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reticulon 4

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https://www.readbyqxmd.com/read/27786289/nogo-a-rtn4a-and-nogo-b-rtn4b-are-simultaneously-expressed-in-epithelial-fibroblast-and-neuronal-cells-and-maintain-er-morphology
#1
Olli Rämö, Darshan Kumar, Erika Gucciardo, Merja Joensuu, Maiju Saarekas, Helena Vihinen, Ilya Belevich, Olli-Pekka Smolander, Kui Qian, Petri Auvinen, Eija Jokitalo
Reticulons (RTNs) are a large family of membrane associated proteins with various functions. NOGO-A/RTN4A has a well-known function in limiting neurite outgrowth and restricting the plasticity of the mammalian central nervous system. On the other hand, Reticulon 4 proteins were shown to be involved in forming and maintaining endoplasmic reticulum (ER) tubules. Using comparative transcriptome analysis and qPCR, we show here that NOGO-B/RTN4B and NOGO-A/RTN4A are simultaneously expressed in cultured epithelial, fibroblast and neuronal cells...
October 27, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27744421/plasticity-related-gene-3-prg3-overcomes-myelin-associated-growth-inhibition-and-promotes-functional-recovery-after-spinal-cord-injury
#2
Thomas Broggini, Lisa Schnell, Ali Ghoochani, José María Mateos, Michael Buchfelder, Kurt Wiendieck, Michael K Schäfer, Ilker Y Eyupoglu, Nicolai E Savaskan
The Plasticity Related Gene family covers five, brain-specific, transmembrane proteins (PRG1-5, also termed LPPR1-5) that operate in neuronal plasticity during development, aging and brain trauma. Here we investigated the role of the PRG family on axonal and filopodia outgrowth. Comparative analysis revealed the strongest outgrowth induced by PRG3 (LPPR1). During development, PRG3 is ubiquitously located at the tip of neuronal processes and at the plasma membrane and declines with age. In utero electroporation of PRG3 induced dendritic protrusions and accelerated spine formations in cortical pyramidal neurons...
October 15, 2016: Aging
https://www.readbyqxmd.com/read/27378925/downregulation-of-gstk1-is-a-common-mechanism-underlying-hypertrophic-cardiomyopathy
#3
Shota Sasagawa, Yuhei Nishimura, Shiko Okabe, Soichiro Murakami, Yoshifumi Ashikawa, Mizuki Yuge, Koki Kawaguchi, Reiko Kawase, Ryuji Okamoto, Masaaki Ito, Toshio Tanaka
Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and is associated with a number of potential outcomes, including impaired diastolic function, heart failure, and sudden cardiac death. Various etiologies have been described for HCM, including pressure overload and mutations in sarcomeric and non-sarcomeric genes. However, the molecular pathogenesis of HCM remains incompletely understood. In this study, we performed comparative transcriptome analysis to identify dysregulated genes common to five mouse HCM models of differing etiology: (i) mutation of myosin heavy chain 6, (ii) mutation of tropomyosin 1, (iii) expressing human phospholamban on a null background, (iv) knockout of frataxin, and (v) transverse aortic constriction...
2016: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/27276652/reticulon-4a-nogo-a-influences-the-distribution-of-kir4-1-but-is-not-essential-for-potassium-conductance-in-retinal-m%C3%A3-ller-glia
#4
Sandrine Joly, Dana A Dodd, Benjamin F Grewe, Vincent Pernet
In the adult retina, we have previously shown that Nogo-A was highly expressed in Müller glia. However, the role of Nogo-A in the glial cell physiology is not clear. In this study, we investigated the possible influence that Nogo-A may exert on other polarized molecules in Müller cells, in particular inwardly rectifying potassium channel 4.1 (Kir4.1) and aquaporin 4 (AQP4) that respectively control potassium and water exchange in glial cells. Our results showed that adenovirus-mediated Nogo-A overexpression with AdNogo-A increased the immunofluorescent signal of Kir4...
August 3, 2016: Neuroscience Letters
https://www.readbyqxmd.com/read/27109183/nogo-a-inhibits-the-migration-and-invasion-of-human-malignant-glioma-u87mg-cells
#5
Shu-Guang Jin, Hyang-Hwa Ryu, Song-Yuan Li, Chun-Hao Li, Sa-Hoe Lim, Woo-Youl Jang, Shin Jung
Nogo or reticulon-4 (RTN4), also known as neurite outgrowth inhibitor, is a member of the reticulon family of genes. Nogo-A, one of the three isoforms, is enriched in the central nervous system (CNS). The extracellular domain of Nogo-A, Nogo-66, has neurite growth inhibitory activity that is specific for neurons and is mediated by the Nogo receptor. However, most of its functions are not known yet. We investigated whether Nogo-A modulates the migration and invasion of a glioblastoma cell line, as well as the factors that have an effect on Nogo-A...
June 2016: Oncology Reports
https://www.readbyqxmd.com/read/26945033/delayed-gelatinase-inhibition-induces-reticulon-4-receptor-expression-in-the-peri-infarct-cortex
#6
Sándor Nardai, Arpád Dobolyi, Judit Skopál, Kinga Lakatos, Béla Merkely, Zoltán Nagy
Matrix metalloproteinase (MMP) inhibition can potentially prevent hemorrhagic transformation following cerebral infarction; however, delayed-phase MMP activity is also necessary for functional recovery after experimental stroke. We sought to identify potential mechanisms responsible for the impaired recovery associated with subacute MMP inhibition in a transient middle cerebral artery occlusion model of focal ischemia in CD rats. Gelatinase inhibition was achieved by intracerebral injection of the Fn-439 MMP inhibitor 7 days after stroke...
April 2016: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/26609158/human-umbilical-tissue-derived-cells-promote-synapse-formation-and-neurite-outgrowth-via-thrombospondin-family-proteins
#7
Sehwon Koh, Namsoo Kim, Henry H Yin, Ian R Harris, Nadine S Dejneka, Cagla Eroglu
UNLABELLED: Cell therapy demonstrates great potential for the treatment of neurological disorders. Human umbilical tissue-derived cells (hUTCs) were previously shown to have protective and regenerative effects in animal models of stroke and retinal degeneration, but the underlying therapeutic mechanisms are unknown. Because synaptic dysfunction, synapse loss, degeneration of neuronal processes, and neuronal death are hallmarks of neurological diseases and retinal degenerations, we tested whether hUTCs contribute to tissue repair and regeneration by stimulating synapse formation, neurite outgrowth, and neuronal survival...
November 25, 2015: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/26605911/shared-molecular-mechanisms-in-alzheimer-s-disease-and-amyotrophic-lateral-sclerosis-neurofilament-dependent-transport-of-sapp-fus-tdp-43-and-sod1-with-endoplasmic-reticulum-like-tubules
#8
Virgil Muresan, Zoia Ladescu Muresan
BACKGROUND: Amyotrophic lateral sclerosis (ALS), a debilitating neurodegenerative disorder of the motor neurons, leads to the disorganization of the neurofilament (NF) cytoskeleton and - ultimately - the deterioration of the neuromuscular junction. Some familial cases of ALS are caused by mutated FUS, TDP-43 or SOD1; it is thought that the mutated proteins inflict pathology either by gain or loss of function. The proper function of the neuromuscular junction requires sAPP, a soluble proteolytic fragment of the amyloid-β precursor protein (APP) - a transmembrane protein implicated in the pathology of Alzheimer's disease (AD)...
2016: Neuro-degenerative Diseases
https://www.readbyqxmd.com/read/26191384/anti-aging-effect-and-gene-expression-profiling-of-aged-rats-treated-with-g-bimaculatus-extract
#9
Mi Young Ahn, Jae Sam Hwang, Eun Young Yun, Min-Ji Kim, Kun-Koo Park
Extract from Gryllus bimaculatus crickets inhibits oxidation at the DNA level, with reduced production of 8-hydroxy-2'-deoxyguanosine (8-OHdG). Microarray analyses were performed with a rat 28K cDNA clone set array to identify the gene expression profiles of aged (10 months old) Wistar Kyoto rats treated for one month with 100 mg/kg G. bimaculatus ethanol extract to assess the effects. The extract produced a meaningful anti-edema effect, evident by the inhibition of creatinine phosphokinase activity. The weights of abdominal and ovarian adipose tissues were reduced and the proportion of unsaturated fatty acids in adipose tissues was increased in an extract dose-dependent manner...
June 2015: Toxicological Research
https://www.readbyqxmd.com/read/26174362/nogo-b-protects-mice-against-lipopolysaccharide-induced-acute-lung-injury
#10
Wujian Xu, Ying Zhu, Yunye Ning, Yuchao Dong, Haidong Huang, Wei Zhang, Qinying Sun, Qiang Li
Nogo-B, a member of the reticulon 4 protein family, plays a critical role in tissue repair and acute inflammation. Its role in acute lung injury (ALI) remains unclear. Here, we assessed the function of Nogo-B during tissue injury in a lipopolysaccharide (LPS)-induced ALI mouse model. We found that pulmonary Nogo-B was significantly repressed after LPS instillation in C57BL/6 mice. Over-expression of pulmonary Nogo-B using an adenovirus vector carrying the Nogo-B-RFP-3flag gene (Ad-Nogo-B) significantly prolonged the survival of mice challenged with a lethal dose of LPS...
July 15, 2015: Scientific Reports
https://www.readbyqxmd.com/read/26099580/endoplasmic-reticulum-tubule-protein-reticulon-4-associates-with-the-legionella-pneumophila-vacuole-and-with-translocated-substrate-ceg9
#11
Eva Haenssler, Vinay Ramabhadran, Connor S Murphy, Matthew I Heidtman, Ralph R Isberg
Intracellular growth of Legionella pneumophila occurs in a replication vacuole constructed by host proteins that regulate vesicular traffic from the host endoplasmic reticulum (ER). This process is promoted by a combination of approximately 300 Icm/Dot translocated substrates (IDTS). One of these proteins, Ceg9, was previously identified in a screen for L. pneumophila IDTS that manipulate secretory traffic when overexpressed in yeast. Using ectopic expression of Ceg9 in mammalian cells, we demonstrate that Ceg9 interacts with isoforms of host reticulon 4 (Rtn4), a protein that regulates ER tubule formation...
September 2015: Infection and Immunity
https://www.readbyqxmd.com/read/26083872/a-common-functional-allele-of-the-nogo-receptor-gene-reticulon-4-receptor-rtn4r-is-associated-with-sporadic-amyotrophic-lateral-sclerosis-in-a-french-population
#12
Maïté Amy, Oliver Staehlin, Frédérique René, Hélène Blasco, Sylviane Marouillat, Hussein Daoud, Patrick Vourc'h, Paul H Gordon, William Camu, Philippe Corcia, Jean-Philippe Loeffler, Miklós Palkovits, Wolfgang H Sommer, Christian R Andres
Amyotrophic lateral sclerosis is sporadic (SALS) in 90% of cases and has complex environmental and genetic influences. Nogo protein inhibits neurite outgrowth and is overexpressed in muscle in ALS. Our aims were to study the reticulon 4 receptor gene RTN4R which encodes Nogo 1 receptor (NgR1) in SALS, to test if the variants were associated with variable expression of the gene and whether NgR1 protein expression was modified in a transgenic mouse model of ALS. We genotyped three single nucleotide polymorphisms (SNPs; rs701421, rs701427, and rs1567871) of the RTN4R gene in 364 SALS French patients and 430 controls...
2015: Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration
https://www.readbyqxmd.com/read/25946643/ras-transformation-results-in-cleavage-of-reticulon-protein-nogo-b-that-is-associated-with-impairment-of-ifn-response
#13
Dae-Gyun Ahn, Tanveer Sharif, Kenneth Chisholm, Devanand M Pinto, Shashi A Gujar, Patrick W K Lee
Dysregulation of Ras signaling is the major cause of various cancers. Aberrant Ras signaling, however, provides a favorable environment for many viruses, making them suitable candidates as cancer-killing therapeutic agents. Susceptibility of cancer cells to such viruses is mainly due to impaired type I interferon (IFN) response, often as a result of activated Ras/ERK signaling in these cells. In this study, we searched for cellular factors modulated by Ras signaling and their potential involvement in promoting viral oncolysis...
2015: Cell Cycle
https://www.readbyqxmd.com/read/25501600/the-endogenous-caspase-8-inhibitor-c-flipl-regulates-er-morphology-and-crosstalk-with-mitochondria
#14
E S Marini, C Giampietri, S Petrungaro, S Conti, A Filippini, L Scorrano, E Ziparo
Components of the death receptor-mediated pathways like caspase-8 have been identified in complexes at intracellular membranes to spatially restrict the processing of local targets. In this study, we report that the long isoform of the cellular FLICE-inhibitory protein (c-FLIP(L)), a well-known inhibitor of the extrinsic cell death initiator caspase-8, localizes at the endoplasmic reticulum (ER) and mitochondria-associated membranes (MAMs). ER morphology was disrupted and ER Ca(2+)-release as well as ER-mitochondria tethering was decreased in c-FLIP(-/-) mouse embryonic fibroblasts (MEFs)...
July 2015: Cell Death and Differentiation
https://www.readbyqxmd.com/read/25040983/rtn4-3-utr-insertion-deletion-polymorphism-and-susceptibility-to-non-small-cell-lung-cancer-in-chinese-han-population
#15
De-Yi Lu, Xu-Hua Mao, Ying-Hui Zhou, Xiao-Long Yan, Wei-Ping Wang, Ya-Biao Zheng, Juan-Juan Xiao, Ping Zhang, Jian-Guo Wang, Neetika Ashwani, Wei-Liang Ding, Hua Jiang, Yan Shang, Ming-Hua Wang
Nogo protein, encoded by gene reticulon-4 (RTN4), includes three major isoforms by different splicing, named Nogo-A Nogo-B and Nogo-C. Nogo proteins play an important role in the apoptosis of cells, especially in tumor cells. RTN4 single nucleotide polymorphisms (SNPs) can influence the efficiency of transcription and translation thus being related with an individual's predisposition to cancer. The CAA insertion/deletion polymorphism (rs34917480) within RTN4 3'-UTR has been reported to be associated with many cancer types...
2014: Asian Pacific Journal of Cancer Prevention: APJCP
https://www.readbyqxmd.com/read/24891604/rab18-and-a-rab18-gef-complex-are-required-for-normal-er-structure
#16
Andreas Gerondopoulos, Ricardo Nunes Bastos, Shin-Ichiro Yoshimura, Rachel Anderson, Sarah Carpanini, Irene Aligianis, Mark T Handley, Francis A Barr
The ancestral Rab GTPase Rab18 and both subunits of the Rab3GAP complex are mutated in the human neurological and developmental disorder Warburg Micro syndrome. Here, we demonstrate that the Rab3GAP complex is a specific Rab18 guanine nucleotide exchange factor (GEF). The Rab3GAP complex localizes to the endoplasmic reticulum (ER) and is necessary for ER targeting of Rab18. It is also sufficient to promote membrane recruitment of Rab18. Disease-associated point mutations of conserved residues in either the Rab3GAP1 (T18P and E24V) or Rab3GAP2 (R426C) subunits result in loss of the Rab18 GEF and membrane-targeting activities...
June 9, 2014: Journal of Cell Biology
https://www.readbyqxmd.com/read/24863057/glutamate-provides-a-key-structural-contact-between-reticulon-4-nogo-66-and-phosphocholine
#17
Ali Alhoshani, Rosemarie Vithayathil, Jonathan Bandong, Katherine M Chrunyk, Gabriel O Moreno, Gregory A Weiss, Melanie J Cocco
Human reticulon 4 (RTN-4) has been identified as the neurite outgrowth inhibitor (Nogo). This protein contains a span of 66 amino acids (Nogo-66) flanked by two membrane helices at the C-terminus. We previously determined the NMR structure of Nogo-66 in a native-like environment and defined the regions of Nogo-66 expected to be membrane embedded. We hypothesize that aromatic groups and a negative charge hyperconserved among RTNs (Glu26) drive the remarkably strong association of Nogo-66 with a phosphocholine surface...
September 2014: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/24668814/protrudin-regulates-endoplasmic-reticulum-morphology-and-function-associated-with-the-pathogenesis-of-hereditary-spastic-paraplegia
#18
Yutaka Hashimoto, Michiko Shirane, Fumiko Matsuzaki, Shotaro Saita, Takafumi Ohnishi, Keiichi I Nakayama
Protrudin is a membrane protein that regulates polarized vesicular trafficking in neurons. The protrudin gene (ZFYVE27) is mutated in a subset of individuals with hereditary spastic paraplegia (HSP), and protrudin is therefore also referred to as spastic paraplegia (SPG) 33. We have now generated mice that express a transgene for dual epitope-tagged protrudin under control of a neuron-specific promoter, and we have subjected highly purified protrudin-containing complexes isolated from the brain of these mice to proteomics analysis to identify proteins that associate with protrudin...
May 9, 2014: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/24618539/subcellular-mechanisms-in-pulmonary-arterial-hypertension-combinatorial-modalities-that-inhibit-anterograde-trafficking-and-cause-bone-morphogenetic-protein-receptor-type-2-mislocalization
#19
Yang-Ming Yang, Kirk B Lane, Pravin B Sehgal
Abstract The natural history of familial pulmonary arterial hypertension (PAH) typically involves mutations in and/or haploinsuffciency of BMPR2 (gene for bone morphogenetic protein receptor type 2) but with low penetrance (10%-15%), delayed onset (in the third or fourth decade), and a gender bias (two- to fourfold more prevalent in postpubertal women). Thus, investigators have sought an understanding of "second-hit" modalities that might affect BMPR2 anterograde trafficking and/or function. Indeed, vascular lung lesions in PAH have been reported to contain enlarged "vacuolated" endothelial and smooth muscle cells with dilated endoplasmic reticulum (ER) cisternae, increased ER structural protein reticulon 4 (also called Nogo-B), and enlarged and fragmented Golgi apparatus...
September 2013: Pulmonary Circulation
https://www.readbyqxmd.com/read/24568601/nogo-b-receptor-modulates-angiogenesis-response-of-pulmonary-artery-endothelial-cells-through-enos-coupling
#20
Ru-Jeng Teng, Ujala Rana, Adeleye J Afolayan, Baofeng Zhao, Qing R Miao, Girija G Konduri
Nogo-B, a reticulon-4 isoform, modulates the motility and adhesion of vascular endothelial cells after binding to its receptor, Nogo-B receptor (NgBR). Nogo-B/NgBR pathway contributes to vascular remodeling and angiogenesis, but the role of this pathway in the angiogenesis of developing lungs remains unknown. We previously reported that angiogenesis function of pulmonary artery endothelial cells (PAECs) is impaired by increased reactive oxygen species formation in a fetal lamb model of intrauterine pulmonary hypertension (IPH)...
August 2014: American Journal of Respiratory Cell and Molecular Biology
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