN-I) signaling is a crucial mechanism of DENV immune evasion...
March 2013: PLoS Pathogens
https://www.readbyqxmd.com/read/23431188/ubr-box-n-recognin-4-ubr4-an-n-recognin-of-the-n-end-rule-pathway-and-its-role-in-yolk-sac-vascular-development-and-autophagy
#19
Takafumi Tasaki, Sung Tae Kim, Adriana Zakrzewska, Bo Eun Lee, Min Jueng Kang, Young Dong Yoo, Hyun Joo Cha-Molstad, Joonsung Hwang, Nak Kyun Soung, Ki Sa Sung, Su-Hyeon Kim, Minh Dang Nguyen, Ming Sun, Eugene C Yi, Bo Yeon Kim, Yong Tae Kwon
The N-end rule pathway is a proteolytic system in which destabilizing N-terminal residues of short-lived proteins act as degradation determinants (N-degrons). Substrates carrying N-degrons are recognized by N-recognins that mediate ubiquitylation-dependent selective proteolysis through the proteasome. Our previous studies identified the mammalian N-recognin family consisting of UBR1/E3α, UBR2, UBR4/p600, and UBR5, which recognize destabilizing N-terminal residues through the UBR box. In the current study, we addressed the physiological function of a poorly characterized N-recognin, 570-kDa UBR4, in mammalian development...
March 5, 2013: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/23206439/interactions-between-e6ap-and-e6-proteins-from-alpha-and-beta-hpv-types
#20
Miranda Thomas, Vjekoslav Tomaić, David Pim, Michael P Myers, Massimo Tommasino, Lawrence Banks
High-risk mucosotropic Human papillomaviruses (HPVs), especially HPV-16, are the aetiological agents of cervical cancer and the cellular targets of their E6 oncoproteins have been much studied. However, much less is known about the cellular targets of the cutaneous HPV E6 proteins. In this study, a proteomic analysis of cells transfected with the E6 proteins from cutaneous HPV types specifically identified E6-interacting proteins involved in the ubiquitination pathways. These include the E3 ubiquitin-protein ligases E6AP and UBR4/p600...
January 20, 2013: Virology
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