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[PMID]:28469040
[Au] Autor:Smith BN; Topp SD; Fallini C; Shibata H; Chen HJ; Troakes C; King A; Ticozzi N; Kenna KP; Soragia-Gkazi A; Miller JW; Sato A; Dias DM; Jeon M; Vance C; Wong CH; de Majo M; Kattuah W; Mitchell JC; Scotter EL; Parkin NW; Sapp PC; Nolan M; Nestor PJ; Simpson M; Weale M; Lek M; Baas F; Vianney de Jong JM; Ten Asbroek ALMA; Redondo AG; Esteban-Pérez J; Tiloca C; Verde F; Duga S; Leigh N; Pall H; Morrison KE; Al-Chalabi A; Shaw PJ; Kirby J; Turner MR; Talbot K; Hardiman O; Glass JD; De Belleroche J; Maki M; Moss SE; Miller C; Gellera C
[Ad] Endereço:United Kingdom Dementia Research Institute Centre, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, 125 Coldharbour Lane, Camberwell, SE5 9NU London, UK.
[Ti] Título:Mutations in the vesicular trafficking protein annexin A11 are associated with amyotrophic lateral sclerosis.
[So] Source:Sci Transl Med;9(388), 2017 May 03.
[Is] ISSN:1946-6242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder. We screened 751 familial ALS patient whole-exome sequences and identified six mutations including p.D40G in the gene in 13 individuals. The p.D40G mutation was absent from 70,000 control whole-exome sequences. This mutation segregated with disease in two kindreds and was present in another two unrelated cases ( = 0.0102), and all mutation carriers shared a common founder haplotype. Annexin A11-positive protein aggregates were abundant in spinal cord motor neurons and hippocampal neuronal axons in an ALS patient carrying the p.D40G mutation. Transfected human embryonic kidney cells expressing with the p.D40G mutation and other N-terminal mutations showed altered binding to calcyclin, and the p.R235Q mutant protein formed insoluble aggregates. We conclude that mutations in are associated with ALS and implicate defective intracellular protein trafficking in disease pathogenesis.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Anexinas/genética
[Mh] Termos MeSH secundário: Anexinas/metabolismo
Células-Tronco Embrionárias Humanas/metabolismo
Seres Humanos
Mutação/genética
Ligação Proteica
Transporte Proteico
Proteína A6 Ligante de Cálcio S100/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Annexins); 0 (S100 Calcium Binding Protein A6)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28765046
[Au] Autor:Sakane K; Nishiguchi M; Denda M; Yamagchi F; Magari M; Kanayama N; Morishita R; Tokumitsu H
[Ad] Endereço:Division of Medical Bioengineering, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
[Ti] Título:Identification and characterization of a centrosomal protein, FOR20 as a novel S100A6 target.
[So] Source:Biochem Biophys Res Commun;491(4):980-985, 2017 Sep 30.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:S100A6 is a Ca -signal transducer that interacts with numerous proteins and regulates their biochemical functions. Here we identified a centrosomal protein, FOR20 (FOP-related protein of 20 kDa) as a novel S100A6 target by screening protein microarrays carrying 19,676 recombinant GST-fused human proteins. Binding experiments revealed that S100A6 interacts with the N-terminal region (residues 1-30) of FOR20 in a Ca -dependent manner in vitro and in living cells. Several S100 proteins including S100A1, A2, A4, A11, B also exhibited Ca -dependent interactions with FOR20 as well as S100A6. We found that two distantly related centrosomal proteins, FOP and OFD1, also possess N-terminal regions with a significant sequence similarity to the putative S100A6-binding site (residues 1-30) in FOR20 and are capable of binding to S100A6 in a Ca -dependent manner. Taken together, these results may indicate that S100A6 interacts with FOR20 and related centrosomal proteins through a conserved N-terminal domain, suggesting a novel Ca -dependent regulation of centrosomal function.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/química
Proteínas de Ciclo Celular/metabolismo
Proteínas/química
Proteínas/metabolismo
Proteínas S100/química
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Animais
Células COS
Células Cultivadas
Centrossomo/química
Centrossomo/metabolismo
Cercopithecus aethiops
Células HeLa
Seres Humanos
Análise Serial de Proteínas
Ligação Proteica
Proteína A6 Ligante de Cálcio S100
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (FOR20 protein, human); 0 (Proteins); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 105504-00-5 (S100A6 protein, human)
[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:170803
[St] Status:MEDLINE


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[PMID]:28646023
[Au] Autor:Tamai H; Yamaguchi H; Miyake K; Takatori M; Kitano T; Yamanaka S; Yui S; Fukunaga K; Nakayama K; Inokuchi K
[Ad] Endereço:Department of Hematology, Nippon Medical School, Tokyo, Japan. s6056@nms.ac.jp.
[Ti] Título:Amlexanox Downregulates S100A6 to Sensitize -Positive Acute Lymphoblastic Leukemia to TNFα Treatment.
[So] Source:Cancer Res;77(16):4426-4433, 2017 Aug 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Acute lymphoblastic leukemias (ALL) positive for ( ) translocation, which constitute 60% of all infant ALL cases, have a poor prognosis even after allogeneic hematopoietic stem cell transplantation (allo-HSCT). This poor prognosis is due to one of two factors, either resistance to TNFα, which mediates a graft-versus-leukemia (GVL) response after allo-HSCT, or immune resistance due to upregulated expression of the immune escape factor S100A6. Here, we report an immune stimulatory effect against -positive ALL cells by treatment with the anti-allergy drug amlexanox, which we found to inhibit S100A6 expression in the presence of TNF-α. In -positive transgenic (Tg) mice, amlexanox enhanced tumor immunity and lowered the penetrance of leukemia development. Similarly, in a NOD/SCID mouse model of human -positive ALL, amlexanox broadened GVL responses and extended survival. Our findings show how amlexanox degrades the resistance of -positive ALL to TNFα by downregulating S100A6 expression, with immediate potential implications for improving clinical management of -positive ALL. .
[Mh] Termos MeSH primário: Aminopiridinas/farmacologia
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Proteínas de Ciclo Celular/metabolismo
Proteínas de Ligação a DNA/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico
Proteínas S100/metabolismo
Fatores de Elongação da Transcrição/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Animais
Antialérgicos/administração & dosagem
Antialérgicos/farmacologia
Proteínas de Ciclo Celular/genética
Proteínas de Ligação a DNA/genética
Modelos Animais de Doenças
Regulação para Baixo
Sinergismo Farmacológico
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos NOD
Camundongos SCID
Camundongos Transgênicos
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/metabolismo
Leucemia-Linfoma Linfoblástico de Células Precursoras/patologia
Proteína A6 Ligante de Cálcio S100
Proteínas S100/genética
Fatores de Elongação da Transcrição/genética
Fator de Necrose Tumoral alfa/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aff1 protein, mouse); 0 (Aminopyridines); 0 (Anti-Allergic Agents); 0 (Cell Cycle Proteins); 0 (DNA-Binding Proteins); 0 (Nuclear Proteins); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 0 (S100a6 protein, mouse); 0 (Transcriptional Elongation Factors); 0 (Tumor Necrosis Factor-alpha); 105504-00-5 (S100A6 protein, human); 150826-18-9 (AFF1 protein, human); BRL1C2459K (amlexanox)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170625
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-16-2974


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[PMID]:28550109
[Au] Autor:Stancill JS; Cartailler JP; Clayton HW; O'Connor JT; Dickerson MT; Dadi PK; Osipovich AB; Jacobson DA; Magnuson MA
[Ad] Endereço:Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN.
[Ti] Título:Chronic ß-Cell Depolarization Impairs ß-Cell Identity by Disrupting a Network of Ca -Regulated Genes.
[So] Source:Diabetes;66(8):2175-2187, 2017 Aug.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We used mice lacking , a key component of the ß-cell K -channel, to analyze the effects of a sustained elevation in the intracellular Ca concentration ([Ca ] ) on ß-cell identity and gene expression. Lineage tracing analysis revealed the conversion of ß-cells lacking into pancreatic polypeptide cells but not to α- or δ-cells. RNA-sequencing analysis of FACS-purified ß-cells confirmed an increase in gene expression and revealed altered expression of more than 4,200 genes, many of which are involved in Ca signaling, the maintenance of ß-cell identity, and cell adhesion. The expression of and , two highly upregulated genes, is closely correlated with membrane depolarization, suggesting their use as markers for an increase in [Ca ] Moreover, a bioinformatics analysis predicts that many of the dysregulated genes are regulated by common transcription factors, one of which, , was confirmed to be directly controlled by Ca influx in ß-cells. Interestingly, among the upregulated genes is , a putative marker of ß-cell dedifferentiation, and other genes associated with ß-cell failure. Taken together, our results suggest that chronically elevated ß-cell [Ca ] in islets contributes to the alteration of ß-cell identity, islet cell numbers and morphology, and gene expression by disrupting a network of Ca -regulated genes.
[Mh] Termos MeSH primário: Sinalização do Cálcio/genética
Polaridade Celular
Regulação da Expressão Gênica/genética
Expressão Gênica/genética
Células Secretoras de Insulina/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/fisiologia
Cálcio/metabolismo
Adesão Celular/genética
Proteínas de Ciclo Celular/metabolismo
Linhagem da Célula/genética
Células Secretoras de Insulina/citologia
Canais KATP/genética
Camundongos
Células Secretoras de Polipeptídeo Pancreático/fisiologia
Proteína A6 Ligante de Cálcio S100
Proteína A4 de Ligação a Cálcio da Família S100/metabolismo
Proteínas S100/metabolismo
Receptores Sulfonilureia/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Abcc8 protein, mouse); 0 (Ascl1 protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Cell Cycle Proteins); 0 (KATP Channels); 0 (S100 Calcium Binding Protein A6); 0 (S100 Calcium-Binding Protein A4); 0 (S100 Proteins); 0 (S100a4 protein, mouse); 0 (S100a6 protein, mouse); 0 (Sulfonylurea Receptors); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1355


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[PMID]:28417162
[Au] Autor:Donato R; Sorci G; Giambanco I
[Ad] Endereço:Department of Experimental Medicine, Centro Universitario per la Ricerca sulla Genomica Funzionale, Perugia Medical School, University of Perugia, Piazza Lucio Severi 1, 06132, Perugia, Italy. rosario.donato@unipg.it.
[Ti] Título:S100A6 protein: functional roles.
[So] Source:Cell Mol Life Sci;74(15):2749-2760, 2017 Aug.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:S100A6 protein belongs to the A group of the S100 protein family of Ca -binding proteins. It is expressed in a limited number of cell types in adult normal tissues and in several tumor cell types. As an intracellular protein, S100A6 has been implicated in the regulation of several cellular functions, such as proliferation, apoptosis, the cytoskeleton dynamics, and the cellular response to different stress factors. S100A6 can be secreted/released by certain cell types which points to extracellular effects of the protein. RAGE (receptor for advanced glycation endproducts) and integrin ß1 transduce some extracellular S100A6's effects. Dosage of serum S100A6 might aid in diagnosis in oncology.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Proliferação Celular
Neoplasias/metabolismo
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Proteínas de Ciclo Celular/sangue
Proteínas de Ciclo Celular/genética
Movimento Celular
Citoesqueleto/genética
Citoesqueleto/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Integrina beta1/metabolismo
Neoplasias/sangue
Neoplasias/genética
Doenças Neurodegenerativas/genética
Doenças Neurodegenerativas/metabolismo
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Proteína A6 Ligante de Cálcio S100
Proteínas S100/sangue
Proteínas S100/genética
Transdução de Sinais
Células-Tronco/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (Integrin beta1); 0 (Receptor for Advanced Glycation End Products); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 105504-00-5 (S100A6 protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2526-9


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[PMID]:28075439
[Au] Autor:Zhang X; Liu Z; Chen M; Cao Q; Huang D
[Ad] Endereço:Department of Gynecology, Jiangxi Maternal and Child Health Hospital, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
[Ti] Título:Effects of S100A6 gene silencing on the biological features of eutopic endometrial stromal cells and ß­catenin expression.
[So] Source:Mol Med Rep;15(3):1279-1285, 2017 Mar.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Protein expression levels of S100 calcium binding protein A6 (S100A6) are increased in various malignancies and are associated with tumor behavior; however, the association between S100A6 and endometriosis remains to be elucidated. In order to investigate the influence of S100A6 protein, recombinant lentivirus siS100A6 was used to transfect the eutopic endometrial stromal cells. CCK­8 assay was performed to identify the proliferation ability of cell and the cell migration was detected by Transwell assay. Flow cytometry was performed to detect cell apoptosis, and western blotting and reverse transcription­quantitative polymerase chain reaction were performed to identify the expression of ß­catenin. The present study investigated the role of S100A6 in endometriosis and its interaction with ß­catenin by transfecting eutopic endometrial stromal cells with a recombinant lentivirus containing S100A6­specific small interfering RNA. Inhibition of S100A6 expression had a significant antiproliferative effect and reduced the migratory ability of eutopic endometrial stromal cells, and induced their apoptosis. In addition, inhibition of S100A6 expression suppressed ß­catenin expression. These results suggested that inhibition of S100A6 may represent a promising novel approach for the targeted therapy of endometriosis.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/genética
Endométrio/metabolismo
Regulação da Expressão Gênica
Inativação Gênica
Proteínas S100/genética
Células Estromais/metabolismo
beta Catenina/genética
[Mh] Termos MeSH secundário: Adulto
Apoptose
Proteínas de Ciclo Celular/metabolismo
Movimento Celular
Proliferação Celular
Endometriose/genética
Endometriose/metabolismo
Endometriose/patologia
Feminino
Expressão Gênica
Genes Reporter
Seres Humanos
Meia-Idade
Ligação Proteica
Interferência de RNA
Proteína A6 Ligante de Cálcio S100
Proteínas S100/metabolismo
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 0 (beta Catenin); 105504-00-5 (S100A6 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2017.6105


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[PMID]:28068373
[Au] Autor:Bartkowska K; Swiatek I; Aniszewska A; Jurewicz E; Turlejski K; Filipek A; Djavadian RL
[Ad] Endereço:Nencki Institute of Experimental Biology Polish Academy of Sciences, Warsaw, Poland.
[Ti] Título:Stress-Dependent Changes in the CacyBP/SIP Interacting Protein S100A6 in the Mouse Brain.
[So] Source:PLoS One;12(1):e0169760, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The CacyBP/SIP target S100A6 is widely present in the nervous system, and its up-regulation is associated with certain neurodegenerative diseases. Here, we examined the involvement of S100A6 protein in stress responses in mice. Using Western blotting, we observed a marked change in brainstem structures, whereby stressed mice showed approximately one-third the protein level produced in the control group. A decreased level of S100A6 protein in stressed animals was also detected in the olfactory bulb and the cerebellum and stress-related structures such as the hippocampus and the hypothalamus. Additionally, using immunohistochemistry, high levels of S100A6 expression were observed in astrocytes localized in the border zones of all brain ventricles, tanycytes of the ventro-lateral walls of the hypothalamus, including the arcuate nucleus (ARH) and low levels of this protein were in neurons of the olfactory bulb, the hippocampus, the thalamus, the cerebral cortex, the brainstem and the cerebellum. Although S100A6-expressing cells in all these brain structures did not change their phenotype in response to stress, the intensity of immunofluorescent labeling in all studied structures was lower in stressed mice than in control animals. For example, in the ARH, where extremely strong immunostaining was observed, the number of immunolabeled fibers was decreased by approximately half in the stressed group compared with the controls. Although these results are descriptive and do not give clue about functional role of S100A6 in stress, they indicate that the level of S100A6 decreases in several brain structures in response to chronic mild stress, suggesting that this protein may modify stress responses.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Proteínas de Ligação ao Cálcio/metabolismo
Proteínas de Ciclo Celular/metabolismo
Proteínas S100/metabolismo
Estresse Fisiológico
[Mh] Termos MeSH secundário: Animais
Tronco Encefálico/metabolismo
Imuno-Histoquímica
Masculino
Camundongos
Microscopia Confocal
Fenótipo
Ligação Proteica
Proteína A6 Ligante de Cálcio S100
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cacybp protein, mouse); 0 (Calcium-Binding Proteins); 0 (Cell Cycle Proteins); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 0 (S100a6 protein, mouse)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169760


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[PMID]:27596819
[Au] Autor:Li A; Shi D; Xu B; Wang J; Tang YL; Xiao W; Shen G; Deng W; Zhao C
[Ad] Endereço:State Key Laboratory of Oncology in South China, Collaborative Innovation Center of Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China.
[Ti] Título:S100A6 promotes cell proliferation in human nasopharyngeal carcinoma via the p38/MAPK signaling pathway.
[So] Source:Mol Carcinog;56(3):972-984, 2017 Mar.
[Is] ISSN:1098-2744
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An elevated level of S100A6 is associated with poor outcomes of many tumor types, but, how S100A6 contributes to nasopharyngeal carcinoma (NPC) progression remains unknown. Here, we investigated the expression and prognostic significance of S100A6 in NPC and explored the molecular mechanisms under-lying the role of S100A6 in NPC development. The results showed that S100A6 was markedly up-regulated in NPC tissues and cell lines compared to paired peritumoral normal tissues and a normal nasopharyngeal epithelial cell line, respectively. In tissues from 92 NPC patients, high S100A6 expression was associated with advanced N stage, locoregional failure and disease progression and was predictive of poor locoregional recurrence-free survival (LRRFS, P = 0.001) and progression-free survival (PFS, P = 0.001). Multivariate analysis showed that S100A6 is an independent prognostic factor for LRRFS and PFS. Silencing S100A6 using siRNA or shRNA significantly suppressed NPC cell proliferation, colony formation and p38/mitogen-activated protein kinase (MAPK) activity in vitro and inhibited tumor growth in a xenograft mouse model of NPC. In contrast, overexpressing S100A6 via plasmid transfection resulted in increased NPC cell proliferation and p38/MAPK activation. S100A6-induced proliferation was abolished by a p38 inhibitor. In summary, S100A6 may be a new prognostic marker of NPC and may promote NPC development via the activation of p38/MAPK signaling pathways. These findings suggest S100A6/p38/MAPK signaling as a potential therapeutic target for NPC. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Carcinoma/patologia
Proteínas de Ciclo Celular/metabolismo
Sistema de Sinalização das MAP Quinases
Neoplasias Nasofaríngeas/patologia
Proteínas S100/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Carcinoma/metabolismo
Linhagem Celular Tumoral
Proliferação Celular
Sobrevivência Celular
Progressão da Doença
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Camundongos
Neoplasias Nasofaríngeas/metabolismo
Estadiamento de Neoplasias
Transplante de Neoplasias
Prognóstico
Estudos Retrospectivos
Proteína A6 Ligante de Cálcio S100
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cell Cycle Proteins); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 105504-00-5 (S100A6 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE
[do] DOI:10.1002/mc.22563


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[PMID]:27818100
[Au] Autor:Yatime L; Betzer C; Jensen RK; Mortensen S; Jensen PH; Andersen GR
[Ad] Endereço:Department of Molecular Biology and Genetics, Aarhus University, Gustav Wieds Vej 10C, 8000 Aarhus, Denmark. Electronic address: laure.yatime@inserm.fr.
[Ti] Título:The Structure of the RAGE:S100A6 Complex Reveals a Unique Mode of Homodimerization for S100 Proteins.
[So] Source:Structure;24(12):2043-2052, 2016 Dec 06.
[Is] ISSN:1878-4186
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:S100 proteins are calcium-dependent regulators of homeostatic processes. Upon cellular response to stress, and notably during tumorigenesis, they relocalize to the extracellular environment where they induce pro-inflammatory signals by activating the receptor for advanced glycation end products (RAGE), thereby facilitating tumor growth and metastasis. Despite its importance in sustaining inflammation, the structural basis for RAGE-S100 crosstalk is still unknown. Here we report two crystal structures of the RAGE:S100A6 complex encompassing a full-length RAGE ectodomain. The structures, in combination with a comprehensive interaction analysis, suggest that the primary S100A6 binding site is formed by the RAGE C1 domain. Complex formation with S100A6 induces a unique dimeric conformation of RAGE that appears suited for signal transduction and intracellular effector recruitment. Intriguingly, S100A6 adopts a dimeric conformation radically different from all known S100 dimers. We discuss the physiological relevance of this non-canonical homodimeric form in vivo.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/química
Proteínas de Ciclo Celular/metabolismo
Receptor para Produtos Finais de Glicação Avançada/química
Receptor para Produtos Finais de Glicação Avançada/metabolismo
Proteínas S100/química
Proteínas S100/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Cristalografia por Raios X
Dimerização
Seres Humanos
Modelos Moleculares
Ligação Proteica
Estrutura Secundária de Proteína
Estrutura Terciária de Proteína
Proteína A6 Ligante de Cálcio S100
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGER protein, human); 0 (Cell Cycle Proteins); 0 (Receptor for Advanced Glycation End Products); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 105504-00-5 (S100A6 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


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[PMID]:27386938
[Au] Autor:Lerchenmüller C; Heißenberg J; Damilano F; Bezzeridis VJ; Krämer I; Bochaton-Piallat ML; Hirschberg K; Busch M; Katus HA; Peppel K; Rosenzweig A; Busch H; Boerries M; Most P
[Ad] Endereço:From the Cardiovascular Research Center, Massachusetts General Hospital (C.L., F.D., A.R.), Cardiovascular Institute, Beth Israel Deaconess Medical Center (F.D.), and Boston Children's Hospital (V.J.B.), Harvard Medical School, Boston, MA; Molecular and Translational Cardiology (MTC), Department of
[Ti] Título:S100A6 Regulates Endothelial Cell Cycle Progression by Attenuating Antiproliferative Signal Transducers and Activators of Transcription 1 Signaling.
[So] Source:Arterioscler Thromb Vasc Biol;36(9):1854-67, 2016 Sep.
[Is] ISSN:1524-4636
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: S100A6, a member of the S100 protein family, has been described as relevant for cell cycle entry and progression in endothelial cells. The molecular mechanism conferring S100A6's proliferative actions, however, remained elusive. APPROACH AND RESULTS: Originating from the clinically relevant observation of enhanced S100A6 protein expression in proliferating endothelial cells in remodeling coronary and carotid arteries, our study unveiled S100A6 as a suppressor of antiproliferative signal transducers and activators of transcription 1 signaling. Discovery of the molecular liaison was enabled by combining gene expression time series analysis with bioinformatic pathway modeling in S100A6-silenced human endothelial cells stimulated with vascular endothelial growth factor A. This unbiased approach led to successful identification and experimental validation of interferon-inducible transmembrane protein 1 and protein inhibitors of activated signal transducers and activators of transcription as key components of the link between S100A6 and signal transducers and activators of transcription 1. CONCLUSIONS: Given the important role of coordinated endothelial cell cycle activity for integrity and reconstitution of the inner lining of arterial blood vessels in health and disease, signal transducers and activators of transcription 1 suppression by S100A6 may represent a promising therapeutic target to facilitate reendothelialization in damaged vessels.
[Mh] Termos MeSH primário: Proteínas de Ciclo Celular/metabolismo
Ciclo Celular
Proliferação Celular
Células Endoteliais/metabolismo
Proteínas S100/metabolismo
Fator de Transcrição STAT1/metabolismo
[Mh] Termos MeSH secundário: Animais
Antígenos de Diferenciação/genética
Antígenos de Diferenciação/metabolismo
Ciclo Celular/efeitos dos fármacos
Proteínas de Ciclo Celular/genética
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Biologia Computacional
Modelos Animais de Doenças
Células Endoteliais/efeitos dos fármacos
Perfilação da Expressão Gênica/métodos
Redes Reguladoras de Genes
Inativação Gênica
Seres Humanos
Masculino
Proteínas Inibidoras de STAT Ativados/genética
Proteínas Inibidoras de STAT Ativados/metabolismo
Interferência de RNA
Ratos Sprague-Dawley
Reepitelização
Proteína A6 Ligante de Cálcio S100
Proteínas S100/genética
Fator de Transcrição STAT1/genética
Transdução de Sinais
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/genética
Proteínas Modificadoras Pequenas Relacionadas à Ubiquitina/metabolismo
Sus scrofa
Fatores de Tempo
Transcriptoma
Transfecção
Fator A de Crescimento do Endotélio Vascular/farmacologia
Lesões do Sistema Vascular/genética
Lesões do Sistema Vascular/metabolismo
Lesões do Sistema Vascular/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation); 0 (Cell Cycle Proteins); 0 (PIAS1 protein, human); 0 (Protein Inhibitors of Activated STAT); 0 (S100 Calcium Binding Protein A6); 0 (S100 Proteins); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (Small Ubiquitin-Related Modifier Proteins); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 0 (leu-13 antigen); 105504-00-5 (S100A6 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160709
[St] Status:MEDLINE
[do] DOI:10.1161/ATVBAHA.115.306415



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