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[PMID]: 25979489
[Au] Autor:Boison D; Aronica E
[Ad] Address:Robert Stone Dow Neurobiology Laboratories, Legacy Research Institute, Portland, OR 97232, USA. Electronic address: dboison@downeurobiology.org.
[Ti] Title:Comorbidities in Neurology: Is adenosine the common link?
[So] Source:Neuropharmacology;97:18-34, 2015 Oct.
[Is] ISSN:1873-7064
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Comorbidities in Neurology represent a major conceptual and therapeutic challenge. For example, temporal lobe epilepsy (TLE) is a syndrome comprised of epileptic seizures and comorbid symptoms including memory and psychiatric impairment, depression, and sleep dysfunction. Similarly, Alzheimer's disease (AD), Parkinson's disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are accompanied by various degrees of memory dysfunction. Patients with AD have an increased likelihood for seizures, whereas all four conditions share certain aspects of psychosis, depression, and sleep dysfunction. This remarkable overlap suggests common pathophysiological mechanisms, which include synaptic dysfunction and synaptotoxicity, as well as glial activation and astrogliosis. Astrogliosis is linked to synapse function via the tripartite synapse, but astrocytes also control the availability of gliotransmitters and adenosine. Here we will specifically focus on the 'adenosine hypothesis of comorbidities' implying that astrocyte activation, via overexpression of adenosine kinase (ADK), induces a deficiency in the homeostatic tone of adenosine. We present evidence from patient-derived samples showing astrogliosis and overexpression of ADK as common pathological hallmark of epilepsy, AD, PD, and ALS. We discuss a transgenic 'comorbidity model', in which brain-wide overexpression of ADK and resulting adenosine deficiency produces a comorbid spectrum of seizures, altered dopaminergic function, attentional impairment, and deficits in cognitive domains and sleep regulation. We conclude that dysfunction of adenosine signaling is common in neurological conditions, that adenosine dysfunction can explain co-morbid phenotypes, and that therapeutic adenosine augmentation might be effective for the treatment of comorbid symptoms in multiple neurological conditions.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 188259 MEDLINE  
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[PMID]: 25616008
[Au] Autor:Tomas-Fernandez X; Warfield SK
[Ti] Title:A Model of Population and Subject (MOPS) Intensities With Application to Multiple Sclerosis Lesion Segmentation.
[So] Source:IEEE Trans Med Imaging;34(6):1349-61, 2015 Jun.
[Is] ISSN:1558-254X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:White matter (WM) lesions are thought to play an important role in multiple sclerosis (MS) disease burden. Recent work in the automated segmentation of white matter lesions from magnetic resonance imaging has utilized a model in which lesions are outliers in the distribution of tissue signal intensities across the entire brain of each patient. However, the sensitivity and specificity of lesion detection and segmentation with these approaches have been inadequate. In our analysis, we determined this is due to the substantial overlap between the whole brain signal intensity distribution of lesions and normal tissue. Inspired by the ability of experts to detect lesions based on their local signal intensity characteristics, we propose a new algorithm that achieves lesion and brain tissue segmentation through simultaneous estimation of a spatially global within-the-subject intensity distribution and a spatially local intensity distribution derived from a healthy reference population. We demonstrate that MS lesions can be segmented as outliers from this intensity model of population and subject. We carried out extensive experiments with both synthetic and clinical data, and compared the performance of our new algorithm to those of state-of-the art techniques. We found this new approach leads to a substantial improvement in the sensitivity and specificity of lesion detection and segmentation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1109/TMI.2015.2393853

  3 / 188259 MEDLINE  
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[PMID]: 26270071
[Au] Autor:Lucena CM; Santos RP
[Ad] Address:Fundação Universitária de Cardiologia, Porto Alegre, RS, BR.
[Ti] Title:Association between Aortic Valve Sclerosis and Adverse Cardiovascular Events.
[So] Source:Arq Bras Cardiol;105(1):99-100, 2015 Jul.
[Is] ISSN:1678-4170
[Cp] Country of publication:Brazil
[La] Language:eng; por
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 188259 MEDLINE  
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[PMID]: 26186011
[Au] Autor:Zhang Y; Zhao KT; Fox SG; Kim J; Kirsch DR; Ferrante RJ; Morimoto RI; Silverman RB
[Ad] Address:†Department of Chemistry, Department of Molecular Biosciences, Chemistry of Life Processes Institute, Center for Molecular Innovation and Drug Discovery, Northwestern University, Evanston, Illinois 60208-3113, United States....
[Ti] Title:Tertiary Amine Pyrazolones and Their Salts as Inhibitors of Mutant Superoxide Dismutase 1-Dependent Protein Aggregation for the Treatment of Amyotrophic Lateral Sclerosis.
[So] Source:J Med Chem;58(15):5942-9, 2015 Aug 13.
[Is] ISSN:1520-4804
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pyrazolone derivatives have previously been found to be inhibitors of Cu/Zn superoxide dismutase 1 (SOD1)-dependent protein aggregation, which extended survival of an amyotrophic lateral sclerosis (ALS) mouse model. On the basis of ADME analysis, we describe herein a new series of tertiary amine-containing pyrazolones and their structure-activity relationships. Further conversion to the conjugate salts greatly improved their solubility. Phosphate compound 17 exhibited numerous benefits both to cellular activity and to CNS-related drug-like properties in vitro and in vivo, including microsomal stability, tolerated toxicity, and blood-brain barrier permeation. These results indicate that tertiary amine pyrazolones comprise a valuable class of ALS drug candidates.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1021/acs.jmedchem.5b00561

  5 / 188259 MEDLINE  
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[PMID]: 26269719
[Au] Autor:Meisel SF; Carere DA; Wardle J; Kalia SS; Moreno TA; Mountain JL; Roberts JS; Green RC; PGen Study Group
[Ad] Address:Cancer Research UK Health Behaviour Research Centre, Department of Epidemiology and Public Health, University College London, London, UK....
[Ti] Title:Explaining, not just predicting, drives interest in personal genomics.
[So] Source:Genome Med;7(1):74, 2015.
[Is] ISSN:1756-994X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: There is a widespread assumption that risk prediction is the major driver of customer interest in personal genomic testing (PGT). However, some customers may also be motivated by finding out whether their existing diseases have a genetic etiology. We evaluated the impact of an existing medical diagnosis on customer interest in condition-specific results from PGT. METHODS: Using a prospective online survey of PGT customers, we measured customer interest prior to receiving PGT results for 11 health conditions, and examined the association between interest and personal medical history of these conditions using logistic regression. RESULTS: We analyzed data from 1,538 PGT customers, mean age 48.7 years, 61 % women, 90 % White, and 47 % college educated. The proportion of customers who were 'very interested' in condition-specific PGT varied considerably, from 28 % for ulcerative colitis to 68% for heart disease. After adjusting for demographic and personal characteristics including family history, having a diagnosis of the condition itself was significantly associated with interest in genetic testing for risk of that condition, with odds ratios ranging from 2.07 (95 % CI 1.28-3.37) for diabetes to 19.99 (95 % CI 4.57-87.35) for multiple sclerosis. CONCLUSIONS: PGT customers are particularly interested in genetic markers for their existing medical conditions, suggesting that the value of genetic testing is not only predictive, but also explanatory.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[St] Status:In-Data-Review
[do] DOI:10.1186/s13073-015-0188-5

  6 / 188259 MEDLINE  
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[PMID]: 26242630
[Au] Autor:Chastain EM; Getts DR; Miller SD
[Ad] Address:Department of Microbiology-Immunology and Interdepartmental Immunobiology Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
[Ti] Title:Deficient Natural Killer Dendritic Cell Responses Underlay the Induction of Theiler's Virus-Induced Autoimmunity.
[So] Source:MBio;6(4), 2015.
[Is] ISSN:2150-7511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: The initiating events in autoimmune disease remain to be completely understood, but it is thought that genetic predisposition synergizes with "environmental" factors, including viral infection, leading to disease. One elegant animal model used to study the pathogenesis of multiple sclerosis that perfectly blends genetics and environmental components in the context of virus-induced autoimmunity is Theiler's murine encephalitis virus-induced demyelinating disease (TMEV-IDD). TMEV-infected disease-susceptible SJL/J mice develop a persistent central nervous system (CNS) infection and later develop autoimmune demyelination, while disease-resistant C57BL/6 (B6) mice rapidly clear the infection and develop no autoimmune pathology. Mice of the (B6 × SJL/J)F1 cross between these two mouse strains are classified as intermediately susceptible. We employed this model to investigate if rapid virus clearance in B6 versus SJL/J mice was perhaps related to differences in the innate immune response in the CNS of the two strains in the first few days following intracerebral virus inoculation. Here we show that SJL/J mice lack, in addition to NK cells, a novel innate immune subset known as natural killer dendritic cells (NKDCs), which express phenotypic markers (CD11c(int) NK1.1(+)) and functional activity of both NK cells and DCs. These NKDCs are activated in the periphery and migrate into the infected CNS in a very late antigen 4 (VLA-4)-dependent fashion. Most significantly, NKDCs are critical for CNS clearance of TMEV, as transfer of NKDCs purified from B6 mice into TMEV-IDD-susceptible (B6 × SJL/J)F1 mice promotes viral clearance. Together the findings of this work show for the first time a link between NKDCs, viral infection, and CNS autoimmunity. IMPORTANCE: Viral infection is an important cofactor, along with genetic susceptibility, in the initiation of a variety of organ-specific autoimmune diseases. Thus, in-depth understanding of how virus infections trigger autoimmunity may lead to novel ways to prevent or treat these diseases. Theiler's murine encephalitis virus-induced demyelinating disease (TMEV-IDD) serves as an important model for the human T cell-mediated autoimmune demyelinating disease multiple sclerosis. Induction of TMEV-IDD is genetically controlled as SJL/J mice develop persistent central nervous system (CNS) infection leading to chronic autoimmune demyelination, while C57BL/6 mice rapidly clear virus and are disease resistant. We determined that, as opposed to resistant B6 mice, disease-susceptible SJL/J mice lacked a unique innate immune population, the natural killer dendritic cell (NKDC), which was shown to play a critical role in early CNS virus clearance via its ability to both present virus antigen to T cells and to lyse target cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 188259 MEDLINE  
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[PMID]: 26083567
[Au] Autor:Ighodaro ET; Jicha GA; Schmitt FA; Neltner JH; Abner EL; Kryscio RJ; Smith CD; Duplessis T; Anderson S; Patel E; Bachstetter A; Van Eldik LJ; Nelson PT
[Ad] Address:From Department of Pathology, Division of Neuropathology (JHN, PTN), Department of Neurology (GAJ, FAS, CDS), Department of Statistics (RJK), Department of Epidemiology (ELA), Sanders-Brown Center on Aging (GAJ, FAS, ELA, RJK, CDS, TD, SA, EL, AB, LVE, PTN), and Department of Anatomy and Neurobiology (ETI, LVE, PTN), University of Kentucky, Lexington, Kentucky.
[Ti] Title:Hippocampal Sclerosis of Aging Can Be Segmental: Two Cases and Review of the Literature.
[So] Source:J Neuropathol Exp Neurol;74(7):642-52, 2015 Jul.
[Is] ISSN:1554-6578
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hippocampal sclerosis of aging (HS-Aging) is a neurodegenerative disease that mimics Alzheimer disease (AD) clinically and has a prevalence rivaling AD in advanced age. Whereas clinical biomarkers are not yet optimized, HS-Aging has distinctive pathological features that distinguish it from other diseases with "hippocampal sclerosis" pathology, such as epilepsy, cerebrovascular perturbations, and frontotemporal lobar degeneration. By definition, HS-Aging brains show neuronal cell loss and gliosis in the hippocampal formation out of proportion to AD-type pathology; it is strongly associated with aberrant TDP-43 pathology and arteriolosclerosis. Here, we describe 2 cases of "segmental" HS-Aging in which "sclerosis" in the hippocampus was evident only in a subset of brain sections by hematoxylin and eosin (H&E) stain. In these cases, TDP-43 pathology was more widespread on immunostained sections than the neuronal cell loss and gliosis seen in H&E stains. The 2 patients were cognitively intact at baseline and were tracked longitudinally over a decade using cognitive studies with at least 1 neuroimaging scan. We discuss the relevant HS-Aging literature, which indicates the need for a clearer consensus-based delineation of "hippocampal sclerosis" and TDP-43 pathologies in aged subjects.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1506
[Cu] Class update date: 150726
[Lr] Last revision date:150726
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1097/NEN.0000000000000204

  8 / 188259 MEDLINE  
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[PMID]: 25934946
[Au] Autor:Oh KW; Moon C; Kim HY; Oh SI; Park J; Lee JH; Chang IY; Kim KS; Kim SH
[Ad] Address:Department of Neurology, College of Medicine and Cell Therapy Center for Neurologic Disorders, Hanyang University Hospital, Seoul, Republic of Korea; Department of Neurology, Busan Paik Hospital, Inje University College of Medicine, Busan, Republic of Korea; Bioengineering Institute, Corestem Inc., ...
[Ti] Title:Phase I trial of repeated intrathecal autologous bone marrow-derived mesenchymal stromal cells in amyotrophic lateral sclerosis.
[So] Source:Stem Cells Transl Med;4(6):590-7, 2015 Jun.
[Is] ISSN:2157-6564
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:UNLABELLED: Stem cell therapy is an emerging alternative therapeutic or disease-modifying strategy for amyotrophic lateral sclerosis (ALS). The aim of this open-label phase I clinical trial was to evaluate the safety of two repeated intrathecal injections of autologous bone marrow (BM)-derived mesenchymal stromal cells (MSCs) in ALS patients. Eight patients with definite or probable ALS were enrolled. After a 3-month lead-in period, autologous MSCs were isolated two times from the BM at an interval of 26 days and were then expanded in vitro for 28 days and suspended in autologous cerebrospinal fluid. Of the 8 patients, 7 received 2 intrathecal injections of autologous MSCs (1 × 10(6) cells per kg) 26 days apart. Clinical or laboratory measurements were recorded to evaluate the safety 12 months after the first MSC injection. The ALS Functional Rating Scale-Revised (ALSFRS-R), the Appel ALS score, and forced vital capacity were used to evaluate the patients' disease status. One patient died before treatment and was withdrawn from the study. With the exception of that patient, no serious adverse events were observed during the 12-month follow-up period. Most of the adverse events were self-limited or subsided after supportive treatment within 4 days. Decline in the ALSFRS-R score was not accelerated during the 6-month follow-up period. Two repeated intrathecal injections of autologous MSCs were safe and feasible throughout the duration of the 12-month follow-up period. SIGNIFICANCE: Stem cell therapy is an emerging alternative therapeutic or disease-modifying strategy for amyotrophic lateral sclerosis (ALS). To the authors' best knowledge, there are no clinical trials to evaluate the safety of repeated intrathecal injections of autologous bone marrow mesenchymal stromal cells in ALS. After the clinical trial (phase I/II) was conducted, the stem cell (HYNR-CS, NEURONATA-R) was included in the revision of the regulations on orphan drug designation (number 160; December 31, 2013) and approved as a New Drug Application (Department of Cell and Gene Therapy 233; July 30, 2014) by the Korean Food and Drug Administration. The phase II trial is expected to be reported later.
[Mh] MeSH terms primary: Amyotrophic Lateral Sclerosis/therapy
Bone Marrow Cells
Mesenchymal Stem Cell Transplantation
Mesenchymal Stromal Cells
[Mh] MeSH terms secundary: Adult
Aged
Amyotrophic Lateral Sclerosis/physiopathology
Autografts
Female
Follow-Up Studies
Humans
Male
Middle Aged
[Pt] Publication type:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1508
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[Da] Date of entry for processing:150530
[St] Status:MEDLINE
[do] DOI:10.5966/sctm.2014-0212

  9 / 188259 MEDLINE  
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[PMID]: 25694449
[Au] Autor:Aditi; Folkmann AW; Wente SR
[Ad] Address:Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN 37232.
[Ti] Title:Cytoplasmic hGle1A regulates stress granules by modulation of translation.
[So] Source:Mol Biol Cell;26(8):1476-90, 2015 Apr 15.
[Is] ISSN:1939-4586
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:When eukaryotic cells respond to stress, gene expression pathways change to selectively export and translate subsets of mRNAs. Translationally repressed mRNAs accumulate in cytoplasmic foci known as stress granules (SGs). SGs are in dynamic equilibrium with the translational machinery, but mechanisms controlling this are unclear. Gle1 is required for DEAD-box protein function during mRNA export and translation. We document that human Gle1 (hGle1) is a critical regulator of translation during stress. hGle1 is recruited to SGs, and hGLE1 small interfering RNA-mediated knockdown perturbs SG assembly, resulting in increased numbers of smaller SGs. The rate of SG disassembly is also delayed. Furthermore, SG hGle1-depletion defects correlate with translation perturbations, and the hGle1 role in SGs is independent of mRNA export. Interestingly, we observe isoform-specific roles for hGle1 in which SG function requires hGle1A, whereas mRNA export requires hGle1B. We find that the SG defects in hGle1-depleted cells are rescued by puromycin or DDX3 expression. Together with recent links of hGLE1 mutations in amyotrophic lateral sclerosis patients, these results uncover a paradigm for hGle1A modulating the balance between translation and SGs during stress and disease.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1504
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1091/mbc.E14-11-1523

  10 / 188259 MEDLINE  
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[PMID]: 24973214
[Au] Autor:Mueller AM; Yoon BH; Sadiq SA
[Ad] Address:From the Tisch Multiple Sclerosis Research Center of New York, New York, New York 10019.
[Ti] Title:Inhibition of hyaluronan synthesis protects against central nervous system (CNS) autoimmunity and increases CXCL12 expression in the inflamed CNS.
[So] Source:J Biol Chem;289(33):22888-99, 2014 Aug 15.
[Is] ISSN:1083-351X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hyaluronan (HA) may have proinflammatory roles in the context of CNS autoimmunity. It accumulates in demyelinated multiple sclerosis (MS) lesions, promotes antigen presentation, and enhances T-cell activation and proliferation. HA facilitates lymphocyte binding to vessels and CNS infiltration at the CNS vascular endothelium. Furthermore, HA signals through Toll-like receptors 2 and 4 to stimulate inflammatory gene expression. We assessed the role of HA in experimental autoimmune encephalomyelitis (EAE), an animal model of MS by administration of 4-methylumbelliferone (4MU), a well established inhibitor of HA synthesis. 4MU decreased hyaluronan synthesis in vitro and in vivo. It was protective in active EAE of C57Bl/6 mice, decreased spinal inflammatory infiltrates and spinal infiltration of Th1 cells, and increased differentiation of regulatory T-cells. In adoptive transfer EAE, feeding of 4MU to donor mice significantly decreased the encephalitogenicity of lymph node cells. The transfer of proteolipid protein (PLP)-stimulated lymph node cells to 4MU-fed mice resulted in a delayed EAE onset and delayed spinal T-cell infiltration. Expression of CXCL12, an anti-inflammatory chemokine, is reduced in MS patients in CSF cells and in spinal cord tissue during EAE. Hyaluronan suppressed production of CXCL12, whereas 4MU increased spinal CXCL12 in naive animals and during neuroinflammation. Neutralization of CXCR4, the most prominent receptor of CXCL12, by administration of AMD3100 diminished the protective impact of 4MU in adoptive transfer EAE. In conclusion, hyaluronan exacerbates CNS autoimmunity, enhances encephalitogenic T-cell responses, and suppresses the protective chemokine CXCL12 in CNS tissue. Inhibition of hyaluronan synthesis with 4MU protects against an animal model of MS and may represent an important therapeutic option in MS and other neuroinflammatory diseases.
[Mh] MeSH terms primary: Central Nervous System/immunology
Chemokine CXCL12/immunology
Encephalomyelitis, Autoimmune, Experimental/immunology
Gene Expression Regulation/immunology
Hyaluronic Acid/immunology
[Mh] MeSH terms secundary: Adoptive Transfer
Animals
Anti-HIV Agents/pharmacology
Central Nervous System/metabolism
Chemokine CXCL12/biosynthesis
Encephalomyelitis, Autoimmune, Experimental/metabolism
Encephalomyelitis, Autoimmune, Experimental/pathology
Female
Gene Expression Regulation/drug effects
Heterocyclic Compounds/pharmacology
Hyaluronic Acid/biosynthesis
Inflammation/immunology
Inflammation/metabolism
Inflammation/pathology
Mice
Rats
T-Lymphocytes, Regulatory/immunology
T-Lymphocytes, Regulatory/metabolism
T-Lymphocytes, Regulatory/pathology
Th1 Cells/immunology
Th1 Cells/metabolism
Th1 Cells/pathology
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Anti-HIV Agents); 0 (CXCL12 protein, rat); 0 (Chemokine CXCL12); 0 (Cxcl12 protein, mouse); 0 (Heterocyclic Compounds); 155148-31-5 (JM 3100); 9004-61-9 (Hyaluronic Acid)
[Em] Entry month:1412
[Cu] Class update date: 150815
[Lr] Last revision date:150815
[Js] Journal subset:IM
[Da] Date of entry for processing:140823
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M114.559583


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