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https://www.readbyqxmd.com/read/28393202/ufm1-inhibits-lps-induced-endothelial-cell-inflammatory-responses-through-the-nf-%C3%AE%C2%BAb-signaling-pathway
#1
Yuan-Yuan Li, Guang-Ya Zhang, Jiang-Ping He, Dan-Dan Zhang, Xiang-Xin Kong, Hui-Min Yuan, Feng-Ling Chen
Endothelial cell dysfunction and inflammatory responses are important early contributors to the occurrence and development of atherosclerosis (AS), which still remains to be decoded. Ubiquitin-fold modifier 1 (Ufm1) is a new member of the ubiquitin-like protein family, and its biological function remains largely unknown, particularly in endothelial cell injury and inflammatory responses. In the present study, we showed that Ufm1 was highly expressed in both the nucleus and cytoplasm of human umbilical vein endothelial cells (HUVECs)...
May 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/28360427/novel-insights-into-the-interaction-of-uba5-with-ufm1-via-a-ufm1-interacting-sequence
#2
Prasanth Padala, Walaa Oweis, Bayan Mashahreh, Nadine Soudah, Einav Cohen-Kfir, Emily A Todd, Christopher E Berndsen, Reuven Wiener
The modification of proteins by ubiquitin-fold modifier 1 (UFM1) is implicated in many human diseases. Prior to conjugation, UFM1 undergoes activation by its cognate activating enzyme, UBA5. UBA5 is a non-canonical E1 activating enzyme that possesses an adenylation domain but lacks a distinct cysteine domain. Binding of UBA5 to UFM1 is mediated via an amino acid sequence, known as the UFM1-interacting sequence (UIS), located outside the adenylation domain that is required for UFM1 activation. However, the precise boundaries of the UIS are yet not clear and are still under debate...
March 30, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28186401/chemoproteomic-screening-of-covalent-ligands-reveals-uba5-as-a-novel-pancreatic-cancer-target
#3
Allison M Roberts, David K Miyamoto, Tucker R Huffman, Leslie A Bateman, Ashley N Ives, David Akopian, Martin J Heslin, Carlo M Contreras, Michael Rape, Christine F Skibola, Daniel K Nomura
Chemical genetic screening of small-molecule libraries has been a promising strategy for discovering unique and novel therapeutic compounds. However, identifying the targets of lead molecules that arise from these screens has remained a major bottleneck in understanding the mechanism of action of these compounds. Here, we have coupled the screening of a cysteine-reactive fragment-based covalent ligand library with an isotopic tandem orthogonal proteolysis-enabled activity-based protein profiling (isoTOP-ABPP) chemoproteomic platform to rapidly couple the discovery of lead small molecules that impair pancreatic cancer pathogenicity with the identification of druggable hotspots for potential cancer therapy...
February 15, 2017: ACS Chemical Biology
https://www.readbyqxmd.com/read/28139377/cpt1a-methylation-is-associated-with-plasma-adiponectin
#4
S Aslibekyan, A N Do, H Xu, S Li, M R Irvin, D Zhi, H K Tiwari, D M Absher, A R Shuldiner, T Zhang, W Chen, K Tanner, C Hong, B D Mitchell, G Berenson, D K Arnett
BACKGROUND AND AIMS: Adiponectin, an adipose-secreted protein that has been linked to insulin sensitivity, plasma lipids, and inflammatory patterns, is an established biomarker for metabolic health. Despite clinical relevance and high heritability, the determinants of plasma adiponectin levels remain poorly understood. METHODS AND RESULTS: We conducted the first epigenome-wide cross-sectional study of adiponectin levels using methylation data on 368,051 cytosine-phosphate-guanine (CpG) sites in CD4+ T-cells from the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN, n = 991)...
March 2017: Nutrition, Metabolism, and Cardiovascular Diseases: NMCD
https://www.readbyqxmd.com/read/28128204/a-critical-role-of-ddrgk1-in-endoplasmic-reticulum-homoeostasis-via-regulation-of-ire1%C3%AE-stability
#5
Jiang Liu, Ying Wang, Lizhi Song, Linghua Zeng, Weiwei Yi, Ting Liu, Huanzhen Chen, Miao Wang, Zhenyu Ju, Yu-Sheng Cong
Disturbance of endoplasmic reticulum (ER) homoeostasis induces ER stress and leads to activation of the unfolded protein response (UPR), which is an adaptive reaction that promotes cell survival or triggers apoptosis, when homoeostasis is not restored. DDRGK1 is an ER membrane protein and a critical component of the ubiquitin-fold modifier 1 (Ufm1) system. However, the functions and mechanisms of DDRGK1 in ER homoeostasis are largely unknown. Here, we show that depletion of DDRGK1 induces ER stress and enhances ER stress-induced apoptosis in both cancer cells and hematopoietic stem cells (HSCs)...
January 27, 2017: Nature Communications
https://www.readbyqxmd.com/read/28104585/rcad-bip-pathway-is-necessary-for-the-proper-synthesis-of-digestive-enzymes-and-secretory-function-of-the-exocrine-pancreas
#6
Camille Miller, Yafei Cai, Tadd Patton, Sarai Hacker Graves, Honglin Li, Maria Eugenia Sabbatini
Alcoholism causes an imbalance of endoplasmic reticulum (ER) homeostasis in pancreatic acini. In those cells, the ER is involved in the synthesis and folding of pancreatic enzymes. Ubiquitin-fold modifier 1 (Ufm1) is part of a novel ubiquitin-like modification system involved in maintaining ER homeostasis. Among the components of the Ufm1 system, Regulator of C53 and DDRGK1 (RCAD) has recently been identified as a Ufm1-specific E3 ligase that promotes ufmylation of DDRGK1, an RCAD-interacting protein. We determined the importance of RCAD in the proper synthesis and secretion of pancreatic enzymes using mice with genetically deleted RCAD...
March 1, 2017: American Journal of Physiology. Gastrointestinal and Liver Physiology
https://www.readbyqxmd.com/read/28098257/a-comprehensive-platform-for-the-analysis-of-ubiquitin-like-protein-modifications-using-in-vivo-biotinylation
#7
Lucia Pirone, Wendy Xolalpa, Jón Otti Sigurðsson, Juanma Ramirez, Coralia Pérez, Monika González, Ainara Ruiz de Sabando, Félix Elortza, Manuel S Rodriguez, Ugo Mayor, Jesper V Olsen, Rosa Barrio, James D Sutherland
Post-translational modification by ubiquitin and ubiquitin-like proteins (UbLs) is fundamental for maintaining protein homeostasis. Efficient isolation of UbL conjugates is hampered by multiple factors, including cost and specificity of reagents, removal of UbLs by proteases, distinguishing UbL conjugates from interactors, and low quantities of modified substrates. Here we describe bioUbLs, a comprehensive set of tools for studying modifications in Drosophila and mammals, based on multicistronic expression and in vivo biotinylation using the E...
January 18, 2017: Scientific Reports
https://www.readbyqxmd.com/read/27545681/biallelic-variants-in-uba5-reveal-that-disruption-of-the-ufm1-cascade-can-result-in-early-onset-encephalopathy
#8
Estelle Colin, Jens Daniel, Alban Ziegler, Jamal Wakim, Aurora Scrivo, Tobias B Haack, Salim Khiati, Anne-Sophie Denommé, Patrizia Amati-Bonneau, Majida Charif, Vincent Procaccio, Pascal Reynier, Kyrieckos A Aleck, Lorenzo D Botto, Claudia Lena Herper, Charlotte Sophia Kaiser, Rima Nabbout, Sylvie N'Guyen, José Antonio Mora-Lorca, Birgit Assmann, Stine Christ, Thomas Meitinger, Tim M Strom, Holger Prokisch, Antonio Miranda-Vizuete, Georg F Hoffmann, Guy Lenaers, Pascale Bomont, Eva Liebau, Dominique Bonneau
Via whole-exome sequencing, we identified rare autosomal-recessive variants in UBA5 in five children from four unrelated families affected with a similar pattern of severe intellectual deficiency, microcephaly, movement disorders, and/or early-onset intractable epilepsy. UBA5 encodes the E1-activating enzyme of ubiquitin-fold modifier 1 (UFM1), a recently identified ubiquitin-like protein. Biochemical studies of mutant UBA5 proteins and studies in fibroblasts from affected individuals revealed that UBA5 mutations impair the process of ufmylation, resulting in an abnormal endoplasmic reticulum structure...
September 1, 2016: American Journal of Human Genetics
https://www.readbyqxmd.com/read/27545674/biallelic-variants-in-uba5-link-dysfunctional-ufm1%C3%A2-ubiquitin-like-modifier-pathway-to-severe-infantile-onset-encephalopathy
#9
Mikko Muona, Ryosuke Ishimura, Anni Laari, Yoshinobu Ichimura, Tarja Linnankivi, Riikka Keski-Filppula, Riitta Herva, Heikki Rantala, Anders Paetau, Minna Pöyhönen, Miki Obata, Takefumi Uemura, Thomas Karhu, Norihisa Bizen, Hirohide Takebayashi, Shane McKee, Michael J Parker, Nadia Akawi, Jeremy McRae, Matthew E Hurles, Outi Kuismin, Mitja I Kurki, Anna-Kaisa Anttonen, Keiji Tanaka, Aarno Palotie, Satoshi Waguri, Anna-Elina Lehesjoki, Masaaki Komatsu
The ubiquitin fold modifier 1 (UFM1) cascade is a recently identified evolutionarily conserved ubiquitin-like modification system whose function and link to human disease have remained largely uncharacterized. By using exome sequencing in Finnish individuals with severe epileptic syndromes, we identified pathogenic compound heterozygous variants in UBA5, encoding an activating enzyme for UFM1, in two unrelated families. Two additional individuals with biallelic UBA5 variants were identified from the UK-based Deciphering Developmental Disorders study and one from the Northern Finland Intellectual Disability cohort...
September 1, 2016: American Journal of Human Genetics
https://www.readbyqxmd.com/read/27520940/a-selective-inhibitor-of-the-ufm1-activating-enzyme-uba5
#10
Sara R da Silva, Stacey-Lynn Paiva, Matthew Bancerz, Mulu Geletu, Andrew M Lewis, Jijun Chen, Yafei Cai, Julie L Lukkarila, Honglin Li, Patrick T Gunning
Protein conjugation with ubiquitin and ubiquitin-like small molecules, such as UFM1, is important for promoting cancer cell survival and proliferation. Herein, the development of the first selective micromolar inhibitor of the UBA5 E1 enzyme that initiates UFM1 protein conjugation is described. This organometallic inhibitor incorporates adenosine and zinc(II)cyclen within its core scaffold and inhibits UBA5 noncompetitively and selectively over other E1 enzymes and a panel of human kinases. Furthermore, this compound selectively impedes the cellular proliferation (above 50μM) of cancer cells containing higher levels of UBA5...
September 15, 2016: Bioorganic & Medicinal Chemistry Letters
https://www.readbyqxmd.com/read/27240952/the-mpn-domain-of-caenorhabditis-elegans-ufsp-modulates-both-substrate-recognition-and-deufmylation-activity
#11
Byung Hak Ha, Kyung Hee Kim, Hee Min Yoo, Weontae Lee, Eunice EunKyeong Kim
Ubiquitin-fold modifier 1 (Ufm1) specific protease (UfSP) is a novel cysteine protease that activates Ufm1 from its precursor by processing the C-terminus to expose the conserved Gly necessary for substrate conjugation and de-conjugates Ufm1 from the substrate. There are two forms: UfSP1 and UfSP2, the later with an additional domain at the N-terminus. Ufm1 and both the conjugating and deconjugating enzymes are highly conserved. However, in Caenorhabditis elegans there is one UfSP which has extra 136 residues at the N terminus compared to UfSP2...
August 5, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27212118/ufmylation-a-unique-fashionable-modification-for-life
#12
REVIEW
Ying Wei, Xingzhi Xu
Ubiquitin-fold modifier 1 (UFM1) is one of the newly-identified ubiquitin-like proteins. Similar to ubiquitin, UFM1 is conjugated to its target proteins by a three-step enzymatic reaction. The UFM1-activating enzyme, ubiquitin-like modifier-activating enzyme 5 (UBA5), serves as the E1 to activate UFM1; UFM1-conjugating enzyme 1 (UFC1) acts as the E2 to transfer the activated UFM1 to the active site of the E2; and the UFM1-specific ligase 1 (UFL1) acts as the E3 to recognize its substrate, transfer, and ligate the UFM1 from E2 to the substrate...
June 2016: Genomics, Proteomics & Bioinformatics
https://www.readbyqxmd.com/read/27033164/essential-role-of-ufm1-conjugation-in-the-hematopoietic-system
#13
REVIEW
Yafei Cai, Nagendra Singh, Honglin Li
Protein modification by ubiquitin (Ub) and ubiquitin-like (Ubl) proteins plays a pivotal role in a wide range of cellular functions and signaling pathways. The Ufm1 conjugation system is a novel ubiquitin-like system that consists of Ufm1, Uba5 (E1), Ufc1 (E2), and less defined E3 ligase(s) and targets. Despite its discovery more than a decade ago, its biological functions and working mechanism remains poorly understood. Recent genetic studies using knockout mouse models provide unambiguous evidence for the indispensable role of the Ufm1 system in animal development and hematopoiesis, especially erythroid development...
June 2016: Experimental Hematology
https://www.readbyqxmd.com/read/26929408/structural-and-functional-analysis-of-a-novel-interaction-motif-within-ufm1-activating-enzyme-5-uba5-required-for-binding-to-ubiquitin-like-proteins-and-ufmylation
#14
Sabrina Habisov, Jessica Huber, Yoshinobu Ichimura, Masato Akutsu, Natalia Rogova, Frank Loehr, David G McEwan, Terje Johansen, Ivan Dikic, Volker Doetsch, Masaaki Komatsu, Vladimir V Rogov, Vladimir Kirkin
The covalent conjugation of ubiquitin-fold modifier 1 (UFM1) to proteins generates a signal that regulates transcription, response to cell stress, and differentiation. Ufmylation is initiated by ubiquitin-like modifier activating enzyme 5 (UBA5), which activates and transfers UFM1 to ubiquitin-fold modifier-conjugating enzyme 1 (UFC1). The details of the interaction between UFM1 and UBA5 required for UFM1 activation and its downstream transfer are however unclear. In this study, we described and characterized a combined linear LC3-interacting region/UFM1-interacting motif (LIR/UFIM) within the C terminus of UBA5...
April 22, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/26872069/uba5-mutations-cause-a-new-form-of-autosomal-recessive-cerebellar-ataxia
#15
Ranhui Duan, Yuting Shi, Li Yu, Gehan Zhang, Jia Li, Yunting Lin, Jifeng Guo, Junling Wang, Lu Shen, Hong Jiang, Guanghui Wang, Beisha Tang
Autosomal recessive cerebellar ataxia (ARCA) comprises a large and heterogeneous group of neurodegenerative disorders. For many affected patients, the genetic cause remains undetermined. Through whole-exome sequencing, we identified compound heterozygous mutations in ubiquitin-like modifier activating enzyme 5 gene (UBA5) in two Chinese siblings presenting with ARCA. Moreover, copy number variations in UBA5 or ubiquitin-fold modifier 1 gene (UFM1) were documented with the phenotypes of global developmental delays and gait disturbances in the ClinVar database...
2016: PloS One
https://www.readbyqxmd.com/read/26544067/ufbp1-a-key-component-of-the-ufm1-conjugation-system-is-essential-for-ufmylation-mediated-regulation-of-erythroid-development
#16
Yafei Cai, Wenhu Pi, Satish Sivaprakasam, Xiaobin Zhu, Mingsheng Zhang, Jijun Chen, Levi Makala, Chunwan Lu, Jianchu Wu, Yong Teng, Betty Pace, Dorothy Tuan, Nagendra Singh, Honglin Li
The Ufm1 conjugation system is an ubiquitin-like modification system that consists of Ufm1, Uba5 (E1), Ufc1 (E2), and less defined E3 ligase(s) and targets. The biological importance of this system is highlighted by its essential role in embryogenesis and erythroid development, but the underlying mechanism is poorly understood. UFBP1 (Ufm1 binding protein 1, also known as DDRGK1, Dashurin and C20orf116) is a putative Ufm1 target, yet its exact physiological function and impact of its ufmylation remain largely undefined...
November 2015: PLoS Genetics
https://www.readbyqxmd.com/read/26486471/genome-wide-association-studies-identify-genetic-loci-for-low-von-willebrand-factor-levels
#17
Janine van Loon, Abbas Dehghan, Tang Weihong, Stella Trompet, Wendy L McArdle, Folkert F W Asselbergs, Ming-Huei Chen, Lorna M Lopez, Jennifer E Huffman, Frank W G Leebeek, Saonli Basu, David J Stott, Ann Rumley, Ron T Gansevoort, Gail Davies, James J F Wilson, Jacqueline C M Witteman, Xiting Cao, Anton J M de Craen, Stephan J L Bakker, Bruce M Psaty, John M Starr, Albert Hofman, J Wouter Jukema, Ian J Deary, Caroline Hayward, Pim van der Harst, Gordon D O Lowe, Aaron R Folsom, David P Strachan, Nicolas Smith, Moniek P M de Maat, Christopher O'Donnell
Low von Willebrand factor (VWF) levels are associated with bleeding symptoms and are a diagnostic criterion for von Willebrand disease, the most common inherited bleeding disorder. To date, it is unclear which genetic loci are associated with reduced VWF levels. Therefore, we conducted a meta-analysis of genome-wide association studies to identify genetic loci associated with low VWF levels. For this meta-analysis, we included 31 149 participants of European ancestry from 11 community-based studies. From all participants, VWF antigen (VWF:Ag) measurements and genome-wide single-nucleotide polymorphism (SNP) scans were available...
July 2016: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/26428751/identification-of-a-mutation-in-the-ubiquitin-fold-modifier-1-specific-peptidase-2-gene-ufsp2-in-an-extended-south-african-family-with-beukes-hip-dysplasia
#18
Christopher Mark Watson, Laura A Crinnion, Lindsay Gleghorn, William G Newman, Rajkumar Ramesar, Peter Beighton, Gillian A Wallis
BACKGROUND: Beukes hip dysplasia (BHD) is an autosomal dominant disorder of variable penetrance that was originally identified in a large South African family of European origin. BHD is characterised by bilateral dysmorphism of the proximal femur, which results in severe degenerative osteoarthropathy. Previous studies mapped the disorder to a 3.34 Mb region on chromosome 4q35. OBJECTIVE: To fine-map the BHD locus and identify the disease-causing mutation by direct sequencing...
July 2015: South African Medical Journal, Suid-Afrikaanse Tydskrif Vir Geneeskunde
https://www.readbyqxmd.com/read/26040753/ufm1-protects-macrophages-from-oxldl-induced-foam-cell-formation-through-a-liver-x-receptor-%C3%AE-dependent-pathway
#19
Qi Pang, Jie Xiong, Xiao-Lei Hu, Jiang-Ping He, Hui-Fang Liu, Guang-Ya Zhang, Yuan-Yuan Li, Feng-Ling Chen
AIM: Macrophage foam cell formation is the most prominent characteristic of the early stages of atherosclerosis. Ubiquitin Fold Modifier 1 (UFM1) is a new member of the ubiquitin-like protein family, and its underlying mechanism of action in macrophage foam cell formation is poorly understood. Our current study focuses on UFM1 and investigates its role in macrophage foam cell formation. METHODS: Using real-time quantitative PCR (qRT-PCR) and western blot analysis, we first analyzed the UFM1 expression in mouse peritoneal macrophages (MPMs) from ApoE-/- mice in vivo and in human macrophages treated with oxLDL in vitro...
2015: Journal of Atherosclerosis and Thrombosis
https://www.readbyqxmd.com/read/25952549/rcad-ufl1-a-ufm1-e3-ligase-is-essential-for-hematopoietic-stem-cell-function-and-murine-hematopoiesis
#20
M Zhang, X Zhu, Y Zhang, Y Cai, J Chen, S Sivaprakasam, A Gurav, W Pi, L Makala, J Wu, B Pace, D Tuan-Lo, V Ganapathy, N Singh, H Li
The Ufm1 conjugation system is a novel ubiquitin-like modification system, consisting of Ufm1, Uba5 (E1), Ufc1 (E2) and poorly characterized E3 ligase(s). RCAD/Ufl1 (also known as KIAA0776, NLBP and Maxer) was reported to function as a Ufm1 E3 ligase in ufmylation (Ufm1-mediated conjugation) of DDRGK1 and ASC1 proteins. It has also been implicated in estrogen receptor signaling, unfolded protein response (UPR) and neurodegeneration, yet its physiological function remains completely unknown. In this study, we report that RCAD/Ufl1 is essential for embryonic development, hematopoietic stem cell (HSC) survival and erythroid differentiation...
December 2015: Cell Death and Differentiation
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