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[PMID]:28467119
[Au] Autor:Wang Y; Li L; Xu C; Cao X; Liu Z; Sun N; Zhang A; Li X; Zhang K
[Ad] Endereço:a Department of Psychiatry , First Hospital of Shanxi Medical University , Taiyuan , People's Republic of China.
[Ti] Título:Polymorphism of ERK/PTPRR Genes in Major Depressive Disorder at Resting-State Brain Function.
[So] Source:Dev Neuropsychol;42(3):231-240, 2017.
[Is] ISSN:1532-6942
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The polymorphism of ERK and PTPRR in MDD is rarely reported. The present study investigated the association between the polymorphism of ERK/PTPRR and MDD at resting-state brain function using genomic imaging. It indicated that the amplitude of low-frequency fluctuation (ALFF) and regional homogeneity (ReHo) in functional magnetic resonance imaging (fMRI) changed significantly in various brain regions of MDD patients. The T/G allele of ERK-rs1267842 and G/C allele of PTPRR-rs1513105 showed abnormal ALFF and ReHo changes in cortex including superior frontal gyrus and middle temporal gyrus. The development of MDD may be related with the polymorphism of ERK-rs12678428 and PTPRR-rs1513105.
[Mh] Termos MeSH primário: Encéfalo/fisiopatologia
Transtorno Depressivo Maior/genética
Sistema de Sinalização das MAP Quinases/genética
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Encéfalo/diagnóstico por imagem
Mapeamento Encefálico
Estudos de Casos e Controles
Transtorno Depressivo Maior/diagnóstico por imagem
Transtorno Depressivo Maior/fisiopatologia
Feminino
Seres Humanos
Imagem por Ressonância Magnética/métodos
Masculino
Meia-Idade
Polimorfismo Genético
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1080/87565641.2017.1306527


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[PMID]:28183446
[Au] Autor:Krisko TI; LeClair KB; Cohen DE
[Ad] Endereço:Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
[Ti] Título:Genetic ablation of phosphatidylcholine transfer protein/StarD2 in ob/ob mice improves glucose tolerance without increasing energy expenditure.
[So] Source:Metabolism;68:145-149, 2017 Mar.
[Is] ISSN:1532-8600
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Phosphatidylcholine transfer protein (PC-TP; synonym StarD2) is highly expressed in liver and oxidative tissues. PC-TP promotes hepatic glucose production during fasting and aggravates glucose intolerance in high fat fed mice. However, because PC-TP also suppresses thermogenesis in brown adipose tissue (BAT), its direct contribution to obesity-associated diabetes in mice remains unclear. Here we examined the effects of genetic PC-TP ablation on glucose homeostasis in leptin-deficient ob/ob mice, which exhibit both diabetes and altered thermoregulation. ANIMALS/METHODS: Mice lacking both PC-TP and leptin (Pctp ;ob/ob) were prepared by crossing Pctp with ob/+ mice. Glucose homeostasis was assessed by standard assays, and energy expenditure was determined by indirect calorimetry using a comprehensive laboratory animal monitoring system, which also recorded physical activity and food intake. Body composition was determined by NMR and hepatic lipids by enzymatic assays. Core body temperature was measured using a rectal thermocouple probe. RESULTS: Pctp ;ob/ob mice demonstrated improved glucose homeostasis, as evidenced by markedly improved glucose and pyruvate tolerance tests, without changes in insulin tolerance. However, there were no differences in EE at any ambient temperature. There were also no effects of PC-TP expression on physical activity, food intake or core body temperature. CONCLUSIONS: Improved glucose tolerance in Pctp ;ob/ob mice in the absence of increases in energy expenditure or core body temperature indicates a direct pathogenic role for PC-TP in diabetes in leptin deficient mice.
[Mh] Termos MeSH primário: Metabolismo Energético/genética
Intolerância à Glucose/genética
Intolerância à Glucose/metabolismo
Proteínas de Transferência de Fosfolipídeos/genética
Proteínas de Transferência de Fosfolipídeos/metabolismo
[Mh] Termos MeSH secundário: Animais
Composição Corporal/genética
Temperatura Corporal/genética
Calorimetria Indireta
Ingestão de Alimentos
Teste de Tolerância a Glucose
Homeostase
Resistência à Insulina/genética
Leptina/deficiência
Leptina/genética
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Piruvatos/metabolismo
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Leptin); 0 (Phospholipid Transfer Proteins); 0 (Pyruvates); EC 3.1.3.48 (Ptprr protein, mouse); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170523
[Lr] Data última revisão:
170523
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE


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[PMID]:26773914
[Au] Autor:Li X; Liu Z; Li W; Sun N; Xu Y; Xie Z; Zhang K
[Ad] Endereço:Department of Psychiatry, First Hospital of Shanxi Medical University, Taiyuan, China.
[Ti] Título:PTPRR regulates ERK dephosphorylation in depression mice model.
[So] Source:J Affect Disord;193:233-41, 2016 Mar 15.
[Is] ISSN:1573-2517
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Protein tyrosine phosphatase receptor type R (PTPRR), which regulates the dephosphorylation of the downstream mitogen-activated protein kinase (MAPK) steering cell proliferation, apoptosis and synaptic plasticity, may be involved in the pathogenesis of depression. METHODS: Lentiviral vectors were utilized to express the PTPRR constitutively in the hippocampal dentate gyrus (DG) of mice before or after chronic mild stress. Behavior tests, MAPK levels, neuronal apoptosis and cell proliferation in the hippocampal DG were examined. RESULTS: Without chronic mild stress (CMS), the lenti-shPTPRR mice showed shorter immobility time in the tail suspension test than controls, while the lenti-PTPRR mice exhibited significantly less sucrose intake and increased immobility time in the forced swim tests than control mice, indicating increased prodepressant-like effects of PTPRR in lenti-PTPRR mice. Similarly, under CMS, the lenti-shPTPRR mice had more sucrose intake, shorter immobility time in the forced swim test and tail suspension test compared to controls, and lenti-PTPRR mice had less sucrose intake and longer immobility time in forced swim test and tail suspension test, exhibiting increased susceptibility to depressive-like behaviors and greater sensitivity to CMS. Besides, the Phospho-ERK1/2(p-ERK) had significant lower phosphorylation in lenti-PTPRR group and higher expression in lenti-shPTPRR group, both without CMS. The Lenti-PTPRR mice exposed to CMS had significant lower p-ERK, and the lenti-shPTPRR mice exposed to CMS had significant higher p-ERK and lower p-P38. Moreover, there were more cells underwent apoptosis in lenti-PTPRR group ,with and without CMS. In cell proliferation, less BrdU positive cells were observed in lenti-PTPRR mice than controls. CONCLUSION: The site-specific lentiviral injections resulted in the PTPRR over-expression in the hippocampal DG and subsequent increased ERK dephosphorylation, which leads to more neuron apoptosis, less cell proliferation, depression onset and increased sensitivity to CMS. PTPRR/ERK pathway could be potential target for depression therapy.
[Mh] Termos MeSH primário: Depressão/metabolismo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Sistema de Sinalização das MAP Quinases
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/metabolismo
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Giro Denteado/metabolismo
Modelos Animais de Doenças
Hipocampo/metabolismo
Masculino
Camundongos
Fosforilação
Natação
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.1.3.48 (Ptprr protein, mouse); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160117
[St] Status:MEDLINE


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[PMID]:26202575
[Au] Autor:Saka S; Hirawa N; Oka A; Yatsu K; Hirukawa T; Yamamoto R; Matsusaka T; Imai E; Narita I; Endoh M; Ichikawa I; Umemura S; Inoko H
[Ad] Endereço:Department of Medical Science and Cardiorenal Medicine, Yokohama City University, Graduate School of Medicine, Yokohama, Japan.
[Ti] Título:Genome-wide association study of IgA nephropathy using 23 465 microsatellite markers in a Japanese population.
[So] Source:J Hum Genet;60(10):573-80, 2015 Oct.
[Is] ISSN:1435-232X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Immunoglobulin A nephropathy (IgAN) is the most common form of primary glomerulonephritis in many parts of the world. Although previous genome-wide association studies (GWAS) identified the major susceptibility loci for IgAN, the causal genes currently remain unknown. We performed a GWAS using 23 465 microsatellite (MS) markers to identify genes related to IgAN in a Japanese population. A pooled sample analysis was conducted in three-stage screenings of three independent case-control populations, and after the final step of individual typing, 11 markers survived. Of these, we focused on two regions on 6p21 and 12q21 because they (i) showed the strongest relationship with IgAN, and (ii) appeared to be highly relevant to IgAN in view of several previous studies. These regions contained the HLA, TSPAN8 and PTPRR genes. This study on GWAS, using >20 000 MS markers, provides a new approach regarding susceptible genes for IgAN for investigators seeking new tools for the prevention and treatment of IgAN.
[Mh] Termos MeSH primário: Cromossomos Humanos Par 12/genética
Cromossomos Humanos Par 6/genética
Glomerulonefrite por IGA/genética
Antígenos HLA/genética
Repetições de Microssatélites
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
Tetraspaninas/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Japão
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA Antigens); 0 (TSPAN8 protein, human); 0 (Tetraspanins); EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150724
[St] Status:MEDLINE
[do] DOI:10.1038/jhg.2015.88


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[PMID]:25592066
[Au] Autor:Munkley J; Lafferty NP; Kalna G; Robson CN; Leung HY; Rajan P; Elliott DJ
[Ad] Endereço:Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, NE1 3BZ, UK. jennifer.munkley@ncl.ac.uk.
[Ti] Título:Androgen-regulation of the protein tyrosine phosphatase PTPRR activates ERK1/2 signalling in prostate cancer cells.
[So] Source:BMC Cancer;15:9, 2015 Jan 16.
[Is] ISSN:1471-2407
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Androgens drive the onset and progression of prostate cancer (PCa) via androgen receptor (AR) signalling. The principal treatment for PCa is androgen deprivation therapy, although the majority of patients eventually develop a lethal castrate-resistant form of the disease, where despite low serum testosterone levels AR signalling persists. Advanced PCa often has hyper-activated RAS/ERK1/2 signalling thought to be due to loss of function of key negative regulators of the pathway, the details of which are not fully understood. METHODS: We recently carried out a genome-wide study and identified a subset of 226 novel androgen-regulated genes (PLOS ONE 6:e29088, 2011). In this study we have meta-analysed this dataset with genes and pathways frequently mutated in PCa to identify androgen-responsive regulators of the RAS/ERK1/2 pathway. RESULTS: We find the PTGER4 and TSPYL2 genes are up-regulated by androgen stimulation and the ADCY1, OPKR1, TRIB1, SPRY1 and PTPRR are down-regulated by androgens. Further characterisation of PTPRR protein in LNCaP cells revealed it is an early and direct target of the androgen receptor which negatively regulates the RAS/ERK1/2 pathway and reduces cell proliferation in response to androgens. CONCLUSION: Our data suggest that loss of PTPRR in clinical PCa is one factor that might contribute to activation of the RAS/ERK1/2 pathway.
[Mh] Termos MeSH primário: Androgênios/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neoplasias da Próstata/genética
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Bases de Dados Genéticas
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Masculino
Neoplasias da Próstata/metabolismo
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/metabolismo
Receptores Androgênicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (AR protein, human); 0 (Androgens); 0 (Receptors, Androgen); EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150117
[St] Status:MEDLINE
[do] DOI:10.1186/s12885-015-1012-8


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[PMID]:25571783
[Au] Autor:Erkens M; Tanaka-Yamamoto K; Cheron G; Márquez-Ruiz J; Prigogine C; Schepens JT; Nadif Kasri N; Augustine GJ; Hendriks WJ
[Ad] Endereço:Department of Cell Biology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Centre, PO Box 9101, Nijmegen, 6500, HB, The Netherlands. mirthe.erkens@gmail.com.
[Ti] Título:Protein tyrosine phosphatase receptor type R is required for Purkinje cell responsiveness in cerebellar long-term depression.
[So] Source:Mol Brain;8:1, 2015 Jan 09.
[Is] ISSN:1756-6606
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Regulation of synaptic connectivity, including long-term depression (LTD), allows proper tuning of cellular signalling processes within brain circuitry. In the cerebellum, a key centre for motor coordination, a positive feedback loop that includes mitogen-activated protein kinases (MAPKs) is required for proper temporal control of LTD at cerebellar Purkinje cell synapses. Here we report that the tyrosine-specific MAPK-phosphatase PTPRR plays a role in coordinating the activity of this regulatory loop. RESULTS: LTD in the cerebellum of Ptprr (-/-) mice is strongly impeded, in vitro and in vivo. Comparison of basal phospho-MAPK levels between wild-type and PTPRR deficient cerebellar slices revealed increased levels in mutants. This high basal phospho-MAPK level attenuated further increases in phospho-MAPK during chemical induction of LTD, essentially disrupting the positive feedback loop and preventing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) phosphorylation and endocytosis. CONCLUSIONS: Our findings indicate an important role for PTPRR in maintaining low basal MAPK activity in Purkinje cells. This creates an optimal 'window' to boost MAPK activity following signals that induce LTD, which can then propagate through feed-forward signals to cause AMPAR internalization and LTD.
[Mh] Termos MeSH primário: Cerebelo/metabolismo
Depressão Sináptica de Longo Prazo
Células de Purkinje/metabolismo
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/metabolismo
[Mh] Termos MeSH secundário: Animais
Estimulação Elétrica
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Retroalimentação Fisiológica
Feminino
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Mutantes Neurológicos
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Modelos Biológicos
Fosforilação
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/deficiência
Receptores de AMPA/metabolismo
Sinapses/metabolismo
Vibrissas
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, AMPA); 0 (glutamate receptor ionotropic, AMPA 2); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases); EC 3.1.3.48 (Ptprr protein, mouse); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150110
[St] Status:MEDLINE
[do] DOI:10.1186/s13041-014-0092-8


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[PMID]:24637728
[Au] Autor:Francis DM; Koveal D; Tortajada A; Page R; Peti W
[Ad] Endereço:Department of Molecular Pharmacology, Physiology and Biotechnology, Brown University, Providence, Rhode Island, United States of America.
[Ti] Título:Interaction of kinase-interaction-motif protein tyrosine phosphatases with the mitogen-activated protein kinase ERK2.
[So] Source:PLoS One;9(3):e91934, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mitogen-activation protein kinase ERK2 is tightly regulated by multiple phosphatases, including those of the kinase interaction motif (KIM) PTP family (STEP, PTPSL and HePTP). Here, we use small angle X-ray scattering (SAXS) and isothermal titration calorimetry (ITC) to show that the ERK2:STEP complex is compact and that residues outside the canonical KIM motif of STEP contribute to ERK2 binding. Furthermore, we analyzed the interaction of PTPSL with ERK2 showing that residues outside of the canonical KIM motif also contribute to ERK2 binding. The integration of this work with previous studies provides a quantitative and structural map of how the members of a single family of regulators, the KIM-PTPs, differentially interact with their corresponding MAPKs, ERK2 and p38α.
[Mh] Termos MeSH primário: Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteínas Tirosina Fosfatases não Receptoras/metabolismo
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/metabolismo
[Mh] Termos MeSH secundário: Fosfatases de Especificidade Dupla/metabolismo
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/química
Proteína Quinase 14 Ativada por Mitógeno/metabolismo
Fosfatases da Proteína Quinase Ativada por Mitógeno/metabolismo
Ligação Proteica
Termodinâmica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 14); EC 3.1.3.16 (Mitogen-Activated Protein Kinase Phosphatases); EC 3.1.3.48 (DUSP16 protein, human); EC 3.1.3.48 (Dual-Specificity Phosphatases); EC 3.1.3.48 (PTPN5 protein, human); EC 3.1.3.48 (PTPN7 protein, human); EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatases, Non-Receptor); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140319
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0091934


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[PMID]:24556203
[Au] Autor:Erkens M; Bakker B; van Duijn LM; Hendriks WJ; Van der Zee CE
[Ad] Endereço:Department of Cell Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Medical Centre, PO Box 9101, 6500 HB Nijmegen, The Netherlands.
[Ti] Título:Protein tyrosine phosphatase receptor type R deficient mice exhibit increased exploration in a new environment and impaired novel object recognition memory.
[So] Source:Behav Brain Res;265:111-20, 2014 May 15.
[Is] ISSN:1872-7549
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mouse gene Ptprr encodes multiple protein tyrosine phosphatase receptor type R (PTPRR) isoforms that negatively regulate mitogen-activated protein kinase (MAPK) signaling pathways. In the mouse brain, PTPRR proteins are expressed in cerebellum, olfactory bulb, hippocampus, amygdala and perirhinal cortex but their precise role in these regions remains to be determined. Here, we evaluated phenotypic consequences of loss of PTPRR activity and found that basal smell was normal for Ptprr(-/-) mice. Also, spatial learning and fear-associated contextual learning were unaffected. PTPRR deficiency, however, resulted in impaired novel object recognition and a striking increase in exploratory activity in a new environment. The data corroborate the importance of proper control of MAPK signaling in cerebral functions and put forward PTPRR as a novel target to modulate synaptic processes.
[Mh] Termos MeSH primário: Condicionamento Clássico/fisiologia
Comportamento Exploratório/fisiologia
Transtornos da Memória/genética
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/deficiência
Recognição (Psicologia)/fisiologia
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Extinção Psicológica
Medo/fisiologia
Feminino
Masculino
Aprendizagem em Labirinto/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
Olfato/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.3.48 (Ptprr protein, mouse); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1411
[Cu] Atualização por classe:140325
[Lr] Data última revisão:
140325
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140222
[St] Status:MEDLINE


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[PMID]:24407576
[Au] Autor:Chang CC; Huang RL; Wang HC; Liao YP; Yu MH; Lai HC
[Ad] Endereço:*Department of Obstetrics and Gynecology, Tri-Service General Hospital; †Laboratory of Epigenetics and Cancer Stem Cells, and ‡Graduate Institute of Medical Sciences, National Defense Medical Center; and §Department of Obstetrics and Gynecology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan, Republic of China.
[Ti] Título:High methylation rate of LMX1A, NKX6-1, PAX1, PTPRR, SOX1, and ZNF582 genes in cervical adenocarcinoma.
[So] Source:Int J Gynecol Cancer;24(2):201-9, 2014 Feb.
[Is] ISSN:1525-1438
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study aimed to investigate the status of DNA methylation of 6 genes, LMX1A, NKX6-1, PAX1, PTPRR, SOX1, and ZNF582, previously found from squamous cell carcinomas in adenocarcinomas (ACs) of the uterine cervix. METHODS: We assessed the methylation status of these genes in 40 ACs, cervical scrapings from 23 ACs, and 67 normal control cervices by real-time quantitative methylation-specific polymerase chain reaction. The results were validated by bisulfite pyrosequencing. RESULTS: The methylation levels of all the 6 genes in the ACs were significantly higher than those in normal cervical tissues, especially for PAX1, PTPRR, SOX1, and ZNF582. The odds ratios and 95% confidence intervals (CIs) of high methylation levels in PAX1, PTPRR, SOX1, and ZNF582 for the risk of developing an AC were 15.7 (95% CI, 7.0-40.6), 16.9 (95% CI, 7.6-43.0), 32.1 (95% CI, 12.1-124.3), and 25.4 (95% CI, 10.4-78.3), respectively (all P < 0.001). The methylation indices of PAX1, PTPRR, SOX1, and ZNF582 recovered from scrapings of ACs were significantly higher than in normal controls. The odds ratios of these indices for the risk of developing an AC in PAX1, PTPRR, SOX1, and ZNF582 were 6.2 (95% CI, 2.6-15.4), 12.1(95% CI, 3.8-46.4), 6.2 (95% CI, 2.6-15.8), and 20.6 (95% CI, 6.9-77.5), respectively (all P < 0.001). CONCLUSIONS: Cervical ACs carry aberrantly high methylation rates of PAX1, PTPRR, SOX1, and ZNF582--commonly methylated in squamous cell carcinomas--which might help for AC screening.
[Mh] Termos MeSH primário: Adenocarcinoma/genética
Biomarcadores Tumorais/genética
Carcinoma de Células Escamosas/genética
Metilação de DNA
Neoplasias do Colo do Útero/genética
[Mh] Termos MeSH secundário: Adenocarcinoma/metabolismo
Carcinoma de Células Escamosas/metabolismo
Estudos de Casos e Controles
Feminino
Proteínas de Homeodomínio/genética
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Proteínas com Homeodomínio LIM/genética
Fatores de Transcrição Box Pareados/genética
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
Fatores de Transcrição SOXB1/genética
Fatores de Transcrição/genética
Neoplasias do Colo do Útero/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Homeodomain Proteins); 0 (Kruppel-Like Transcription Factors); 0 (LIM-Homeodomain Proteins); 0 (LMX1A protein, human); 0 (NKX6-1 protein, human); 0 (Paired Box Transcription Factors); 0 (SOX1 protein, human); 0 (SOXB1 Transcription Factors); 0 (Transcription Factors); 0 (ZNF582 protein, human); 142661-96-9 (PAX1 transcription factor); EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140111
[St] Status:MEDLINE
[do] DOI:10.1097/IGC.0000000000000054


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[PMID]:24242166
[Au] Autor:Wozniak M; Gamian E; Laczmanska I; Sasiadek MM; Dus-Szachniewicz K; Ziólkowski P
[Ad] Endereço:Department of Pathology, Wroclaw Medical University, Poland.
[Ti] Título:Immunohistochemical and Western blot analysis of two protein tyrosine phosphatase receptors, R and Z1, in colorectal carcinoma, colon adenoma and normal colon tissues.
[So] Source:Histol Histopathol;29(5):635-9, 2014 May.
[Is] ISSN:1699-5848
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Two classes of proteins, namely tyrosine kinases (PTK) and phosphatases (PTP), play an important role in cell proliferation and differentiation, thus leading to an acceleration or inhibition of tumour growth. The role of the above proteins in colorectal carcinoma (CRC) growth is a well-known event. In this study we carried out immunohistochemical and Western blot analysis of colorectal carcinoma, adenoma and normal colon tissue in relation to two protein tyrosine phosphatase receptors, R and Z1. Twenty-five cases of CRC were analyzed and the results were compared with similar data obtained in non-malignant tissues. High expression of both PTP receptors was observed in all examined cases of CRC, adenoma and normal colon tissue in this study. These results are not in line with recently published data, showing that genetic coding for PTPRR and PTPRZ1 were hypermethylated in CRC's. We presume that the protein tyrosine phosphatase overexpression in colorectal carcinoma is not enough to protect from the progression of disease.
[Mh] Termos MeSH primário: Adenoma/enzimologia
Colo/enzimologia
Neoplasias do Colo/enzimologia
Neoplasias Colorretais/enzimologia
Proteínas Tirosina Fosfatases Classe 5 Semelhantes a Receptores/metabolismo
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/metabolismo
[Mh] Termos MeSH secundário: Adenoma/genética
Adenoma/patologia
Western Blotting
Colo/anatomia & histologia
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Metilação de DNA
Seres Humanos
Imuno-Histoquímica
Proteínas Tirosina Fosfatases Classe 5 Semelhantes a Receptores/genética
Proteínas Tirosina Fosfatases Classe 7 Semelhantes a Receptores/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.3.48 (PTPRR protein, human); EC 3.1.3.48 (PTPRZ1 protein, human); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 5); EC 3.1.3.48 (Receptor-Like Protein Tyrosine Phosphatases, Class 7)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:161202
[Lr] Data última revisão:
161202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131119
[St] Status:MEDLINE
[do] DOI:10.14670/HH-29.10.635



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