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Pesquisa : D12.776.543.750.705.940.742 [Categoria DeCS]
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[PMID]:27396949
[Au] Autor:Schade J; Weidenmaier C
[Ad] Endereço:Interfaculty Institute for Microbiology and Infection Medicine (IMIT), University of Tübingen, Germany.
[Ti] Título:Cell wall glycopolymers of Firmicutes and their role as nonprotein adhesins.
[So] Source:FEBS Lett;590(21):3758-3771, 2016 Nov.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cell wall glycopolymers (CWGs) of gram-positive bacteria have gained increasing interest with respect to their role in colonization and infection. In most gram-positive pathogens they constitute a large fraction of the cell wall biomass and represent major cell envelope determinants. Depending on their chemical structure they modulate interaction with complement factors and play roles in immune evasion or serve as nonprotein adhesins that mediate, especially under dynamic conditions, attachment to different host cell types. In particular, covalently peptidoglycan-attached CWGs that extend well above the cell wall seem to interact with glyco-receptors on host cell surfaces. For example, in the case of Staphylococcus aureus, the cell wall-attached teichoic acid (WTA) has been identified as a major CWG adhesin. A recent report indicates that a type-F scavenger receptor, termed SR-F1 (SREC-I), is the predominant WTA receptor in the nasal cavity and that WTA-SREC-I interaction plays an important role in S. aureus nasal colonization. Therefore, understanding the role of CWGs in complex processes that mediate colonization and infection will allow novel insights into the mechanisms of host-microbiota interaction.
[Mh] Termos MeSH primário: Parede Celular/metabolismo
Firmicutes/metabolismo
Polissacarídeos Bacterianos/metabolismo
Receptores Depuradores Classe F/metabolismo
[Mh] Termos MeSH secundário: Adesinas Bacterianas/química
Adesinas Bacterianas/metabolismo
Parede Celular/química
Firmicutes/química
Infecções por Bactérias Gram-Positivas/microbiologia
Interações Hospedeiro-Patógeno
Seres Humanos
Cavidade Nasal/microbiologia
Polissacarídeos Bacterianos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adhesins, Bacterial); 0 (Polysaccharides, Bacterial); 0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class F)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160712
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12288


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[PMID]:27375131
[Au] Autor:Niederhoffer KY; Fahiminiya S; Eydoux P; Mawson J; Nishimura G; Jerome-Majewska LA; Patel MS
[Ad] Endereço:Department of Medical Genetics, University of British Columbia, Vancouver, British Columbia, Canada.
[Ti] Título:Diagnosis of Van den Ende-Gupta syndrome: Approach to the Marden-Walker-like spectrum of disorders.
[So] Source:Am J Med Genet A;170(9):2310-21, 2016 Sep.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Marden-Walker syndrome is challenging to diagnose, as there is significant overlap with other multi-system congenital contracture syndromes including Beals congenital contractural arachnodactyly, D4ST1-Deficient Ehlers-Danlos syndrome (adducted thumb-clubfoot syndrome), Schwartz-Jampel syndrome, Freeman-Sheldon syndrome, Cerebro-oculo-facio-skeletal syndrome, and Van den Ende-Gupta syndrome. We discuss this differential diagnosis in the context of a boy from a consanguineous union with Van den Ende-Gupta syndrome, a diagnosis initially confused by the atypical presence of intellectual disability. SNP microarray and whole exome sequencing identified a homozygous frameshift mutation (p.L870V) in SCARF2 and predicted damaging mutations in several genes, most notably DGCR2 (p.P75L) and NCAM2 (p.S147G), both possible candidates for this child's intellectual disability. We review distinguishing features for each Marden-Walker-like syndrome and propose a clinical algorithm for diagnosis among this spectrum of disorders. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Anormalidades Múltiplas/diagnóstico
Anormalidades Múltiplas/genética
Aracnodactilia/diagnóstico
Aracnodactilia/genética
Blefarofimose/diagnóstico
Blefarofimose/genética
Contratura/diagnóstico
Contratura/genética
Estudos de Associação Genética
[Mh] Termos MeSH secundário: Anormalidades Múltiplas/metabolismo
Aracnodactilia/metabolismo
Blefarofimose/metabolismo
Criança
Contratura/metabolismo
Variações do Número de Cópias de DNA
Exoma
Mutação da Fase de Leitura
Sequenciamento de Nucleotídeos em Larga Escala
Homozigoto
Seres Humanos
Masculino
Imagem Multimodal
Análise de Sequência com Séries de Oligonucleotídeos
Fenótipo
Polimorfismo de Nucleotídeo Único
Receptores Depuradores Classe F/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SCARF2 protein, human); 0 (Scavenger Receptors, Class F)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160705
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.37831


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[PMID]:27187611
[Au] Autor:Hytönen MK; Arumilli M; Lappalainen AK; Owczarek-Lipska M; Jagannathan V; Hundi S; Salmela E; Venta P; Sarkiala E; Jokinen T; Gorgas D; Kere J; Nieminen P; Drögemüller C; Lohi H
[Ad] Endereço:Department of Veterinary Biosciences, University of Helsinki, Helsinki, Finland.
[Ti] Título:Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes.
[So] Source:PLoS Genet;12(5):e1006037, 2016 May.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:One to two percent of all children are born with a developmental disorder requiring pediatric hospital admissions. For many such syndromes, the molecular pathogenesis remains poorly characterized. Parallel developmental disorders in other species could provide complementary models for human rare diseases by uncovering new candidate genes, improving the understanding of the molecular mechanisms and opening possibilities for therapeutic trials. We performed various experiments, e.g. combined genome-wide association and next generation sequencing, to investigate the clinico-pathological features and genetic causes of three developmental syndromes in dogs, including craniomandibular osteopathy (CMO), a previously undescribed skeletal syndrome, and dental hypomineralization, for which we identified pathogenic variants in the canine SLC37A2 (truncating splicing enhancer variant), SCARF2 (truncating 2-bp deletion) and FAM20C (missense variant) genes, respectively. CMO is a clinical equivalent to an infantile cortical hyperostosis (Caffey disease), for which SLC37A2 is a new candidate gene. SLC37A2 is a poorly characterized member of a glucose-phosphate transporter family without previous disease associations. It is expressed in many tissues, including cells of the macrophage lineage, e.g. osteoclasts, and suggests a disease mechanism, in which an impaired glucose homeostasis in osteoclasts compromises their function in the developing bone, leading to hyperostosis. Mutations in SCARF2 and FAM20C have been associated with the human van den Ende-Gupta and Raine syndromes that include numerous features similar to the affected dogs. Given the growing interest in the molecular characterization and treatment of human rare diseases, our study presents three novel physiologically relevant models for further research and therapy approaches, while providing the molecular identity for the canine conditions.
[Mh] Termos MeSH primário: Anormalidades Múltiplas/genética
Aracnodactilia/genética
Blefarofimose/genética
Fissura Palatina/genética
Contratura/genética
Exoftalmia/genética
Hiperostose Cortical Congênita/genética
Microcefalia/genética
Osteosclerose/genética
[Mh] Termos MeSH secundário: Anormalidades Múltiplas/patologia
Animais
Antiporters/genética
Aracnodactilia/patologia
Blefarofimose/patologia
Doenças Ósseas/genética
Doenças Ósseas/patologia
Caseína Quinase I/genética
Fissura Palatina/patologia
Contratura/patologia
Transtornos Craniomandibulares/genética
Transtornos Craniomandibulares/patologia
Modelos Animais de Doenças
Cães
Exoftalmia/patologia
Proteínas da Matriz Extracelular/genética
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
Seres Humanos
Hiperostose Cortical Congênita/patologia
Microcefalia/patologia
Osteosclerose/patologia
Receptores Depuradores Classe F/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiporters); 0 (Extracellular Matrix Proteins); 0 (SCARF2 protein, human); 0 (Scavenger Receptors, Class F); 0 (Slc37a2 protein, human); EC 2.7.11.1 (Casein Kinase I); EC 2.7.11.1 (FAM20C protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160518
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006037


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[PMID]:26343178
[Au] Autor:He J; Liu W; Wang S; Liu W; Liu H
[Ad] Endereço:National Engineering Research Center of Marine Facilities Aquaculture, Zhejiang Ocean University, Zhoushan 316022, PR China.
[Ti] Título:The SREC-I and SREC-II associated with epidermal growth factor in scavenger receptor family are the potential regulative transmembrane receptors in Larimichthys crocea.
[So] Source:Fish Shellfish Immunol;47(1):182-95, 2015 Nov.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In innate immunity, the regulation of the immunologic gene expression plays a vital role in defense against pathogenic threat. The class F scavenger receptors (SCARFs), a kind of crucial immunologic type I transmembrane receptors, mainly involve in the signal transmission and eliminating pathogens in host immune system. In this study, the SREC-I and SREC-II of SCARFs in Larimichthys crocea (designated as LycSREC1 and LycSREC2 respectively) were first identified, the potential genetic locus relationships with other species were depicted and the features of gene expression after Vibrio alginolyticus stimulation were tested. The results demonstrated that the complete ORF sequences of two candidates were 3024 bp and 2832 bp (KM884873 and KM884874) respectively including some important domains and motifs, such as EGF/EGF-like domains, TRAF2-binding consensus motif, generic motif and atipical motif. The gene location maps and genetic locus interpreted that the DNA sequences of LycSREC1 and LycSREC2 were 7603 bp and 4883 bp, and some locus had changed compared with human being, but three more crucial genetic locus were conservative among ten species. Furthermore, quantitative real-time PCR (qRT-PCR) analysis indicated that the highest mRNA expression of LycSREC1 and LycSREC2 were both in liver among eight detected tissues, and their expression were up-regulated by V. alginolyticus stimulation. All these findings would contribute to better understanding the biologic function of SCARFs in defending against pathogenic bacteria challenge and further exploring the innate immune of sciaenidae fish.
[Mh] Termos MeSH primário: Doenças dos Peixes/genética
Proteínas de Peixes/genética
Perciformes
Receptores Depuradores Classe F/genética
Vibrioses/veterinária
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Clonagem Molecular
Fator de Crescimento Epidérmico/genética
Fator de Crescimento Epidérmico/metabolismo
Doenças dos Peixes/imunologia
Doenças dos Peixes/metabolismo
Proteínas de Peixes/química
Proteínas de Peixes/metabolismo
Imunidade Inata
Dados de Sequência Molecular
Fases de Leitura Aberta
Especificidade de Órgãos
Filogenia
Receptores Depuradores Classe F/química
Receptores Depuradores Classe F/metabolismo
Alinhamento de Sequência/veterinária
Vibrioses/genética
Vibrioses/imunologia
Vibrioses/metabolismo
Vibrio alginolyticus/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Scavenger Receptors, Class F); 62229-50-9 (Epidermal Growth Factor)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151103
[Lr] Data última revisão:
151103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150908
[St] Status:MEDLINE


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[PMID]:25767073
[Au] Autor:Murshid A; Borges TJ; Calderwood SK
[Ad] Endereço:Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, United States.
[Ti] Título:Emerging roles for scavenger receptor SREC-I in immunity.
[So] Source:Cytokine;75(2):256-60, 2015 Oct.
[Is] ISSN:1096-0023
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:SREC-I is a class F scavenger receptor with key role in the immune response, particularly in antigen presenting cell (APC) such as macrophages and dendritic cells (DC). This receptor is able to mediate engulfment of dead cells as well as endocytosis of heat shock protein (HSP)-antigen complexes. SREC-I could thus potentially mediate the tolerizing influence of apoptotic cells or the immunostimulatory effects of HSP-peptide complexes, depending on context. This receptor was able to mediate presentation of external antigens, bound to HSPs through both the class II pathway as well as cross presentation via MHC class I complexes. In addition to its recently established role in adaptive immunity, emerging studies are indicating a broad role in innate immunity and regulation of cell signaling through Toll Like Receptors (TLR). SREC-I may thus play a key role in APC function by coordinating immune responses to internal and external antigens in APC.
[Mh] Termos MeSH primário: Apresentação do Antígeno/imunologia
Apresentação Cruzada/imunologia
Células Dendríticas/imunologia
Macrófagos/imunologia
Receptores Depuradores Classe F/imunologia
[Mh] Termos MeSH secundário: Apoptose/imunologia
Endocitose/imunologia
Proteínas de Choque Térmico HSP70/imunologia
Seres Humanos
Fagocitose/imunologia
Transdução de Sinais/imunologia
Linfócitos T/imunologia
Receptores Toll-Like/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (HSP70 Heat-Shock Proteins); 0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class F); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150314
[St] Status:MEDLINE


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[PMID]:25641411
[Au] Autor:Murshid A; Gong J; Ahmad R; Borges TJ; Calderwood SK
[Ad] Endereço:Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States.
[Ti] Título:Scavenger receptor SREC-I promotes double stranded RNA-mediated TLR3 activation in human monocytes.
[So] Source:Immunobiology;220(6):823-32, 2015 Jun.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Scavenger receptor associated with endothelial cells (SREC-I) was previously shown to be expressed by immune cells and to play a role in CD8(+)-mediated T cell immunity. SREC-I was also shown to modulate the function of Toll like receptors with essential roles in innate immunity. Here we have shown that SREC-I enhanced double stranded RNA (dsRNA)-mediated Toll like receptor-3 (TLR3) activation. Viral double stranded RNA (dsRNA) was demonstrated to be a pathogen associated molecular pattern (PAMP) signaling viral infection. We found that in human monocyte/macrophage THP1 cells as well as murine bone marrow derived macrophages SREC-I led to elevated responses to the dsRNA-like molecule polyinosine-polycytidylic acid (Poly I:C) and enhanced production of inflammatory cytokines. Our data also showed that intracellular/endocytic TLR3 could directly interact with SREC-I in the presence of Poly I:C. The internalized ligand, along with TLR3 and SREC-I localized in endosomes within macrophages and in HEK293 cells engineered to express TLR3 and SREC-I. SREC-I also stimulated dsRNA-mediated TLR3 activation of signaling through the NFκß, MAP kinase and interferon regulatory factor 3 (IRF3) pathways leading to expression of cytokines, most notably interleukin-8 and interferon-ß. We therefore hypothesized that SREC-I could be a receptor capable of internalizing Poly I:C, boosting TLR3 mediated inflammatory signaling and stimulating cytokine production in macrophages.
[Mh] Termos MeSH primário: Monócitos/imunologia
Monócitos/metabolismo
RNA de Cadeia Dupla/metabolismo
Receptores Depuradores Classe F/metabolismo
Receptor 3 Toll-Like/metabolismo
[Mh] Termos MeSH secundário: Citocinas/biossíntese
Expressão Gênica
Células HEK293
Seres Humanos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Modelos Biológicos
NF-kappa B/metabolismo
Poli I-C/imunologia
Ligação Proteica
Transporte Proteico
Receptores Depuradores Classe F/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (NF-kappa B); 0 (RNA, Double-Stranded); 0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class F); 0 (Toll-Like Receptor 3); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150203
[St] Status:MEDLINE


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[PMID]:25155057
[Au] Autor:Murshid A; Gong J; Calderwood SK
[Ad] Endereço:Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston MA02215, United States.
[Ti] Título:Hsp90-peptide complexes stimulate antigen presentation through the class II pathway after binding scavenger receptor SREC-I.
[So] Source:Immunobiology;219(12):924-31, 2014 Dec.
[Is] ISSN:1878-3279
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Molecular chaperones such as heat shock protein 90 (Hsp90) have been shown to form complexes with tumor antigens and can be used to prepare anticancer vaccines largely due to this property. Earlier studies had suggested that mice immunized with a molecular chaperone-based vaccine derived from tumors became immune to further vaccination and that both CD8(+) and CD4(+) T cells were activated by the chaperone vaccine in a manner dependent on scavenger receptor SREC-I. Here we have investigated mechanisms whereby SREC-I might facilitate uptake of Hsp90-conjugated peptides by APC into the MHC class II pathway for presentation to CD4(+) T cells. Our studies showed that antigenic peptides associated with Hsp90 were taken up into the class II pathway by a mechanism dependent on SREC-I binding and internalization and presented to CD4(+) T cells. In addition our studies showed that SREC-I could associate with MHC class II molecules on the cell surface and in intracellular endosomes, suggesting a mechanism involving facilitated uptake of peptides into the MHC class II pathway. These studies in addition to our earlier findings showed SREC-I to play a primary role in chaperone-associated antigen uptake both through cross priming of MHC class I molecules and entry into the class II pathway.
[Mh] Termos MeSH primário: Antígenos de Neoplasias/imunologia
Proteínas de Choque Térmico HSP90/metabolismo
Antígenos de Histocompatibilidade Classe II/metabolismo
Peptídeos/imunologia
Peptídeos/metabolismo
Receptores Depuradores Classe F/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Apresentação do Antígeno/imunologia
Antígenos de Neoplasias/química
Linhagem Celular
Membrana Celular/metabolismo
Apresentação Cruzada
Antígenos de Histocompatibilidade Classe II/imunologia
Seres Humanos
Espaço Intracelular
Camundongos
Modelos Biológicos
Ligação Proteica
Transporte Proteico
Receptores Depuradores Classe F/genética
Proteína cdc42 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Antigens, Neoplasm); 0 (HSP90 Heat-Shock Proteins); 0 (Histocompatibility Antigens Class II); 0 (Peptides); 0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class F); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140827
[St] Status:MEDLINE


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[PMID]:25119377
[Au] Autor:Piccolo P; Annunziata P; Mithbaokar P; Brunetti-Pierri N
[Ad] Endereço:Telethon Institute of Genetics and Medicine, Naples, Italy.
[Ti] Título:SR-A and SREC-I binding peptides increase HDAd-mediated liver transduction.
[So] Source:Gene Ther;21(11):950-7, 2014 Nov.
[Is] ISSN:1476-5462
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Helper-dependent adenoviral (HDAd) vectors can mediate long-term, high-level transgene expression from transduced hepatocytes without inducing chronic toxicity. However, vector therapeutic index is narrow because of a toxic acute response with potentially lethal consequences elicited by high vector doses. Kupffer cells (KCs) and liver sinusoidal endothelial cells (LSECs) are major barriers to efficient hepatocyte transduction. We investigated two small peptides (PP1 and PP2) developed by phage display to block scavenger receptor type A (SR-A) and scavenger receptor expressed on endothelial cells type I (SREC-I), respectively, for enhancement of HDAd-mediated hepatocyte transduction efficiency. Pre-incubation of J774A.1 macrophages with either PP1 or PP2 prior to HDAd infection significantly reduced viral vector uptake. In vivo, fluorochrome-conjugated PP1 and PP2 injected intravenously into mice co-localized with both CD68 and CD31 on KCs and LSECs, respectively. Compared with saline pre-treated animals, intravenous injections of both peptides prior to the injection of an HDAd resulted in up to 3.7- and 2.9-fold increase of hepatic transgene expression with PP1 and PP2, respectively. In addition to greater hepatocyte transduction, compared with control saline injected mice, pre-treatment with either peptide resulted in no increased levels of serum interleukin-6, the major marker of adenoviral vector acute toxicity. In summary, we developed small peptides that significantly increase hepatocyte transduction efficacy and improve HDAd therapeutic index with potential for clinical applications.
[Mh] Termos MeSH primário: Adenoviridae/genética
Hepatócitos/metabolismo
Peptídeos/farmacologia
Receptores Depuradores Classe A/antagonistas & inibidores
Receptores Depuradores Classe F/antagonistas & inibidores
Transdução Genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Vetores Genéticos
Vírus Auxiliares/genética
Hepatócitos/efeitos dos fármacos
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Biblioteca de Peptídeos
Peptídeos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Peptide Library); 0 (Peptides); 0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class A); 0 (Scavenger Receptors, Class F)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140815
[St] Status:MEDLINE
[do] DOI:10.1038/gt.2014.71


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[PMID]:24788600
[Au] Autor:Baur S; Rautenberg M; Faulstich M; Faulstich M; Grau T; Severin Y; Unger C; Hoffmann WH; Rudel T; Autenrieth IB; Weidenmaier C
[Ad] Endereço:Interfacultary Institute for Microbiology and Infection Medicine Tübingen, Department of Medical Microbiology and Hygiene, University of Tübingen, Tübingen, Germany.
[Ti] Título:A nasal epithelial receptor for Staphylococcus aureus WTA governs adhesion to epithelial cells and modulates nasal colonization.
[So] Source:PLoS Pathog;10(5):e1004089, 2014 May.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nasal colonization is a major risk factor for S. aureus infections. The mechanisms responsible for colonization are still not well understood and involve several factors on the host and the bacterial side. One key factor is the cell wall teichoic acid (WTA) of S. aureus, which governs direct interactions with nasal epithelial surfaces. We report here the first receptor for the cell wall glycopolymer WTA on nasal epithelial cells. In several assay systems this type F-scavenger receptor, termed SREC-I, bound WTA in a charge dependent manner and mediated adhesion to nasal epithelial cells in vitro. The impact of WTA and SREC-I interaction on epithelial adhesion was especially pronounced under shear stress, which resembles the conditions found in the nasal cavity. Most importantly, we demonstrate here a key role of the WTA-receptor interaction in a cotton rat model of nasal colonization. When we inhibited WTA mediated adhesion with a SREC-I antibody, nasal colonization in the animal model was strongly reduced at the early onset of colonization. More importantly, colonization stayed low over an extended period of 6 days. Therefore we propose targeting of this glycopolymer-receptor interaction as a novel strategy to prevent or control S. aureus nasal colonization.
[Mh] Termos MeSH primário: Aderência Bacteriana/genética
Células Epiteliais/microbiologia
Cavidade Nasal/microbiologia
Receptores Depuradores Classe F/fisiologia
Staphylococcus aureus/crescimento & desenvolvimento
Staphylococcus aureus/fisiologia
Ácidos Teicoicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células CHO
Parede Celular/metabolismo
Células Cultivadas
Cricetinae
Cricetulus
Interações Hospedeiro-Patógeno/genética
Seres Humanos
Ratos
Receptores Depuradores Classe F/metabolismo
Sigmodontinae
Infecções Estafilocócicas/genética
Infecções Estafilocócicas/metabolismo
Infecções Estafilocócicas/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (SCARF1 protein, human); 0 (Scavenger Receptors, Class F); 0 (Teichoic Acids)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150806
[Lr] Data última revisão:
150806
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140503
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1004089


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Brunoni, Décio
PubMed Central Texto completo
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[PMID]:24478002
[Au] Autor:Migliavacca MP; Sobreira NL; Antonialli GP; Oliveira MM; Melaragno MI; Casteels I; de Ravel T; Brunoni D; Valle D; Perez AB
[Ad] Endereço:Clinical Genetics, Department of Morphology and Genetics, UNIFESP, São Paulo, Brazil.
[Ti] Título:Sclerocornea in a patient with van den Ende-Gupta syndrome homozygous for a SCARF2 microdeletion.
[So] Source:Am J Med Genet A;164A(5):1170-4, 2014 May.
[Is] ISSN:1552-4833
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Van den Ende-Gupta Syndrome (VDEGS) is an autosomal recessive disorder characterized by blepharophimosis, distinctive nose, hypoplastic maxilla, and skeletal abnormalities. Using homozygosity mapping in four VDEGS patients from three consanguineous families, Anastacio et al. [Anastacio et al. (2010); Am J Hum Genet 87:553-559] identified homozygous mutations in SCARF2, located at 22q11.2. Bedeschi et al. [2010] described a VDEGS patient with sclerocornea and cataracts with compound heterozygosity for the common 22q11.2 microdeletion and a hemizygous SCARF2 mutation. Because sclerocornea had been described in DiGeorge-velo-cardio-facial syndrome but not in VDEGS, they suggested that the ocular abnormalities were caused by the 22q11.2 microdeletion. We report on a 23-year-old male who presented with bilateral sclerocornea and the VDGEGS phenotype who was subsequently found to be homozygous for a 17 bp deletion in exon 4 of SCARF2. The occurrence of bilateral sclerocornea in our patient together with that of Bedeschi et al., suggests that the full VDEGS phenotype may include sclerocornea resulting from homozygosity or compound heterozygosity for loss of function variants in SCARF2.
[Mh] Termos MeSH primário: Anormalidades Múltiplas/diagnóstico
Anormalidades Múltiplas/genética
Aracnodactilia/diagnóstico
Aracnodactilia/genética
Blefarofimose/diagnóstico
Blefarofimose/genética
Contratura/diagnóstico
Contratura/genética
Córnea/anormalidades
Doenças da Córnea/diagnóstico
Doenças da Córnea/genética
Homozigoto
Receptores Depuradores Classe F/genética
Deleção de Sequência
[Mh] Termos MeSH secundário: Adulto
Osso e Ossos/diagnóstico por imagem
Osso e Ossos/patologia
Cromossomos Humanos Par 22
Éxons
Facies
Deformidades Congênitas da Mão
Seres Humanos
Masculino
Fenótipo
Radiografia
Análise de Sequência de DNA
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (SCARF2 protein, human); 0 (Scavenger Receptors, Class F)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140131
[St] Status:MEDLINE
[do] DOI:10.1002/ajmg.a.36425



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