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  1 / 1918 MEDLINE  
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[PMID]:29480856
[Au] Autor:Yuan B; Ji W; Fan B; Zhang B; Zhao Y; Li J
[Ad] Endereço:Department of Orthopaedics.
[Ti] Título:Association analysis between thrombospondin-2 gene polymorphisms and intervertebral disc degeneration in a Chinese Han population.
[So] Source:Medicine (Baltimore);97(2):e9586, 2018 Jan.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study is to determine the contribution of 2 single nucleotide polymorphisms (SNPs) in thrombospondin 2 (THBS2) gene to the development of intervertebral disc degeneration (IDD) in a Chinese Han population.We studied 138 patients with radiographically proven IDD and 136 healthy volunteers with no history of back problems. Magnetic resonance images (MRIs) were obtained for all the patients and controls. Image evaluation for IDD was performed to evaluate the severity of IDD. All patients and controls were genotyped for rs6422747 and rs6422748. Associations between genotypes and development of IDD were analyzed.We found that 2 SNPs in the intron region of THBS2 gene (rs6422747 and rs6422748) were associated with susceptibility of IDD. However, they were not related with severity of IDD, including the total number of degenerative disc and level of IDD. G allele in both SNPs was associated with a higher risk of IDD.The 2 SNPs (rs6422747 and rs6422748) in the THBS2 gene were associated with susceptibility of IDD but not severity of IDD in a Chinese Han population. Our results indicated that THBS2 gene polymorphisms might be the risk factors for IDD. More studies with larger sample size need to be perfected to make sure the functions of THBS2 gene polymorphisms in IDD development.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Degeneração do Disco Intervertebral/genética
Polimorfismo de Nucleotídeo Único
Trombospondinas/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
China
Feminino
Técnicas de Genotipagem
Seres Humanos
Degeneração do Disco Intervertebral/diagnóstico por imagem
Íntrons
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Índice de Gravidade de Doença
Coluna Vertebral/diagnóstico por imagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Thrombospondins); 0 (thrombospondin 2)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180227
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009586


  2 / 1918 MEDLINE  
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[PMID]:28467820
[Au] Autor:Yan KS; Janda CY; Chang J; Zheng GXY; Larkin KA; Luca VC; Chia LA; Mah AT; Han A; Terry JM; Ootani A; Roelf K; Lee M; Yuan J; Li X; Bolen CR; Wilhelmy J; Davies PS; Ueno H; von Furstenberg RJ; Belgrader P; Ziraldo SB; Ordonez H; Henning SJ; Wong MH; Snyder MP; Weissman IL; Hsueh AJ; Mikkelsen TS; Garcia KC; Kuo CJ
[Ad] Endereço:Department of Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
[Ti] Título:Non-equivalence of Wnt and R-spondin ligands during Lgr5 intestinal stem-cell self-renewal.
[So] Source:Nature;545(7653):238-242, 2017 05 11.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The canonical Wnt/ß-catenin signalling pathway governs diverse developmental, homeostatic and pathological processes. Palmitoylated Wnt ligands engage cell-surface frizzled (FZD) receptors and LRP5 and LRP6 co-receptors, enabling ß-catenin nuclear translocation and TCF/LEF-dependent gene transactivation. Mutations in Wnt downstream signalling components have revealed diverse functions thought to be carried out by Wnt ligands themselves. However, redundancy between the 19 mammalian Wnt proteins and 10 FZD receptors and Wnt hydrophobicity have made it difficult to attribute these functions directly to Wnt ligands. For example, individual mutations in Wnt ligands have not revealed homeostatic phenotypes in the intestinal epithelium-an archetypal canonical, Wnt pathway-dependent, rapidly self-renewing tissue, the regeneration of which is fueled by proliferative crypt Lgr5 intestinal stem cells (ISCs). R-spondin ligands (RSPO1-RSPO4) engage distinct LGR4-LGR6, RNF43 and ZNRF3 receptor classes, markedly potentiate canonical Wnt/ß-catenin signalling, and induce intestinal organoid growth in vitro and Lgr5 ISCs in vivo. However, the interchangeability, functional cooperation and relative contributions of Wnt versus RSPO ligands to in vivo canonical Wnt signalling and ISC biology remain unknown. Here we identify the functional roles of Wnt and RSPO ligands in the intestinal crypt stem-cell niche. We show that the default fate of Lgr5 ISCs is to differentiate, unless both RSPO and Wnt ligands are present. However, gain-of-function studies using RSPO ligands and a new non-lipidated Wnt analogue reveal that these ligands have qualitatively distinct, non-interchangeable roles in ISCs. Wnt proteins are unable to induce Lgr5 ISC self-renewal, but instead confer a basal competency by maintaining RSPO receptor expression that enables RSPO ligands to actively drive and specify the extent of stem-cell expansion. This functionally non-equivalent yet cooperative interaction between Wnt and RSPO ligands establishes a molecular precedent for regulation of mammalian stem cells by distinct priming and self-renewal factors, with broad implications for precise control of tissue regeneration.
[Mh] Termos MeSH primário: Autorrenovação Celular
Intestinos/citologia
Receptores Acoplados a Proteínas-G/metabolismo
Células-Tronco/citologia
Células-Tronco/metabolismo
Trombospondinas/metabolismo
Proteínas Wnt/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem da Célula
Proliferação Celular
Feminino
Seres Humanos
Ligantes
Masculino
Camundongos
Organoides/citologia
Organoides/crescimento & desenvolvimento
Análise de Célula Única
Nicho de Células-Tronco
Transcriptoma
Ubiquitina-Proteína Ligases/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (LGR5 protein, human); 0 (Ligands); 0 (Receptors, G-Protein-Coupled); 0 (Thrombospondins); 0 (Wnt Proteins); 0 (beta Catenin); EC 2.3.2.27 (RNF43 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.3.2.27 (Znrf3 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1038/nature22313


  3 / 1918 MEDLINE  
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[PMID]:28953973
[Au] Autor:Wang S; Hu T; Wang Z; Li N; Zhou L; Liao L; Wang M; Liao L; Wang H; Zeng L; Fan C; Zhou H; Xiong K; Huang J; Chen D
[Ad] Endereço:Department of Anatomy and Neurobiology, Central South University School of Basic Medical Sciences, Changsha, Hunan, China.
[Ti] Título:Macroglia-derived thrombospondin 2 regulates alterations of presynaptic proteins of retinal neurons following elevated hydrostatic pressure.
[So] Source:PLoS One;12(9):e0185388, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many studies on retinal injury and repair following elevated intraocular pressure suggest that the survival ratio of retinal neurons has been improved by various measures. However, the visual function recovery is far lower than expected. The homeostasis of retinal synapses in the visual signal pathway is the key structural basis for the delivery of visual signals. Our previous studies found that complicated changes in the synaptic structure between retinal neurons occurred much earlier than obvious degeneration of retinal ganglion cells in rat retinae. The lack of consideration of these earlier retinal synaptic changes in the rescue strategy may be partly responsible for the limited visual function recovery with the types of protective methods for retinal neurons used following elevated intraocular pressure. Thus, research on the modulatory mechanisms of the synaptic changes after elevated intraocular pressure injury may give new light to visual function rescue. In this study, we found that thrombospondin 2, an important regulator of synaptogenesis in central nervous system development, was distributed in retinal macroglia cells, and its receptor α2δ-1 was in retinal neurons. Cell cultures including mixed retinal macroglia cells/neuron cultures and retinal neuron cultures were exposed to elevated hydrostatic pressure for 2 h. The expression levels of glial fibrillary acidic protein (the marker of activated macroglia cells), thrombospondin 2, α2δ-1 and presynaptic proteins were increased following elevated hydrostatic pressure in mixed cultures, but the expression levels of postsynaptic proteins were not changed. SiRNA targeting thrombospondin 2 could decrease the upregulation of presynaptic proteins induced by the elevated hydrostatic pressure. However, in retinal neuron cultures, elevated hydrostatic pressure did not affect the expression of presynaptic or postsynaptic proteins. Rather, the retinal neuron cultures with added recombinant thrombospondin 2 protein upregulated the level of presynaptic proteins. Finally, gabapentin decreased the expression of presynaptic proteins in mixed cultures by blocking the interaction of thrombospondin 2 and α2δ-1. Taken together, these results indicate that activated macroglia cells may participate in alterations of presynaptic proteins of retinal neurons following elevated hydrostatic pressure, and macroglia-derived thrombospondin 2 may modulate these changes via binding to its neuronal receptor α2δ-1.
[Mh] Termos MeSH primário: Pressão Hidrostática
Neuroglia/metabolismo
Terminações Pré-Sinápticas/metabolismo
Neurônios Retinianos/metabolismo
Trombospondinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Canais de Cálcio/metabolismo
Proteínas de Transporte/metabolismo
Células Cultivadas
Proteína 4 Homóloga a Disks-Large
Proteína Glial Fibrilar Ácida/metabolismo
Proteínas de Arcabouço Homer/metabolismo
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas de Membrana/metabolismo
Ratos Sprague-Dawley
Sinapsinas/metabolismo
Sinaptofisina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cacna2d2 protein, rat); 0 (Calcium Channels); 0 (Carrier Proteins); 0 (Disks Large Homolog 4 Protein); 0 (Dlg4 protein, rat); 0 (Glial Fibrillary Acidic Protein); 0 (Homer Scaffolding Proteins); 0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Synapsins); 0 (Synaptophysin); 0 (Thrombospondins); 0 (gephyrin); 0 (thrombospondin 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185388


  4 / 1918 MEDLINE  
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[PMID]:28945253
[Au] Autor:Huang PY; Kandyba E; Jabouille A; Sjolund J; Kumar A; Halliwill K; McCreery M; DelRosario R; Kang HC; Wong CE; Seibler J; Beuger V; Pellegrino M; Sciambi A; Eastburn DJ; Balmain A
[Ad] Endereço:Helen Diller Family Comprehensive Cancer Center University of California, San Francisco, San Francisco, California, USA.
[Ti] Título:Lgr6 is a stem cell marker in mouse skin squamous cell carcinoma.
[So] Source:Nat Genet;49(11):1624-1632, 2017 Nov.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The G-protein-coupled receptors LGR4, LGR5 and LGR6 are Wnt signaling mediators, but their functions in squamous cell carcinoma (SCC) are unclear. Using lineage tracing in Lgr5-EGFP-CreERT2/Rosa26-Tomato and Lgr6-EGFP-CreERT2/Rosa26-Tomato reporter mice, we demonstrate that Lgr6, but not Lgr5, acts as an epithelial stem cell marker in SCCs in vivo. We identify, by single-molecule in situ hybridization and cell sorting, rare cells positive for Lgr6 expression in immortalized keratinocytes and show that their frequency increases in advanced SCCs. Lgr6 expression is enriched in cells with stem cell characteristics, and Lgr6 downregulation in vivo causes increased epidermal proliferation with expanded lineage tracing from epidermal stem cells positive for Lgr6 expression. Surprisingly, mice with germline knockout of Lgr6 are predisposed to SCC development, through a mechanism that includes compensatory upregulation of Lgr5. These data provide a model for human patients with germline loss-of-function mutations in Wnt pathway genes, including RSPO1 or LGR4, who show increased susceptibility to squamous tumor development.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/genética
Regulação Neoplásica da Expressão Gênica
Queratinócitos/metabolismo
Células-Tronco Neoplásicas/metabolismo
Receptores Acoplados a Proteínas-G/genética
Neoplasias Cutâneas/genética
[Mh] Termos MeSH secundário: Animais
Carcinoma de Células Escamosas/metabolismo
Carcinoma de Células Escamosas/patologia
Linhagem Celular Transformada
Epiderme/metabolismo
Epiderme/patologia
Seres Humanos
Queratinócitos/patologia
Camundongos
Camundongos Transgênicos
Células-Tronco Neoplásicas/patologia
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/metabolismo
Transdução de Sinais
Neoplasias Cutâneas/metabolismo
Neoplasias Cutâneas/patologia
Trombospondinas/genética
Trombospondinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (LGR4 protein, mouse); 0 (Lgr5 protein, mouse); 0 (Lgr6 protein, mouse); 0 (RNA, Small Interfering); 0 (RSPO1 protein, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Thrombospondins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170926
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3957


  5 / 1918 MEDLINE  
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[PMID]:28847812
[Au] Autor:Yu Y; Moberly AH; Bhattarai JP; Duan C; Zheng Q; Li F; Huang H; Olson W; Luo W; Wen T; Yu H; Ma M
[Ad] Endereço:School of Life Sciences, Shanghai University, Shanghai, China 200444, Yiqun_Yu@shu.edu.cn minghong@upenn.edu.
[Ti] Título:The Stem Cell Marker Lgr5 Defines a Subset of Postmitotic Neurons in the Olfactory Bulb.
[So] Source:J Neurosci;37(39):9403-9414, 2017 Sep 27.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lgr5, leucine-rich repeat-containing G-protein coupled receptor 5, is a biomarker for stem cells in multiple tissues. Lgr5 is also expressed in the brain, but the identities and properties of these Lgr5 cells are still elusive. Using an Lgr5-EGFP reporter mouse line, we found that, from early development to adulthood, Lgr5 is highly expressed in the olfactory bulb (OB), an area with ongoing neurogenesis. Immunostaining with stem cell, glial, and neuronal markers reveals that Lgr5 does not label stem cells in the OB but instead labels a heterogeneous population of neurons with preference in certain subtypes. Patch-clamp recordings in OB slices reveal that Lgr5-EGFP cells fire action potentials and display spontaneous excitatory postsynaptic events, indicating that these neurons are integrated into OB circuits. Interestingly, R-spondin 3, a potential ligand of Lgr5, is also expressed in the adult OB. Collectively, our data indicate that Lgr5-expressing cells in the OB are fully differentiated neurons and imply distinct roles of Lgr5 and its ligand in postmitotic cells. Lgr5 (leucine-rich repeat-containing G-protein coupled receptor 5) is a stem cell marker in many body organs. Here we report that Lgr5 is also highly expressed in the olfactory bulb (OB), the first relay station in the brain for processing odor information and one of the few neural structures that undergo continuous neurogenesis. Surprisingly, Lgr5 is not expressed in the OB stem cells, but instead in a few subtypes of terminally differentiated neurons, which are incorporated into the OB circuit. This study reveals that Lgr5 cells in the brain represent a nonstem cell lineage, implying distinct roles of Lgr5 in postmitotic neurons.
[Mh] Termos MeSH primário: Neurônios/metabolismo
Bulbo Olfatório/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Divisão Celular
Potenciais Pós-Sinápticos Excitadores
Feminino
Masculino
Camundongos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Neurônios/citologia
Neurônios/fisiologia
Bulbo Olfatório/citologia
Bulbo Olfatório/crescimento & desenvolvimento
Receptores Acoplados a Proteínas-G/genética
Trombospondinas/genética
Trombospondinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lgr5 protein, mouse); 0 (R-spondin3 protein, mouse); 0 (Receptors, G-Protein-Coupled); 0 (Thrombospondins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171015
[Lr] Data última revisão:
171015
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0500-17.2017


  6 / 1918 MEDLINE  
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[PMID]:28814510
[Au] Autor:Tomas NM; Meyer-Schwesinger C; von Spiegel H; Kotb AM; Zahner G; Hoxha E; Helmchen U; Endlich N; Koch-Nolte F; Stahl RAK
[Ad] Endereço:III. Medizinische Klinik, n.tomas@uke.de.
[Ti] Título:A Heterologous Model of Thrombospondin Type 1 Domain-Containing 7A-Associated Membranous Nephropathy.
[So] Source:J Am Soc Nephrol;28(11):3262-3277, 2017 Nov.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thrombospondin type 1 domain-containing 7A (THSD7A) is a target for autoimmunity in patients with membranous nephropathy (MN). Circulating autoantibodies from patients with THSD7A-associated MN have been demonstrated to cause MN in mice. However, THSD7A-associated MN is a rare disease, preventing the use of patient antibodies for larger experimental procedures. Therefore, we generated antibodies against the human and mouse orthologs of THSD7A in rabbits by coimmunization with the respective cDNAs. Injection of these anti-THSD7A antibodies into mice induced a severe nephrotic syndrome with proteinuria, weight gain, and hyperlipidemia. Immunofluorescence analyses revealed granular antigen-antibody complexes in a subepithelial location along the glomerular filtration barrier 14 days after antibody injection, and immunohistochemistry for rabbit IgG and THSD7A as well as ultrastructural analyses showed the typical characteristics of human MN. Mice injected with purified IgG from rabbit serum that was taken before immunization failed to develop any of these changes. Notably, MN developed in the absence of detectable complement activation, and disease was strain dependent. , anti-THSD7A antibodies caused cytoskeletal rearrangement and activation of focal adhesion signaling. Knockdown of the THSD7A ortholog, thsd7aa, in zebrafish larvae resulted in altered podocyte differentiation and impaired glomerular filtration barrier function, with development of pericardial edema, suggesting an important role of THSD7A in glomerular filtration barrier integrity. In summary, our study introduces a heterologous mouse model that allows further investigation of the molecular events that underlie MN.
[Mh] Termos MeSH primário: Anticorpos/fisiologia
Antígenos de Superfície/imunologia
Glomerulonefrite Membranosa/imunologia
Proteínas de Membrana/imunologia
Trombospondinas/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos de Superfície/fisiologia
Modelos Animais de Doenças
Seres Humanos
Masculino
Proteínas de Membrana/fisiologia
Camundongos
Camundongos Endogâmicos BALB C
Coelhos
Ratos
Ratos Sprague-Dawley
Trombospondinas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Antigens, Surface); 0 (Membrane Proteins); 0 (Thrombospondins); 0 (Thsd7A protein, mouse); 0 (thrombospondin type I domain containing 7A protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2017010030


  7 / 1918 MEDLINE  
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[PMID]:28679845
[Au] Autor:Farnoodian M; Wang S; Dietz J; Nickells RW; Sorenson CM; Sheibani N
[Ad] Endereço:Department of Ophthalmology and Visual Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, U.S.A.
[Ti] Título:Negative regulators of angiogenesis: important targets for treatment of exudative AMD.
[So] Source:Clin Sci (Lond);131(15):1763-1780, 2017 Aug 01.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Angiogenesis contributes to the pathogenesis of many diseases including exudative age-related macular degeneration (AMD). It is normally kept in check by a tightly balanced production of pro- and anti-angiogenic factors. The up-regulation of the pro-angiogenic factor, vascular endothelial growth factor (VEGF), is intimately linked to the pathogenesis of exudative AMD, and its antagonism has been effectively targeted for treatment. However, very little is known about potential changes in expression of anti-angiogenic factors and the role they play in choroidal vascular homeostasis and neovascularization associated with AMD. Here, we will discuss the important role of thrombospondins and pigment epithelium-derived factor, two major endogenous inhibitors of angiogenesis, in retinal and choroidal vascular homeostasis and their potential alterations during AMD and choroidal neovascularization (CNV). We will review the cell autonomous function of these proteins in retinal and choroidal vascular cells. We will also discuss the potential targeting of these molecules and use of their mimetic peptides for therapeutic development for exudative AMD.
[Mh] Termos MeSH primário: Inibidores da Angiogênese/fisiologia
Neovascularização de Coroide/fisiopatologia
Proteínas do Olho/fisiologia
Degeneração Macular/fisiopatologia
Fatores de Crescimento Neural/fisiologia
Serpinas/fisiologia
Trombospondinas/fisiologia
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/uso terapêutico
Angiostatinas/uso terapêutico
Neovascularização de Coroide/tratamento farmacológico
Endostatinas/uso terapêutico
Seres Humanos
Degeneração Macular/tratamento farmacológico
Terapia de Alvo Molecular/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Endostatins); 0 (Eye Proteins); 0 (Nerve Growth Factors); 0 (Serpins); 0 (Thrombospondins); 0 (pigment epithelium-derived factor); 86090-08-6 (Angiostatins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170707
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170066


  8 / 1918 MEDLINE  
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[PMID]:28674044
[Au] Autor:Beck LH
[Ad] Endereço:Renal Section, Boston Medical Center, Boston University School of Medicine, Boston, Massachusetts Laurence.Beck@bmc.org lhbeckjr@bu.edu.
[Ti] Título:PLA2R and THSD7A: Disparate Paths to the Same Disease?
[So] Source:J Am Soc Nephrol;28(9):2579-2589, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The phospholipase A2 receptor (PLA2R) and thrombospondin type-1 domain-containing 7A (THSD7A) are the two major autoantigens in primary membranous nephropathy (MN), and define two molecular subclasses of this disease. Both proteins are large transmembrane glycoproteins expressed by the podocyte, and both induce IgG4-predominant humoral immune responses that produce circulating autoantibodies that can be used clinically for diagnostic and monitoring purposes. The biologic roles of these proteins remain speculative, although several features of THSD7A suggest a role in adhesion. PLA2R-associated MN was initially found to associate with risk alleles within , but subsequent studies have shifted the focus to the HLA-DRB locus. Three distinct humoral epitope-containing regions have been defined within the extracellular portion of PLA2R, and it appears that the number of targeted epitopes may determine disease severity. Although similar information is not yet available for THSD7A-associated MN, this form of MN may have a unique association with malignancy. Finally, it appears likely that other autoantigens in primary MN exist. Although protocols similar to those that identified PLA2R and THSD7A may be successful in the identification of novel antigenic targets in MN, newer techniques such as laser-capture mass spectrometry or protein arrays may be helpful as well.
[Mh] Termos MeSH primário: Autoantígenos/imunologia
Glomerulonefrite Membranosa/imunologia
Neoplasias/imunologia
Receptores da Fosfolipase A2/genética
Receptores da Fosfolipase A2/imunologia
Trombospondinas/imunologia
[Mh] Termos MeSH secundário: Autoanticorpos
Autoantígenos/genética
Epitopos/genética
Cadeias alfa de HLA-DQ/genética
Cadeias beta de HLA-DR/genética
Seres Humanos
Imunoglobulina G
Podócitos/metabolismo
Receptores da Fosfolipase A2/isolamento & purificação
Receptores da Fosfolipase A2/metabolismo
Trombospondinas/isolamento & purificação
Trombospondinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (Epitopes); 0 (HLA-DQ alpha-Chains); 0 (HLA-DQA1 antigen); 0 (HLA-DR beta-Chains); 0 (Immunoglobulin G); 0 (Receptors, Phospholipase A2); 0 (Thrombospondins); 0 (thrombospondin type I domain containing 7A protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2017020178


  9 / 1918 MEDLINE  
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[PMID]:28586642
[Au] Autor:Huels DJ; Sansom OJ
[Ad] Endereço:Laboratory for Experimental Oncology and Radiobiology (LEXOR), Center for Experimental Molecular Medicine (CEMM), Academic Medical Center (AMC), University of Amsterdam, Amsterdam, the Netherlands; Cancer Genomics Netherlands, Academic Medical Center, the Netherlands.
[Ti] Título:R-spondin Is More Than Just Wnt's Sidekick.
[So] Source:Dev Cell;41(5):456-458, 2017 06 05.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The intestinal crypt and its stem cells are dependent on the Wnt pathway. Reporting in Nature, Yan et al. (2017) show that Wnts and Wnt signaling potentiator R-spondins have non-interchangeable roles. Both are necessary for intestinal stem cell (ISC) maintenance, and R-spondins are the limiting factor that defines ISC number.
[Mh] Termos MeSH primário: Trombospondinas
Via de Sinalização Wnt
[Mh] Termos MeSH secundário: Seres Humanos
Intestinos
Células-Tronco
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Thrombospondins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE


  10 / 1918 MEDLINE  
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[PMID]:28576485
[Au] Autor:Xu Z; Rui YN; Balzeau J; Menezes MR; Niu A; Hagan JP; Kim DH
[Ad] Endereço:Department of Neurosurgery, The University of Texas Health Science Center at Houston, TX, United States. Electronic address: Zhen.Xu@uth.tmc.edu.
[Ti] Título:Highly efficient one-step scarless protein tagging by type IIS restriction endonuclease-mediated precision cloning.
[So] Source:Biochem Biophys Res Commun;490(1):8-16, 2017 Aug 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Protein tagging with a wide variety of epitopes and/or fusion partners is used routinely to dissect protein function molecularly. Frequently, the required DNA subcloning is inefficient, especially in cases where multiple constructs are desired for a given protein with unique tags. Additionally, the generated clones have unwanted junction sequences introduced. To add versatile tags into the extracellular domain of the transmembrane protein THSD1, we developed a protein tagging technique that utilizes non-classical type IIS restriction enzymes that recognize non-palindromic DNA sequences and cleave outside of their recognition sites. Our results demonstrate that this method is highly efficient and can precisely fuse any tag into any position of a protein in a scarless manner. Moreover, this method is cost-efficient and adaptable because it uses commercially available type IIS restriction enzymes and is compatible with the traditional cloning system used by many labs. Therefore, precision tagging technology will benefit a number of researchers by providing an alternate method to integrate an array of tags into protein expression constructs.
[Mh] Termos MeSH primário: Clonagem Molecular/métodos
Desoxirribonucleases de Sítio Específico do Tipo II/metabolismo
Trombospondinas/genética
[Mh] Termos MeSH secundário: Células Cultivadas
Células HEK293
Seres Humanos
Trombospondinas/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (THSD1 protein, human); 0 (Thrombospondins); EC 3.1.21.4 (Deoxyribonucleases, Type II Site-Specific)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170604
[St] Status:MEDLINE



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