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Pesquisa : G05.308.370 [Categoria DeCS]
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Id: biblio-889036
Autor: Zhang, X; Song, Y; Song, N; Zhang, L; Wang, Y; Li, D; Wang, Z; Qu, X; Liu, Y.
Título: Rankl expression predicts poor prognosis in gastric cancer patients: results from a retrospective and single-center analysis
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(3):e6265, 2018. tab, graf.
Idioma: en.
Projeto: National Science and Technology Major Project; . Science and Technology Plan Project; . Chinese National Foundation of National Sciences; . Liaoning BaiQianWan Talents Program.
Resumo: The receptor activator of nuclear factor κB ligand (RANKL)/RANK pathway plays an important role in the prognosis of several solid tumor types, but its role in gastric cancer prognosis has been poorly characterized. A total of 116 gastric cancer patients who underwent surgical resection were enrolled in this study. Expressions of RANKL and RANK in gastric cancer tissues were detected using immunohistochemical staining. Thirty-eight patients (33%) showed a high level of RANKL expression and 61 patients (53%) showed a high level of RANK expression. There was a positive correlation between expressions of RANKL and RANK (P=0.014, r=0.221). A high level of RANKL expression indicated shorter overall survival (OS) (P=0.008), and was associated with a higher pathological tumor/lymph node/metastasis (pTNM) stage (P=0.035), while no significant correlation was detected between RANK expression and clinicopathological parameters. RANKL also predicted poor prognosis in patients with high RANK expression (P=0.008) and Bormann's type III/IV (P=0.002). Furthermore, RANKL expression correlated with pTNM stage according to high RANK expression (P=0.009), while no significance was found in patients with low RANK expression (P=1.000). Together, our results revealed that high expression of RANKL could predict worse outcomes in gastric cancer especially combined with RANK detection, and thereby this pathway could be a useful prognostic indicator of gastric cancer.
Descritores: Neoplasias Gástricas/metabolismo
Adenocarcinoma/metabolismo
Ligante RANK/metabolismo
Proteínas de Neoplasias/metabolismo
-Prognóstico
Neoplasias Gástricas/cirurgia
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/patologia
Imuno-Histoquímica
Adenocarcinoma/cirurgia
Adenocarcinoma/mortalidade
Adenocarcinoma/patologia
Regulação Neoplásica da Expressão Gênica
China/epidemiologia
Estudos Retrospectivos
Estatísticas não Paramétricas
Gradação de Tumores
Estadiamento de Neoplasias
Limites: Seres Humanos
Masculino
Feminino
Meia-Idade
Responsável: BR1.1 - BIREME


  2 / 128 LILACS  
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Id: biblio-1024773
Autor: Lima, M A; Dos Santos, L; Turri, J A; Nonogaki, S; Buim, M; Lima, J F; de Jesus Viana Pinheiro, J; Osório, C A Bueno de Toledo; Soares, F A; Freitas, V M.
Título: Prognostic Value of ADAMTS Proteases and Their Substrates in Epithelial Ovarian Cancer
Fonte: Pathobiology;83(6):316-326, 2016.
Idioma: en.
Resumo: Background: ADAMTS are metalloproteases with disintegrin and thrombospondin motifs. They are secreted proteases playing a role in biological processes such as inflammation, angiogenesis, and urogenital development. ADAMTS have specific substrates, such as the proteoglycans (PG) versican, aggrecan, and brevican. Despite data indicating a role of ADAMTS in tumor invasion and metastases, effects played by these molecules in cancer progression are still controversial. In ovarian cancer, the importance of ADAMTS gene mutations was recently described and related to chemotherapy outcome. Objective: To analyze protein levels of ADAMTS-1, -4, and -5, and TIMP-3 in human ovarian cancer classified as benign, borderline, or malignant. We also assessed the expression of the ADAMTS substrates aggrecan, brevican, and versican in these neoplasms. Correlations between overall survival and protein expression were performed. Methods: Tumors were classified according to the WHO Classification of Tumors of Female Reproductive Organs. Protein and PG expression was studied by immunohistochemistry. Differences in labeling were analyzed by percent measurements of stained areas. Results: ADAMTS-1, ADAMTS-5, and its tissue inhibitor TIMP-3 are increased in borderline and malignant tumors compared to benign neoplasms. Aggrecan and versican levels were increased in malignant subtypes compared to benign ovarian cancer. Higher ADAMTS-1, TIMP-3, and versican expression was associated with a shorter overall survival. Conclusions: Comparison of protease, TIMP-3, and substrate expression showed that in malignant tumors all ADAMTS and TIMP-3 expression levels were significantly raised compared to the substrates studied.
Descritores: Neoplasias Ovarianas
Seres Humanos
Biomarcadores Tumorais/metabolismo
Regulação Neoplásica da Expressão Gênica
Neoplasias Epiteliais e Glandulares/diagnóstico
Inibidor Tecidual de Metaloproteinase-3/metabolismo
Proteína ADAMTS1/metabolismo
Proteína ADAMTS4/metabolismo
FREUDIAN THEORY1
Responsável: BR91.2 - Centro de Documentação


  3 / 128 LILACS  
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Id: biblio-889107
Autor: Wu, Wei; Huang, Bo; Yan, Yan; Zhong, Zhi-Qiang.
Título: Exploration of gene functions for esophageal squamous cell carcinoma using network-based guilt by association principle
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(6):e6801, 2018. tab, graf.
Idioma: en.
Resumo: Gene networks have been broadly used to predict gene functions based on guilt by association (GBA) principle. Thus, in order to better understand the molecular mechanisms of esophageal squamous cell carcinoma (ESCC), our study was designed to use a network-based GBA method to identify the optimal gene functions for ESCC. To identify genomic bio-signatures for ESCC, microarray data of GSE20347 were first downloaded from a public functional genomics data repository of Gene Expression Omnibus database. Then, differentially expressed genes (DEGs) between ESCC patients and controls were identified using the LIMMA method. Afterwards, construction of differential co-expression network (DCN) was performed relying on DEGs, followed by gene ontology (GO) enrichment analysis based on a known confirmed database and DEGs. Eventually, the optimal gene functions were predicted using GBA algorithm based on the area under the curve (AUC) for each GO term. Overall, 43 DEGs and 67 GO terms were gained for subsequent analysis. GBA predictions demonstrated that 13 GO functions with AUC>0.7 had a good classification ability. Significantly, 6 out of 13 GO terms yielded AUC>0.8, which were determined as the optimal gene functions. Interestingly, there were two GO categories with AUC>0.9, which included cell cycle checkpoint (AUC=0.91648), and mitotic sister chromatid segregation (AUC=0.91597). Our findings highlight the clinical implications of cell cycle checkpoint and mitotic sister chromatid segregation in ESCC progression and provide the molecular foundation for developing therapeutic targets.
Descritores: Carcinoma de Células Escamosas/genética
Biologia Computacional/métodos
Neoplasias Esofágicas/genética
Perfilação da Expressão Gênica/métodos
Regulação Neoplásica da Expressão Gênica/genética
Redes Reguladoras de Genes/genética
-Área Sob a Curva
Limites: Seres Humanos
Responsável: BR1.1 - BIREME


  4 / 128 LILACS  
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Id: biblio-889104
Autor: Yang, Shaofeng; Sheng, Nan; Pan, Lili; Cao, Jing; Liu, Jiao; Ma, Ran.
Título: microRNA-3129 promotes cell proliferation in gastric cancer cell line SGC7901 via positive regulation of pRb
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(6):e6452, 2018. tab, graf.
Idioma: en.
Resumo: Several microRNAs (miRNAs) have been reported as oncogenes or tumor suppressors in many cancers, including gastric cancer (GC). However, the role and molecular mechanism of miR-3129 in GC is largely unknown. We aimed to explore the function and the underlying molecular mechanism of miR-3129 in GC. Cancer tissues and corresponding adjacent tissues were collected from 50 patients with GC, and the expression of miR-3129 was detected by RT-qPCR. The expression of miR-3129 and pRb in human GC cell line SCG7091 was altered by transient transfection. Thereafter, MTT and flow cytometry assays were used to analyze cell viability and cell cycle. The expression of cyclin E, CDK2, CDK2 inhibitors (p16 and 21), and pRb were detected by RT-qPCR and western blot. A significant up-regulation of miR-3129 was observed in GC tissues compared to adjacent tissues. Overexpression of miR-3129 significantly improved cell viability after 4 days of post-transfection. Flow cytometry assay results showed that the miR-3129 overexpression arrested more SGC7901 cells at S phase. Moreover, overexpression of miR-3129 down-regulated the expression of CDK2 inhibitors while it up-regulated the expression levels of cyclin E, CDK2, and pRb. Interestingly, we found that pRb inhibition reversed the effect of miR-3129 inhibitor on cell proliferation in SGC7901 cells, increased cell viability, reduced cells at G0/1 phase, and modulated the expression of proliferation-related factors. Our results revealed that miR-3129 functioned as an oncogene through positive regulation of pRb and may prove to be a promising option for molecular therapy of GC.
Descritores: Proliferação Celular/genética
Proteína do Retinoblastoma/genética
Neoplasias Gástricas/genética
-Linhagem Celular Tumoral
Sobrevivência Celular
Regulação para Baixo
Citometria de Fluxo
Regulação Neoplásica da Expressão Gênica/genética
Estadiamento de Neoplasias
Reação em Cadeia da Polimerase em Tempo Real
Proteína do Retinoblastoma/metabolismo
Transdução de Sinais
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
Transfecção
Regulação para Cima
Limites: Seres Humanos
Masculino
Feminino
Adulto
Meia-Idade
Responsável: BR1.1 - BIREME


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Id: biblio-889094
Autor: Yang, Tianzheng; Zhai, Hongyan; Yan, Ruihong; Zhou, Zhenhu; Gao, Lei; Wang, Luqing.
Título: lncRNA CCAT1 promotes cell proliferation, migration, and invasion by down-regulation of miR-143 in FTC-133 thyroid carcinoma cell line
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(6):e7046, 2018. graf.
Idioma: en.
Resumo: Thyroid cancer is a common malignant tumor. Long non-coding RNA colon cancer-associated transcript 1 (lncRNA CCAT1) is highly expressed in many cancers; however, the molecular mechanism of CCAT1 in thyroid cancer remains unclear. Hence, this study aimed to investigate the effect of CCAT1 on human thyroid cancer cell line FTC-133. FTC-133 cells were transfected with CCAT1 expressing vector, CCAT1 shRNA, miR-143 mimic, and miR-143 inhibitor, respectively. After different treatments, cell viability, proliferation, migration, invasion, and apoptosis were measured. Moreover, the regulatory relationship of CCAT1 and miR-143, as well as miR-143 and VEGF were tested using dual-luciferase reporter assay. The relative expressions of CCAT1, miR-143, and VEGF were tested by qRT-PCR. The expressions of apoptosis-related factors and corresponding proteins in PI3K/AKT and MAPK pathways were analyzed using western blot analysis. The results suggested that CCAT1 was up-regulated in the FTC-133 cells. CCAT1 suppression decreased FTC-133 cell viability, proliferation, migration, invasion, and miR-143 expression, while it increased apoptosis and VEGF expression. CCAT1 might act as a competing endogenous RNA (ceRNA) for miR-143. Moreover, CCAT1 activated PI3K/AKT and MAPK signaling pathways through inhibition of miR-143. This study demonstrated that CCAT1 exhibited pro-proliferative and pro-metastasis functions on FTC-133 cells and activated PI3K/AKT and MAPK signaling pathways via down-regulation of miR-143. These findings will provide a possible target for clinical treatment of thyroid cancer.
Descritores: MicroRNAs/metabolismo
RNA Longo não Codificante/metabolismo
Neoplasias da Glândula Tireoide/patologia
-Apoptose
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Sobrevivência Celular
Regulação para Baixo
Regulação Neoplásica da Expressão Gênica
MicroRNAs/genética
Invasividade Neoplásica/patologia
RNA Longo não Codificante/genética
Transfecção
Limites: Seres Humanos
Responsável: BR1.1 - BIREME


  6 / 128 LILACS  
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Id: biblio-889056
Autor: Song, Zhonghua; Zhao, Wenhua; Cao, Danfeng; Zhang, Jinqing; Chen, Shouhua.
Título: Elementary screening of lymph node metastatic-related genes in gastric cancer based on the co-expression network of messenger RNA, microRNA and long non-coding RNA
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;51(4):e6685, 2018. tab, graf.
Idioma: en.
Resumo: Gastric cancer (GC) is the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. The high mortality might be attributed to delay in detection and is closely related to lymph node metastasis. Therefore, it is of great importance to explore the mechanism of lymph node metastasis and find strategies to block GC metastasis. Messenger RNA (mRNA), microRNA (miRNA) and long non-coding RNA (lncRNA) expression data and clinical data were downloaded from The Cancer Genome Atlas (TCGA) database. A total of 908 differentially expressed factors with variance >0.5 including 542 genes, 42 miRNA, and 324 lncRNA were screened using significant analysis microarray algorithm, and interaction networks were constructed using these differentially expressed factors. Furthermore, we conducted functional modules analysis in the network, and found that yellow and turquoise modules could separate samples efficiently. The groups classified in the yellow and turquoise modules had a significant difference in survival time, which was verified in another independent GC mRNA dataset (GSE62254). The results suggested that differentially expressed factors in the yellow and turquoise modules may participate in lymph node metastasis of GC and could be applied as potential biomarkers or therapeutic targets for GC.
Descritores: Regulação Neoplásica da Expressão Gênica/genética
Redes Reguladoras de Genes/genética
MicroRNAs/genética
RNA Longo não Codificante/genética
RNA Mensageiro/genética
Neoplasias Gástricas/genética
-China/epidemiologia
Perfilação da Expressão Gênica
Linfonodos/metabolismo
Linfonodos/patologia
Metástase Linfática/genética
Prognóstico
RNA Mensageiro/metabolismo
Neoplasias Gástricas/mortalidade
Neoplasias Gástricas/secundário
Limites: Seres Humanos
Responsável: BR1.1 - BIREME


  7 / 128 LILACS  
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Id: biblio-888994
Autor: Zhu, TG; Xiao, X; Wei, Q; Yue, M; Zhang, LX.
Título: Revealing potential long non-coding RNA biomarkers in lung adenocarcinoma using long non-coding RNA-mediated competitive endogenous RNA network
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(9):e6297, 2017. tab, graf.
Idioma: en.
Resumo: In our study, we aimed to reveal potential long non-coding RNAs (lncRNA) biomarkers in lung adenocarcinoma (LAD) using lncRNA-mediated competing endogenous RNAs (ceRNAs) network (LMCN). Competing lncRNA-mRNA interactions were identified using the hypergeometric test. Co-expression analysis for the competing lncRNA-mRNA interactions was implemented, and relying on the weight value >0.8, a highly competitive LMCN was further constructed. Degree distribution, betweenness and closeness for LMCN were carried out to analyze the network structure. Functional analyses of mRNAs in LMCN were carried out to further explore the biological functions of lncRNAs. Biclique algorithm was utilized to extract competing modules from the LMCN. Finally, we verified our findings in an independent sample set using qRT-PCR. Based on degrees >60, we identified 4 hubs, including DLEU2, SNHG12, HCP5, and LINC00472. Furthermore, 2 competing modules were identified, and LINC00472 in module 1 functioned as a hub in both LMCN and module. Functional implications of lncRNAs demonstrated that lncRNAs were related to histone modification, negative regulation of cell cycle, neuroactive ligand-receptor interaction, and regulation of actin cytoskeleton. qRT-PCR results demonstrated that lncRNAs LINC00472, and HCP5 were down-regulated in LAD tissues, while the expression level of SNHG12 was up-regulated in LAD tissues. Our study sheds novel light on the roles of lncRNA-related ceRNA network in LAD and facilitates the detection of potential lncRNA biomarkers for LAD diagnosis and treatment. Remarkably, in our study, LINC00472, HCP5, and SNHG12 might be potential biomarkers for LAD management.
Descritores: Adenocarcinoma/genética
Biomarcadores Tumorais/genética
Regulação Neoplásica da Expressão Gênica/genética
Redes Reguladoras de Genes/genética
Neoplasias Pulmonares/genética
RNA Longo não Codificante/genética
-Prognóstico
Limites: Seres Humanos
Responsável: BR1.1 - BIREME


  8 / 128 LILACS  
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Id: biblio-888985
Autor: Zhou, LL; Dong, JL; Huang, G; Sun, ZL; Wu, J.
Título: MicroRNA-143 inhibits cell growth by targeting ERK5 and MAP3K7 in breast cancer
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(8):e5891, 2017. graf.
Idioma: en.
Resumo: This study aimed to investigate the function and mechanism of microRNA-143 (miR-143) in the occurrence and development of breast cancer (BC). A total of 30 BC tissues, 30 corresponding noncancerous tissues, and 10 normal control (NC) breast tissues were obtained to detect the levels of miR-143, extracellular signal-regulated kinase 5 (ERK5) and mitogen-activated protein 3 kinase 7 (MAP3K7) using RT-qPCR, western blotting or immunohistochemistry. The correlation of miR-143 with ERK5 or MAP3K7 was evaluated using Pearson correlation analysis. MCF-7 cells were transiently transfected with miR-143 mimic, miR-143 inhibitor, miR-143 mimic/inhibitor + si-ERK5, si-MAP3K7 or si-cyclin D1. Then, cell growth was evaluated by MTT assay and the expressions of phospho-ERK5 (p-ERK5), ERK5, p-MAP3K7, MAP3K7 and cyclin D1 were detected by western blotting. Results showed that, compared with noncancerous tissues or NC breast tissues, miR-143 level was decreased, while p-ERK5, ERK5, p-MAP3K7 and MAP3K7 expressions were increased in BC tissues (all P<0.01). The miR-143 level was negatively correlated with the mRNA level of ERK5 or MAP3K7 (r=-4.231 or r=-4.280, P<0.01). In addition, up-regulated miR-143 significantly decreased the expressions of p-ERK5, ERK5, p-MAP3K7, MAP3K7 and cyclin D1 (all P<0.01), as well as cell viability in MCF-7 cells (all P<0.05) while the effect of down-regulated miR-143 was the opposite. In conclusion, both ERK5 and MAP3K7 may be the target genes of miR-143. Increased expression of miR-143 can inhibit cell growth, which may be associated with ERK5 and MAP3K7 expressions in BC.
Descritores: Neoplasias da Mama/metabolismo
MicroRNAs/metabolismo
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
-Biomarcadores Tumorais/metabolismo
Western Blotting
Estudos de Casos e Controles
Linhagem Celular Tumoral
Proliferação Celular
Regulação Neoplásica da Expressão Gênica
Imuno-Histoquímica
Proteína Quinase 7 Ativada por Mitógeno/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Limites: Seres Humanos
Feminino
Responsável: BR1.1 - BIREME


  9 / 128 LILACS  
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Id: biblio-888984
Autor: Wanandi, SI; Yustisia, I; Neolaka, GMG; Jusman, SWA.
Título: Impact of extracellular alkalinization on the survival of human CD24-/CD44+ breast cancer stem cells associated with cellular metabolic shifts
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(8):e6538, 2017. tab, graf.
Idioma: en.
Resumo: Cancer stem cells reside in a distinct region within the tumor microenvironment that it is believed to play a fundamental role in regulating stemness, proliferation, survival, and metabolism of cancer cells. This study aimed to analyze the effect of extracellular alkalinization on metabolism and survival of human CD24-/CD44+ breast cancer stem cells (BCSCs). BCSCs were cultured in alkalinized DMEM-F12 and incubated at 37°C, 5% CO2, and 20% O2 for 30 min, 6, 24, and 48 h. After each incubation period, we analyzed the modulation of various mRNA expressions related to pH and cellular metabolic regulation using the qRT-PCR. Metabolic state was measured using colorimetric and fluorometric assays. To examine cell proliferation and apoptosis, we used trypan blue and annexin V/propidium iodide assay, respectively. This study demonstrated that alkalinization could stimulate extracellular carbonic anhydrase (CAe) activity, as well as CA9 and HIF1α expression. Under alkaline pH and HIF1α regulation, glucose consumption, extracellular lactate production, and LDH activity of BCSCs were upregulated while O2 consumption was downregulated. These metabolic shifts seemed to promote apoptosis and suppress the proliferation of BCSCs. To conclude, modulation of the extracellular environment through alkalinization could change the metabolic states of BCSCs, which in turn affect the cell survival.
Descritores: Neoplasias da Mama/metabolismo
Antígeno CD24/metabolismo
Receptores de Hialuronatos/metabolismo
Células-Tronco Neoplásicas/metabolismo
-Apoptose
Proliferação Celular
Sobrevivência Celular
Espaço Extracelular
Regulação Neoplásica da Expressão Gênica
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Limites: Seres Humanos
Feminino
Responsável: BR1.1 - BIREME


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Id: biblio-888976
Autor: Jiang, T; Jiang, CY; Shu, JH; Xu, YJ.
Título: Excavation of attractor modules for nasopharyngeal carcinoma via integrating systemic module inference with attract method
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(8):e6416, 2017. tab, graf.
Idioma: en.
Resumo: The molecular mechanism of nasopharyngeal carcinoma (NPC) is poorly understood and effective therapeutic approaches are needed. This research aimed to excavate the attractor modules involved in the progression of NPC and provide further understanding of the underlying mechanism of NPC. Based on the gene expression data of NPC, two specific protein-protein interaction networks for NPC and control conditions were re-weighted using Pearson correlation coefficient. Then, a systematic tracking of candidate modules was conducted on the re-weighted networks via cliques algorithm, and a total of 19 and 38 modules were separately identified from NPC and control networks, respectively. Among them, 8 pairs of modules with similar gene composition were selected, and 2 attractor modules were identified via the attract method. Functional analysis indicated that these two attractor modules participate in one common bioprocess of cell division. Based on the strategy of integrating systemic module inference with the attract method, we successfully identified 2 attractor modules. These attractor modules might play important roles in the molecular pathogenesis of NPC via affecting the bioprocess of cell division in a conjunct way. Further research is needed to explore the correlations between cell division and NPC.
Descritores: Carcinoma/genética
Regulação Neoplásica da Expressão Gênica/genética
Redes Reguladoras de Genes/genética
Neoplasias Nasofaríngeas/genética
-Perfilação da Expressão Gênica
Mapeamento de Interação de Proteínas
Limites: Seres Humanos
Responsável: BR1.1 - BIREME



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