Base de dados : MEDLINE
Pesquisa : D12.644.276.374.480.700 [Categoria DeCS]
Referências encontradas : 1548 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 155 ir para página                         

  1 / 1548 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28257871
[Au] Autor:Yang L; Zang S; Bai Y; Yao X; Zhang L
[Ad] Endereço:Department of Animal Science, College of Life Science and Food Engineering, Hebei University of Engineering, Handan 056021, China. Electronic address: yangling@hebeu.edu.cn.
[Ti] Título:Effect of early pregnancy on the expression of progesterone receptor and progesterone-induced blocking factor in ovine lymph node.
[So] Source:Theriogenology;93:78-83, 2017 Apr 15.
[Is] ISSN:1879-3231
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Lymph nodes are the sites where the immune reaction or suppression takes place. Progesterone (P4) exerts an essential effect of the immunomodulation on the maternal uterus during early pregnancy in ruminants. At present study, the inguinal lymph nodes were obtained at day 16 of non-pregnancy, days 13, 16 and 25 of pregnancy (n = 3 for each group) in ewes, and RT-PCR assay, western blot and immunohistochemistry analysis were used to analyze to the effect of early pregnancy on the expression of P4 receptor (PGR) and progesterone-induced blocking factor (PIBF) in the lymph nodes. Our results showed that the PGR and PIBF mRNA were up-regulated in the lymph nodes in pregnant ewes, and the PGR isoform (60 kDa) and the PIBF variant (75 kDa) were expressed constantly in the lymph nodes. However, there was no expression of the PGR isoform (40 kDa) and the PIBF variant (48 kDa) at day 16 of the estrous cycle. The immunohistochemistry results confirmed that the PGR and PIBF proteins were limited to the subcapsular sinus and trabeculae in the cortex, medullary sinuses, and were localized in the cytoplasm of the specific cells. This paper reports for the first time that early pregnancy exerts its effect on the specific cells in the lymph nodes through P4, which results in the up-regulated expression of the PGR mRNA and 40 kDa isoform, the PIBF mRNA and 48 kDa variant, and is involved in the immunoregulation of the lymph nodes through a cytosolic pathway in ewes.
[Mh] Termos MeSH primário: Linfonodos/química
Proteínas da Gravidez/genética
Progesterona/farmacologia
Receptores de Progesterona/genética
Ovinos
Fatores Supressores Imunológicos/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Expressão Gênica/efeitos dos fármacos
Idade Gestacional
Imuno-Histoquímica/veterinária
Linfonodos/imunologia
Gravidez
Proteínas da Gravidez/análise
RNA Mensageiro/análise
Receptores de Progesterona/análise
Fatores Supressores Imunológicos/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pregnancy Proteins); 0 (RNA, Messenger); 0 (Receptors, Progesterone); 0 (Suppressor Factors, Immunologic); 4G7DS2Q64Y (Progesterone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170305
[St] Status:MEDLINE


  2 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28168193
[Au] Autor:Gutiérrez-Rodríguez A; Hansberg-Pastor V; Camacho-Arroyo I
[Ad] Endereço:Unidad de Investigación en Reproducción Humana, Instituto Nacional de Perinatología-Facultad de Química, Universidad Nacional Autónoma de México (UNAM), Ciudad Universitaria, Coyoacán, 04510 Ciudad de México, Mexico.
[Ti] Título:Proliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells.
[So] Source:Biomed Res Int;2017:1295087, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Progesterone-induced blocking factor (PIBF) is a progesterone (P ) regulated protein expressed in different types of high proliferative cells including astrocytomas, the most frequent and aggressive brain tumors. It has been shown that PIBF increases the number of human astrocytoma cells. In this work, we evaluated PIBF regulation by P and the effects of PIBF on proliferation, migration, and invasion of U87 and U251 cells, both derived from human glioblastomas. PIBF mRNA expression was upregulated by P (10 nM) from 12 to 24 h. Glioblastoma cells expressed two PIBF isoforms, 90 and 57 kDa. The content of the shorter isoform was increased by P at 24 h, while progesterone receptor antagonist RU486 (10 M) blocked this effect. PIBF (100 ng/mL) increased the number of U87 cells on days 4 and 5 of treatment and induced cell proliferation on day 4. Wound-healing assays showed that PIBF increased the migration of U87 (12-48 h) and U251 (24 and 48 h) cells. Transwell invasion assays showed that PIBF augmented the number of invasive cells in both cell lines at 24 h. These data suggest that PIBF promotes proliferation, migration, and invasion of human glioblastoma cells.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/patologia
Glioblastoma/patologia
Proteínas da Gravidez/metabolismo
Fatores Supressores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Neoplasias Encefálicas/genética
Contagem de Células
Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Glioblastoma/genética
Seres Humanos
Peso Molecular
Invasividade Neoplásica
Proteínas da Gravidez/genética
Progesterona/farmacologia
Isoformas de Proteínas/metabolismo
Fatores Supressores Imunológicos/genética
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PIBF1 protein, human); 0 (Pregnancy Proteins); 0 (Protein Isoforms); 0 (Suppressor Factors, Immunologic); 4G7DS2Q64Y (Progesterone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170208
[St] Status:MEDLINE
[do] DOI:10.1155/2017/1295087


  3 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27717886
[Au] Autor:Marquina-Sánchez B; González-Jorge J; Hansberg-Pastor V; Wegman-Ostrosky T; Baranda-Ávila N; Mejía-Pérez S; Camacho-Arroyo I; González-Arenas A
[Ad] Endereço:Departamento de Medicina Genómica y Toxicología Ambiental, Programa de Investigación en Cancer de Mama, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, Ciudad de México, Mexico.
[Ti] Título:The interplay between intracellular progesterone receptor and PKC plays a key role in migration and invasion of human glioblastoma cells.
[So] Source:J Steroid Biochem Mol Biol;172:198-206, 2017 Sep.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Intracellular progesterone receptors (PRs) and protein kinases C (PKCs) are known regulators of cancer cell proliferation and metastasis. Both PRs and PKCs are found overexpressed in grade IV human astrocytomas, also known as glioblastomas, which are the most frequent and aggressive brain tumors. In the present study, we investigated whether PR activation by PKC induces the migration and invasion of glioblastoma derived cell lines and if PKCα and δ isoforms are involved in PR activation. We observed that PKC activation with tetradecanoylphorbol acetate (TPA) increases the migration and invasion capacity of two human glioblastoma derived human cell lines (U251 MG and U87) and that the treatment with the PR receptor antagonist RU486 blocks these processes. Interestingly, the pharmacological inhibition of the isoenzymes PKCα and PKCδ also resulted in a blocked PR transcriptional activity. Also, TPA-dependent PR activation increases the expression of progesterone-induced blocking factor (PIBF), a known PR target gene. These results hint to an existing cross-talk between PKCs and PRs in regulating the infiltration process of human glioblastomas.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica
Neuroglia/metabolismo
Proteína Quinase C-alfa/genética
Proteína Quinase C-delta/genética
Receptores de Progesterona/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Antagonistas de Hormônios/farmacologia
Seres Humanos
Mifepristona/farmacologia
Neuroglia/efeitos dos fármacos
Neuroglia/patologia
Proteínas da Gravidez/genética
Proteínas da Gravidez/metabolismo
Proteína Quinase C-alfa/metabolismo
Proteína Quinase C-delta/metabolismo
Receptores de Progesterona/antagonistas & inibidores
Receptores de Progesterona/metabolismo
Transdução de Sinais
Fatores Supressores Imunológicos/genética
Fatores Supressores Imunológicos/metabolismo
Acetato de Tetradecanoilforbol/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hormone Antagonists); 0 (PIBF1 protein, human); 0 (Pregnancy Proteins); 0 (Receptors, Progesterone); 0 (Suppressor Factors, Immunologic); 320T6RNW1F (Mifepristone); EC 2.7.11.13 (PRKCA protein, human); EC 2.7.11.13 (PRKCD protein, human); EC 2.7.11.13 (Protein Kinase C-alpha); EC 2.7.11.13 (Protein Kinase C-delta); NI40JAQ945 (Tetradecanoylphorbol Acetate)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161009
[St] Status:MEDLINE


  4 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28139583
[Au] Autor:Agarkov NM; Gontarev SN; Gontareva IS; Lutzenko VD; Yakovlev AP
[Ad] Endereço:South West State University, Kursk, Russia, Belgorod State National Research University, Belgorod, Russia.
[Ti] Título:[Modeling shifts and correlation of hematological and immunological parameters in chronic generalized periodontitis].
[Ti] Título:Modelirovanie sdvigov i korrelyatsionnykh svyazei gematologicheskikh i immunologicheskikh pokazatelei u bol'nykh khronicheskim generalizovannym parodontitom..
[So] Source:Stomatologiia (Mosk);95(6):12-16, 2016.
[Is] ISSN:0039-1735
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Simulation of shifts and correlations of hematological and immunological parameters of the T-cell immunity in 106 patients with chronic periodontal disease and 65 individuals of the control group allowed us to identify leading diagnostic parameters with the quantitative evaluation and enhanced contingency of intersystem communications in peripheral blood and cellular immunity. Mathematical modelling of systemic immunity revealed the most significant shift in absolute number of T-helpers and T-lymphocytes in peripheral blood. Less significant shifts were seen in relative numbers of T-helpers and T-suppressors as well as neutrophilic activity. The revealed changes may play an important role in both diagnosis and therapy of periodontal disease.
[Mh] Termos MeSH primário: Periodontite Crônica/sangue
Periodontite Crônica/imunologia
Modelos Biológicos
[Mh] Termos MeSH secundário: Adulto
Periodontite Crônica/diagnóstico
Feminino
Seres Humanos
Imunidade Celular
Contagem de Linfócitos
Masculino
Meia-Idade
Neutrófilos/imunologia
Fatores Supressores Imunológicos/imunologia
Linfócitos T/imunologia
Linfócitos T Auxiliares-Indutores/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Suppressor Factors, Immunologic)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE
[do] DOI:10.17116/stomat201695612-16


  5 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27874025
[Au] Autor:Alsultan AM; Chin DY; Howard CB; de Bakker CJ; Jones ML; Mahler SM
[Ad] Endereço:Australian Institute for Bioengineering and Nanotechnology (AIBN), University of Queensland (UQ), Brisbane, QLD 4072, Australia.
[Ti] Título:Beyond Antibodies: Development of a Novel Protein Scaffold Based on Human Chaperonin 10.
[So] Source:Sci Rep;5:37348, 2016 11 22.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Human Chaperonin 10 (hCpn10) was utilised as a novel scaffold for presenting peptides of therapeutic and diagnostic significance. Molecular dynamic simulations and protein sizing analyses identified a peptide linker (P1) optimal for the formation of the quarternary hCpn10 heptamer structure. hCpn10 scaffold displaying peptides targeting Factor VIIa (CE76 ) and CD44 (CP7) were expressed in E. coli. Functional studies of CE76 indicated nanomolar affinity for Factor VIIa (3 nM) similar to the E-76 peptide (6 nM), with undetectable binding to Factor X. CE76 was a potent inhibitor of FX activity (via inhibition of Factor VIIa) and prolonged clot formation 4 times longer than achieved by E-76 peptide as determined by prothrombin time (PT) assays. This improvement in clotting function by CE76 , highlights the advantages of a heptamer-based scaffold for improving avidity by multiple peptide presentation. In another example of hCPn10 utility as a scaffold, CP7 bound to native CD44 overexpressed on cancer cells and bound rCD44 with high affinity (K 9.6 nM). The ability to present various peptides through substitution of the hCpn10 mobile loop demonstrates its utility as a novel protein scaffold.
[Mh] Termos MeSH primário: Chaperonina 10/química
Fator VIIa/farmacologia
Receptores de Hialuronatos/metabolismo
Peptídeos/química
Peptídeos/farmacologia
Proteínas da Gravidez/química
Fatores Supressores Imunológicos/química
[Mh] Termos MeSH secundário: Sítios de Ligação
Coagulação Sanguínea/efeitos dos fármacos
Seres Humanos
Modelos Moleculares
Simulação de Dinâmica Molecular
Biblioteca de Peptídeos
Ligação Proteica
Estrutura Quaternária de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD44 protein, human); 0 (Chaperonin 10); 0 (Hyaluronan Receptors); 0 (Peptide Library); 0 (Peptides); 0 (Pregnancy Proteins); 0 (Suppressor Factors, Immunologic); 0 (early pregnancy factor); EC 3.4.21.21 (Factor VIIa)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.1038/srep37348


  6 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27840373
[Au] Autor:Chen Q; Zhu X; Chen R; Liu J; Liu P; Hu A; Wu L; Hua H; Yuan H
[Ad] Endereço:Laboratory Animal Center, Xuzhou Medical University.
[Ti] Título:Early Pregnancy Factor Enhances the Generation and Function of CD4 CD25 Regulatory T Cells.
[So] Source:Tohoku J Exp Med;240(3):215-220, 2016 11.
[Is] ISSN:1349-3329
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The mechanisms of fetal semi-allograft acceptance by the mother's immune system have been the target of many immunological studies. Early pregnancy factor (EPF) is a molecule present in the serum of pregnant mammals soon after conception that has been reported to have immunomodulatory effects. In the present study, we aimed to determine whether immune cells such as CD4 CD25 regulatory T cells (Tregs) are involved in the suppressive mechanism of EPF. Accordingly, CD4 CD25 T cells were isolated from spleens of female C57BL/6 mice and stimulated with anti-CD3 antibody, anti-CD28 antibody and IL-2 in the presence or absence of EPF. Flow cytometry was used to analyze the differentiation of CD4 CD25 T cells to CD4 CD25 Tregs. We thus found a remarkable rise in the Treg ratio in the EPF-treated cells. Higher mRNA and protein levels of fork head box P3 (Foxp3), a marker of the Treg lineage, were also observed in cells treated with EPF. Furthermore, the effect of EPF on Treg immunosuppressive capacity was evaluated. EPF treatment induced the expression of interleukin-10 and transforming growth factor ß1 in Tregs. The suppressive capacity of Tregs was further measured by their capability to inhibit T cell receptor-mediated proliferation of CD4 CD25 T cells. We thus found that EPF exposure can enhance the immunosuppressive functions of Tregs. Overall, our data suggest that EPF induces the differentiation of Tregs and increases their immunosuppressive activities, which might be an important mechanism to inhibit immune responses during pregnancy.
[Mh] Termos MeSH primário: Antígenos CD4/metabolismo
Chaperonina 10/farmacologia
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Proteínas da Gravidez/farmacologia
Fatores Supressores Imunológicos/farmacologia
Linfócitos T Reguladores/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Imunossupressão
Camundongos Endogâmicos C57BL
Receptores de Antígenos de Linfócitos T/metabolismo
Linfócitos T Reguladores/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD4 Antigens); 0 (Chaperonin 10); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Pregnancy Proteins); 0 (Receptors, Antigen, T-Cell); 0 (Suppressor Factors, Immunologic); 0 (early pregnancy factor)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161115
[St] Status:MEDLINE


  7 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27581120
[Au] Autor:Notsu K; Nakagawa M; Nakamura M
[Ad] Endereço:The Department of Cooperative Medical Research, Collaboration Center, Shimane University, Izumo, 693-8501, Japan.
[Ti] Título:Ubiquitin-like protein MNSFß noncovalently binds to molecular chaperone HSPA8 and regulates osteoclastogenesis.
[So] Source:Mol Cell Biochem;421(1-2):149-56, 2016 Oct.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:MNSFß, a ubiquitin-like protein, covalently binds to various target proteins including proapoptotic Bcl-G. During the course of isolation of MNSFß-conjugating enzyme(s), we identified a novel target protein for MNSFß. MALDI-TOF MS fingerprinting revealed that the MNSFß-interacting protein is HSPA8 (heat shock 70-kDa protein 8). We observed that MNSFß noncovalently binds to HSPA8 in the presence of ATP in vitro. Double knockdown of MNSFß and HSPA8 strongly inhibited RANKL-induced osteoclastogenesis from Raw264.7 macrophage-like cells. The same treatment inhibited RANKL-induced ERK1/2 and p38 phosphorylation and TNFα production, suggesting that the association of MNSFß with HSPA8 may promote RANKL-induced osteoclastogenesis. This is the first report that MNSFß binds to a protein substrate via the noncovalent association and exerts biological effects.
[Mh] Termos MeSH primário: Proteínas de Choque Térmico HSC70/metabolismo
Sistema de Sinalização das MAP Quinases
Osteoclastos/metabolismo
Fatores Supressores Imunológicos/metabolismo
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/química
Trifosfato de Adenosina/metabolismo
Animais
Linhagem Celular
Proteínas de Choque Térmico HSC70/química
Camundongos
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Ligação Proteica
Ligante RANK/metabolismo
Fatores Supressores Imunológicos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HSC70 Heat-Shock Proteins); 0 (Hspa8 protein, mouse); 0 (RANK Ligand); 0 (Suppressor Factors, Immunologic); 0 (Tnfsf11 protein, mouse); 0 (monoclonal nonspecific suppressor factor); 8L70Q75FXE (Adenosine Triphosphate); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160902
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-016-2795-x


  8 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27132407
[Au] Autor:Check JH; DiAntonio G; DiAntonio A; Duroseau M
[Ti] Título:The progesterone receptor antagonist mifepristone does not lower serum progesterone induced blocking factor (PIBF) in the presence of progesterone.
[So] Source:Clin Exp Obstet Gynecol;43(2):189-91, 2016.
[Is] ISSN:0390-6663
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:PURPOSE: To determine if mifepristone can lower serum levels of a progesterone (P) induced immunomodulatory protein believed to be needed for the fetus to escape immune surveillance. MATERIALS AND METHODS: A female volunteer had her serum P induced blocking factor (PIBF) increased by ingestion of oral micronized P. While remaining on P mifepristone, 200 mg/day was given for six days when another serum PIBF level was obtained. RESULTS: The serum PIBF was 273 ng/ml after five days of oral micronized P. It increased further to 737 ng/ml despite taking six days of 200 mg mifepristone. CONCLUSIONS: The mechanism for inducing abortion by mifepristone does not seem to be related to decreasing serum levels of PIBF. This does not eliminate the possibility that the mechanism involves reducing the intracytoplasmic PIBF levels.
[Mh] Termos MeSH primário: Antagonistas de Hormônios/farmacologia
Mifepristona/farmacologia
Proteínas da Gravidez/efeitos dos fármacos
Progesterona/farmacologia
Progestinas/farmacologia
Fatores Supressores Imunológicos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Proteínas da Gravidez/sangue
Receptores de Progesterona/antagonistas & inibidores
Fatores Supressores Imunológicos/sangue
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hormone Antagonists); 0 (PIBF1 protein, human); 0 (Pregnancy Proteins); 0 (Progestins); 0 (Receptors, Progesterone); 0 (Suppressor Factors, Immunologic); 320T6RNW1F (Mifepristone); 4G7DS2Q64Y (Progesterone)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160502
[Lr] Data última revisão:
160502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160503
[St] Status:MEDLINE


  9 / 1548 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27038657
[Au] Autor:Webb DR
[Ad] Endereço:Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 N. Torrey Pines Rd, La Jolla, CA 92037, United States. Electronic address: dwebb@scripps.edu.
[Ti] Título:Soluble Immune Response Suppressor (SIRS): Reassessing the immunosuppressant potential of an elusive peptide.
[So] Source:Biochem Pharmacol;117:1-9, 2016 Oct 01.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A previously studied immunosuppressive cytokine, Soluble Immune Response Suppressor (SIRS), may have relevance to current studies of immune suppression in a variety of human disease states. Despite extensive efforts using experimental models, mainly in mice, much remains to be discovered as to how autoimmune cells in mice and humans escape normal regulation and, conversely, how tumor cells evade evoking an immune response. It is the contention of this commentary that the literature pre-2000 contain results that might inform current studies. The broadly immunosuppressive protein, SIRS, was studied extensively from the 1970s to 1990s and culminated in the determination of the n-terminal 21mer sequence of this 15kDa protein which had high homology to the short neurotoxins from sea snakes, that are canonical members of the three finger neurotoxin superfamily (3FTx). It was not until 2007 that the prophylactic administration of the synthetic N-terminal peptide of the SIRS 21mer, identical to the published sequence, was reported to inhibit or delay the development of two autoimmune diseases in mice: experimental allergic encephalomyelitis (EAE) and type I diabetes (T1D). These findings were consistent with other studies of the 3FTx superfamily as important probes in the study of mammalian pharmacology. It is the perspective of this commentary that SIRS, SIRS peptide and the anti-peptide mAb, represent useful, pharmacologically-active probes for the study of the immune response as well as in the potential treatment of autoimmune, inflammatory diseases and cancer.
[Mh] Termos MeSH primário: Doenças Autoimunes/tratamento farmacológico
Imunossupressores/uso terapêutico
Modelos Moleculares
Fatores Supressores Imunológicos/uso terapêutico
[Mh] Termos MeSH secundário: Algoritmos
Animais
Anticorpos Monoclonais/farmacologia
Anticorpos Monoclonais/uso terapêutico
Doenças Autoimunes/imunologia
Doenças Autoimunes/terapia
Biologia Computacional
Sistemas Especialistas
Seres Humanos
Imunomodulação/efeitos dos fármacos
Imunossupressão/métodos
Imunossupressores/antagonistas & inibidores
Imunossupressores/química
Imunossupressores/farmacologia
Neurotoxinas/química
Neurotoxinas/toxicidade
Fragmentos de Peptídeos/antagonistas & inibidores
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/farmacologia
Fragmentos de Peptídeos/uso terapêutico
Conformação Proteica
Homologia de Sequência de Aminoácidos
Venenos de Serpentes/química
Venenos de Serpentes/toxicidade
Fatores Supressores Imunológicos/antagonistas & inibidores
Fatores Supressores Imunológicos/química
Fatores Supressores Imunológicos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Monoclonal); 0 (Immunosuppressive Agents); 0 (Neurotoxins); 0 (Peptide Fragments); 0 (Snake Venoms); 0 (Suppressor Factors, Immunologic); 0 (soluble immune response suppressor)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160404
[St] Status:MEDLINE


  10 / 1548 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26980572
[Au] Autor:Chu SJ; Wang G; Zhang PF; Zhang R; Huang YX; Lu YM; Da W; Sun Q; Zhang J; Zhu JS
[Ad] Endereço:Department of Gerontology, Shanghai Jiao Tong University Affiliated Shanghai Sixth People's Hospital, Shanghai, 200233, China.
[Ti] Título:MicroRNA-203 suppresses gastric cancer growth by targeting PIBF1/Akt signaling.
[So] Source:J Exp Clin Cancer Res;35:47, 2016 Mar 15.
[Is] ISSN:1756-9966
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: MicroRNAs (miRNAs) have been proved involved in many tumorigenic behaviors including tumor growth. But, the clinical significance and functions of miRNA-203 in gastric cancer (GC) remain elusive. RESULTS: Decreased expression of miRNA-203 was correlated with tumor size, poor prognosis and recurrence in GC patients. Overexpression of miR-203 or knockdown of its target progesterone immunomodulatory binding factor 1 (PIBF1) inhibited GC growth in vitro and in vivo, while miR-203 knockdown promoted GC proliferation. In addition, PIBF1 overexpression attenuated the inhibitory effects of miR-203 on GC growth and enhanced that effect on p-Akt expression. CONCLUSIONS: MiR-203 as a tumor biomarker suppresses GC growth through targeting the PIBF1/Akt signaling, suggesting that it may have the important therapeutic potential for the treatment of GC.
[Mh] Termos MeSH primário: MicroRNAs/genética
Recidiva Local de Neoplasia/genética
Proteínas da Gravidez/genética
Proteínas Proto-Oncogênicas c-akt/genética
Neoplasias Gástricas/patologia
Fatores Supressores Imunológicos/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular
Feminino
Seres Humanos
Masculino
Prognóstico
Transdução de Sinais
Neoplasias Gástricas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RETRACTED PUBLICATION
[Nm] Nome de substância:
0 (MIRN203 microRNA, human); 0 (MicroRNAs); 0 (PIBF1 protein, human); 0 (Pregnancy Proteins); 0 (Suppressor Factors, Immunologic); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170504
[Lr] Data última revisão:
170504
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160317
[St] Status:MEDLINE
[do] DOI:10.1186/s13046-016-0323-1



página 1 de 155 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde