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[PMID]:29279050
[Au] Autor:Madrigal A; Tan L; Zhao Y
[Ad] Endereço:Biological Sciences Department, California State Polytechnic University at Pomona, 3801 W. Temple Ave., Pomona, CA, 91768, USA.
[Ti] Título:Expression regulation and functional analysis of RGS2 and RGS4 in adipogenic and osteogenic differentiation of human mesenchymal stem cells.
[So] Source:Biol Res;50(1):43, 2017 Dec 26.
[Is] ISSN:0717-6287
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Understanding the molecular basis underlying the formation of bone-forming osteocytes and lipid-storing adipocytes will help provide insights into the cause of disorders originating in stem/progenitor cells and develop therapeutic treatments for bone- or adipose-related diseases. In this study, the role of RGS2 and RGS4, two members of the regulators of G protein signaling (RGS) family, was investigated during adipogenenic and osteogenenic differentiation of human mesenchymal stem cells (hMSCs). RESULTS: Expression of RGS2 and RGS4 were found to be inversely regulated during adipogenesis induced by dexamethasone (DEX) and 3-isobutyl-methylxanthine, regardless if insulin was present, with RGS2 up-regulated and RGS4 down-regulated in response to adipogenic induction. RGS2 expression was also up-regulated during osteogenesis at a level similar to that induced by treatment of DEX alone, a shared component of adipogenic and osteogenic differentiation inducing media, but significantly lower than the level induced by adipogenic inducing media. RGS4 expression was down-regulated during the first 48 h of osteogenesis but up-regulated afterwards, in both cases at levels similar to that induced by DEX alone. Expression knock-down using small interfering RNA against RGS2 resulted in decreased differentiation efficiency during both adipogenesis and osteogenesis. On the other hand, expression knock-down of RGS4 also resulted in decreased adipogenic differentiation but increased osteogenic differentiation. CONCLUSIONS: RGS2 and RGS4 are differentially regulated during adipogenic and osteogenic differentiation of hMSCs. In addition, both RGS2 and RGS4 play positive roles during adipogenesis but opposing roles during osteogenesis, with RGS2 as a positive regulator and RGS4 as a negative regulator. These results imply that members of RGS proteins may play multifaceted roles during human adipogenesis and osteogenesis to balance or counterbalance each other's function during those processes.
[Mh] Termos MeSH primário: Adipogenia/fisiologia
Regulação da Expressão Gênica/fisiologia
Células Mesenquimais Estromais/citologia
Osteócitos/citologia
Osteogênese/fisiologia
Proteínas RGS/metabolismo
[Mh] Termos MeSH secundário: Adipogenia/genética
Regulação da Expressão Gênica/genética
Seres Humanos
Osteogênese/genética
Proteínas RGS/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RGS Proteins); 175335-35-0 (RGS4 protein)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1186/s40659-017-0148-1


  2 / 1666 MEDLINE  
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[PMID]:29212007
[Au] Autor:Wijesinghe P; Johansen NJ; Curatolo A; Sampson DD; Ganss R; Kennedy BF
[Ad] Endereço:BRITElab, Harry Perkins Institute of Medical Research, QEII Medical Centre, Nedlands and Centre for Medical Research, The University of Western Australia, Perth, Western Australia, Australia; Optical+Biomedical Engineering Laboratory, School of Electrical, Electronic and Computer Engineering, The Un
[Ti] Título:Ultrahigh-Resolution Optical Coherence Elastography Images Cellular-Scale Stiffness of Mouse Aorta.
[So] Source:Biophys J;113(11):2540-2551, 2017 Dec 05.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cellular-scale imaging of the mechanical properties of tissue has helped to reveal the origins of disease; however, cellular-scale resolution is not readily achievable in intact tissue volumes. Here, we demonstrate volumetric imaging of Young's modulus using ultrahigh-resolution optical coherence elastography, and apply it to characterizing the stiffness of mouse aortas. We achieve isotropic resolution of better than 15 µm over a 1-mm lateral field of view through the entire depth of an intact aortic wall. We employ a method of quasi-static compression elastography that measures volumetric axial strain and uses a compliant, transparent layer to measure surface axial stress. This combination is used to estimate Young's modulus throughout the volume. We demonstrate differentiation by stiffness of individual elastic lamellae and vascular smooth muscle. We observe stiffening of the aorta in regulator of G protein signaling 5-deficient mice, a model that is linked to vascular remodeling and fibrosis. We observe increased stiffness with proximity to the heart, as well as regions with micro-structural and micro-mechanical signatures characteristic of fibrous and lipid-rich tissue. High-resolution imaging of Young's modulus with optical coherence elastography may become an important tool in vascular biology and in other fields concerned with understanding the role of mechanics within the complex three-dimensional architecture of tissue.
[Mh] Termos MeSH primário: Aorta/diagnóstico por imagem
Aorta/fisiologia
Técnicas de Imagem por Elasticidade
Fenômenos Ópticos
Razão Sinal-Ruído
Rigidez Vascular
[Mh] Termos MeSH secundário: Animais
Aorta/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Proteínas RGS/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RGS Proteins); 0 (Rgs5 protein, mouse)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171207
[St] Status:MEDLINE


  3 / 1666 MEDLINE  
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[PMID]:28934222
[Au] Autor:Branch MR; Hepler JR
[Ad] Endereço:Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia, United States of America.
[Ti] Título:Endogenous RGS14 is a cytoplasmic-nuclear shuttling protein that localizes to juxtanuclear membranes and chromatin-rich regions of the nucleus.
[So] Source:PLoS One;12(9):e0184497, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulator of G protein signaling 14 (RGS14) is a multifunctional scaffolding protein that integrates G protein and H-Ras/MAPkinase signaling pathways to regulate synaptic plasticity important for hippocampal learning and memory. However, to date, little is known about the subcellular distribution and roles of endogenous RGS14 in a neuronal cell line. Most of what is known about RGS14 cellular behavior is based on studies of tagged, recombinant RGS14 ectopically overexpressed in unnatural host cells. Here, we report for the first time a comprehensive assessment of the subcellular distribution and dynamic localization of endogenous RGS14 in rat B35 neuroblastoma cells. Using confocal imaging and 3D-structured illumination microscopy, we find that endogenous RGS14 localizes to subcellular compartments not previously recognized in studies of recombinant RGS14. RGS14 localization was observed most notably at juxtanuclear membranes encircling the nucleus, at nuclear pore complexes (NPC) on both sides of the nuclear envelope and within intranuclear membrane channels, and within both chromatin-poor and chromatin-rich regions of the nucleus in a cell cycle-dependent manner. In addition, a subset of nuclear RGS14 localized adjacent to active RNA polymerase II. Endogenous RGS14 was absent from the plasma membrane in resting cells; however, the protein could be trafficked to the plasma membrane from juxtanuclear membranes in endosomes derived from ER/Golgi, following constitutive activation of endogenous RGS14 G protein binding partners using AlF4¯. Finally, our findings show that endogenous RGS14 behaves as a cytoplasmic-nuclear shuttling protein confirming what has been shown previously for recombinant RGS14. Taken together, the findings highlight possible cellular roles for RGS14 not previously recognized that are distinct from the regulation of conventional GPCR-G protein signaling, in particular undefined roles for RGS14 in the nucleus.
[Mh] Termos MeSH primário: Núcleo Celular/metabolismo
Cromatina/metabolismo
Citoplasma/metabolismo
Membrana Nuclear/metabolismo
Proteínas RGS/metabolismo
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/fisiologia
Encéfalo/citologia
Encéfalo/metabolismo
Células COS
Ciclo Celular/fisiologia
Linhagem Celular Tumoral
Cercopithecus aethiops
Células HEK293
Seres Humanos
Imagem Tridimensional
Camundongos
Microscopia Confocal
Neurônios/citologia
Neurônios/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (RGS Proteins); 0 (Rgs14 protein, rat)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184497


  4 / 1666 MEDLINE  
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[PMID]:28845525
[Au] Autor:Xu F; Liu Y; Shi L; Cai H; Liu W; Hu Y; Li Y; Yuan W
[Ad] Endereço:Department of Pathophysiology, Binzhou Medical University, Yantai, China.
[Ti] Título:RGS3 inhibits TGF-ß1/Smad signalling in adventitial fibroblasts.
[So] Source:Cell Biochem Funct;35(6):334-338, 2017 Aug.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Recent evidence suggests that adventitial fibroblasts (AFs) are crucially implicated in atherosclerosis. However, the mechanisms by which AFs are dysfunctional and contribute to atherosclerosis remain unclear. This study aimed to investigate the role of regulator of G-protein signalling 3 (RGS3) in the regulation of AFs using apoE knockout mouse as the model. Pathological changes in aortic arteries of apoE knockout mice fed with hyperlipid diet were examined by Movat staining. The expression of RGS3, α-SMA, TGF-ß1, Smad2, and Smad3 in the adventitia was detected by immunohistochemistry. Adventitial fibroblasts were isolated from aortic arteries of apoE knockout mice and infected with RGS3 overexpression lentivirus or empty lentivirus. The expression of RGS3, α-SMA, TGF-ß1, Smad2, and Smad3 in AFs was detected by real-time polymerase chain reaction and Western blot analysis. We found that hyperlipidic diet caused significant aortic intima thickening and atherosclerotic plaques in 15-week-old apoE knockout mice. Compared to wild-type mice, RGS3 expression was lower while α-SMA, TGF-ß1, Smad2, and Smad3 expression was higher in the adventitia of apoE knockout mice. In addition, lentivirus mediated overexpression of RGS3 caused decreased expression of α-SMA, TGF-ß1, Smad2, and Smad3 in AFs derived from apoE(-/-) mice. In conclusion, these results suggest that RGS3 may provide protection against pathological changes of AFs and the development of atherosclerosis by inhibiting TGF-ß1/Smad signalling. RGS3 may be a potential therapeutic target for atherosclerosis.
[Mh] Termos MeSH primário: Proteínas RGS/metabolismo
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Actinas/genética
Actinas/metabolismo
Animais
Aorta/citologia
Aorta/patologia
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Células Cultivadas
Dieta Hiperlipídica
Regulação para Baixo
Fibroblastos/citologia
Fibroblastos/metabolismo
Vetores Genéticos/genética
Vetores Genéticos/metabolismo
Imuno-Histoquímica
Lentivirus/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas RGS/genética
RNA Mensageiro/metabolismo
Transdução de Sinais
Proteína Smad2/genética
Proteína Smad3/genética
Fator de Crescimento Transformador beta1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Apolipoproteins E); 0 (RGS Proteins); 0 (RNA, Messenger); 0 (Rgs3 protein, mouse); 0 (Smad2 Protein); 0 (Smad3 Protein); 0 (Transforming Growth Factor beta1); 0 (alpha-smooth muscle actin, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3280


  5 / 1666 MEDLINE  
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[PMID]:28784619
[Au] Autor:Phan HTN; Sjögren B; Neubig RR
[Ad] Endereço:Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
[Ti] Título:Human Missense Mutations in Regulator of G Protein Signaling 2 Affect the Protein Function Through Multiple Mechanisms.
[So] Source:Mol Pharmacol;92(4):451-458, 2017 Oct.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulator of G protein signaling 2 (RGS2) plays a significant role in alleviating vascular contraction and promoting vascular relaxation due to its GTPase accelerating protein activity toward G q. Mice lacking RGS2 display a hypertensive phenotype, and several RGS2 missense mutations have been found predominantly in hypertensive human subjects. However, the mechanisms whereby these mutations could impact blood pressure is unknown. Here, we selected 16 rare, missense mutations in RGS2 identified in various human exome sequencing projects and evaluated their ability to inhibit intracellular calcium release mediated by angiotensin II receptor type 1 (AT1R). Four of them had reduced function and were further investigated to elucidate underlying mechanisms. Low protein expression, protein mislocalization, and reduced G protein binding were identified as likely mechanisms of the malfunctioning mutants. The Q2L mutant had 50% lower RGS2 than wild-type (WT) protein detected by Western blot. Confocal microscopy demonstrated that R44H and D40Y had impaired plasma membrane targeting; only 46% and 35% of those proteins translocated to the plasma membrane when coexpressed with G Q209L compared with 67% for WT RGS2. The R188H mutant had a significant reduction in G binding affinity (10-fold increase in compared with WT RGS2 in a flow cytometry competition binding assay). This study provides functional data for 16 human RGS2 missense variants on their effects on AT1R-mediated calcium mobilization and provides molecular understanding of those variants with functional loss in vitro. These molecular behaviors can provide insight to inform antihypertensive therapeutics in individuals with variants having reduced function.
[Mh] Termos MeSH primário: Mutação de Sentido Incorreto/fisiologia
Proteínas RGS/química
Proteínas RGS/fisiologia
[Mh] Termos MeSH secundário: Angiotensina II/farmacologia
Animais
Células CHO
Cricetinae
Cricetulus
Relação Dose-Resposta a Droga
Células HEK293
Seres Humanos
Estrutura Secundária de Proteína
Proteínas RGS/agonistas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RGS Proteins); 0 (RGS2 protein, human); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE
[do] DOI:10.1124/mol.117.109215


  6 / 1666 MEDLINE  
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[PMID]:28665981
[Au] Autor:Li S; Jin X; Wu H; Wang Y; Li X; Guo Y; Liang S
[Ad] Endereço:Department of Gastrointestinal Surgery and Neonatal Surgery, Children's Hospital of Chongqing Medical University, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing, China.
[Ti] Título:HA117 endows HL60 cells with a stem-like signature by inhibiting the degradation of DNMT1 via its ability to down-regulate expression of the GGL domain of RGS6.
[So] Source:PLoS One;12(6):e0180142, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:All-trans retinoic acid (ATRA) induces complete remission in almost all patients with acute promyelocytic leukemia (APL) via its ability to induce the in vivo differentiation of APL blasts. However, prolonged ATRA treatment can result in drug resistance. In previous studies, we generated a multi-drug-resistant HL60/ATRA cell line and found it to contain a new drug resistance-related gene segment, HA117. In this study, we demonstrate that ATRA induces multi-drug-resistant subpopulations of HL60 cells with a putative stem-like signature by up-regulating the expression of the new gene segment HA117. Western blot analysis and quantitative real-time PCR demonstrated that HA117 causes alternative splicing of regulator of G-protein signaling 6 (RGS6) and down-regulation of the expression of the GGL domain of RGS6, which plays an important role in DNA methyltransferase 1 (DNMT1) degradation. Moreover, DNMT1 expression was increased in multi-drug resistance HL60/ATRA cells. Knockdown of HA117 restored expression of the GGL domain and blocked DNMT1 expression. Moreover, resistant cells displayed a putative stem-like signature with increased expression of cancer steam cell markers CD133 and CD123. The stem cell marker, Nanog, was significantly up-regulated. In conclusion, our study shows that HA117 potentially promotes the stem-like signature of the HL60/ATRA cell line by inhibiting by the ubiquitination and degradation of DNMT1 and by down-regulating the expression of the GGL domain of RGS6. These results throw light on the cellular events associated with the ATRA-induced multi-drug resistance phenotype in acute leukemia.
[Mh] Termos MeSH primário: Regulação para Baixo
Proteínas de Neoplasias/fisiologia
Células-Tronco Neoplásicas/patologia
Proteínas RGS/metabolismo
Proteínas Repressoras/metabolismo
[Mh] Termos MeSH secundário: Resistência a Medicamentos Antineoplásicos
Células HL-60
Seres Humanos
Leucemia Promielocítica Aguda/tratamento farmacológico
Leucemia Promielocítica Aguda/patologia
Células-Tronco Neoplásicas/metabolismo
Proteólise
Proteínas RGS/química
Tretinoína/farmacologia
Tretinoína/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DMAP1 protein, human); 0 (HA117 protein, human); 0 (Neoplasm Proteins); 0 (RGS Proteins); 0 (RGS6 protein, human); 0 (Repressor Proteins); 5688UTC01R (Tretinoin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180142


  7 / 1666 MEDLINE  
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[PMID]:28611045
[Au] Autor:Wang Y; Wang J; Zhang L; Karatas OF; Shao L; Zhang Y; Castro P; Creighton CJ; Ittmann M
[Ad] Endereço:Department of Urology, Southwest Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:RGS12 Is a Novel Tumor-Suppressor Gene in African American Prostate Cancer That Represses AKT and MNX1 Expression.
[So] Source:Cancer Res;77(16):4247-4257, 2017 Aug 15.
[Is] ISSN:1538-7445
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:African American (AA) men exhibit a relatively high incidence and mortality due to prostate cancer even after adjustment for socioeconomic factors, but the biological basis for this disparity is unclear. Here, we identify a novel region on chromosome 4p16.3 that is lost selectively in AA prostate cancer. The negative regulator of G-protein signaling RGS12 was defined as the target of 4p16.3 deletions, although it has not been implicated previously as a tumor-suppressor gene. RGS12 transcript levels were relatively reduced in AA prostate cancer, and prostate cancer cell lines showed decreased RGS12 expression relative to benign prostate epithelial cells. Notably, RGS12 exhibited potent tumor-suppressor activity in prostate cancer and prostate epithelial cell lines and We found that RGS12 expression correlated negatively with the oncogene MNX1 and regulated its expression and Further, MNX1 was regulated by AKT activity, and RGS12 expression decreased total and activated AKT levels. Our findings identify RGS12 as a candidate tumor-suppressor gene in AA prostate cancer, which acts by decreasing expression of AKT and MNX1, establishing a novel oncogenic axis in this disparate disease setting. .
[Mh] Termos MeSH primário: Afroamericanos/genética
Genes Supressores de Tumor
Proteínas de Homeodomínio/biossíntese
Proteína Oncogênica v-akt/biossíntese
Neoplasias da Próstata/genética
Proteínas RGS/genética
Fatores de Transcrição/biossíntese
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proliferação Celular/genética
Xenoenxertos
Proteínas de Homeodomínio/genética
Seres Humanos
Masculino
Camundongos
Proteína Oncogênica v-akt/genética
Neoplasias da Próstata/etnologia
Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
Fatores de Transcrição/genética
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (MNX1 protein, human); 0 (RGS Proteins); 0 (RGS12 protein, human); 0 (Transcription Factors); EC 2.7.11.1 (Oncogene Protein v-akt)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1158/0008-5472.CAN-17-0669


  8 / 1666 MEDLINE  
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[PMID]:28545052
[Au] Autor:Tunc-Ozdemir M; Jones AM
[Ad] Endereço:Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC, United States of America.
[Ti] Título:BRL3 and AtRGS1 cooperate to fine tune growth inhibition and ROS activation.
[So] Source:PLoS One;12(5):e0177400, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Plasma membrane-localized leucine-rich repeat receptor-like kinases directly activates G protein complex via interaction with seven transmembrane domain Regulator of G-protein Signaling 1 (AtRGS1) protein. Brassinosteroid insensitive 1 (BRI1) LIKE3 (BRL3) phosphorylates AtRGS1 in vitro. FRET analysis showed that BRL3 and AtRGS1 interaction dynamics change in response to glucose and flg22. Both BRL3 and AtRGS1 function in glucose sensing and brl3 and rgs1-2 single mutants are hyposensitive to high glucose as well as the brl3/rgs1 double mutant. BRL3 and AtRGS1 function in the same pathway linked to high glucose sensing. Hypocotyl elongation, another sugar-mediated pathway, is also implicated to be partially mediated by BRL3 and AtRGS1 because rgs1-2, brl3-2 and brl3-2/ rgs1-2 mutants share the long hypocotyl phenotype. BRL3 and AtRGS1 modulate the flg22-induced ROS burst and block one or more components positively regulating ROS production because the brl3/rgs1 double mutant has ~60% more ROS production than wild type while rgs1-2 has a partial ROS burst impairment and brl3 has slightly more ROS production. Here, we proposed a simple model where both BRL3 and AtRGS1 are part of a fine-tuning mechanism sensing glucose and flg22 to prevent excess ROS burst and control growth inhibition.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/metabolismo
Arabidopsis/crescimento & desenvolvimento
Arabidopsis/metabolismo
Proteínas RGS/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Receptores de Superfície Celular/metabolismo
[Mh] Termos MeSH secundário: Arabidopsis/efeitos dos fármacos
Arabidopsis/genética
Proteínas de Arabidopsis/genética
Glucose/farmacologia
Mutação
Peptídeos/farmacologia
Proteínas RGS/genética
Receptores de Superfície Celular/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (BRL3 protein, Arabidopsis); 0 (Peptides); 0 (RGS Proteins); 0 (RGS1 protein, Arabidopsis); 0 (Reactive Oxygen Species); 0 (Receptors, Cell Surface); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177400


  9 / 1666 MEDLINE  
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[PMID]:28432124
[Au] Autor:Scherer SL; Cain MD; Kanai SM; Kaltenbronn KM; Blumer KJ
[Ad] Endereço:From the Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110.
[Ti] Título:Regulation of neurite morphogenesis by interaction between R7 regulator of G protein signaling complexes and G protein subunit Gα .
[So] Source:J Biol Chem;292(24):9906-9918, 2017 Jun 16.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The R7 regulator of G protein signaling family (R7-RGS) critically regulates nervous system development and function. Mice lacking all R7-RGS subtypes exhibit diverse neurological phenotypes, and humans bearing mutations in the retinal R7-RGS isoform RGS9-1 have vision deficits. Although each R7-RGS subtype forms heterotrimeric complexes with Gß and R7-RGS-binding protein (R7BP) that regulate G protein-coupled receptor signaling by accelerating deactivation of G α-subunits, several neurological phenotypes of R7-RGS knock-out mice are not readily explained by dysregulated G signaling. Accordingly, we used tandem affinity purification and LC-MS/MS to search for novel proteins that interact with R7-RGS heterotrimers in the mouse brain. Among several proteins detected, we focused on Gα because it had not been linked to R7-RGS complexes before. Split-luciferase complementation assays indicated that Gα in its active or inactive state interacts with R7-RGS heterotrimers containing any R7-RGS isoform. LARG (leukemia-associated Rho guanine nucleotide exchange factor (GEF)), PDZ-RhoGEF, and p115RhoGEF augmented interaction between activated Gα and R7-RGS heterotrimers, indicating that these effector RhoGEFs can engage Gα ·R7-RGS complexes. Because Gα /R7-RGS interaction required R7BP, we analyzed phenotypes of neuronal cell lines expressing RGS7 and Gß with or without R7BP. We found that neurite retraction evoked by Gα -dependent lysophosphatidic acid receptors was augmented in R7BP-expressing cells. R7BP expression blunted neurite formation evoked by serum starvation by signaling mechanisms involving Gα but not Gα These findings provide the first evidence that R7-RGS heterotrimers interact with Gα to augment signaling pathways that regulate neurite morphogenesis. This mechanism expands the diversity of functions whereby R7-RGS complexes regulate critical aspects of nervous system development and function.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Proteínas de Transporte/metabolismo
Subunidades alfa G12-G13 de Proteínas de Ligação ao GTP/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neuritos/metabolismo
Neurônios/metabolismo
Proteínas RGS/metabolismo
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Encéfalo/citologia
Encéfalo/enzimologia
Proteínas de Transporte/química
Proteínas de Transporte/genética
Linhagem Celular
Subunidades alfa G12-G13 de Proteínas de Ligação ao GTP/química
Subunidades alfa G12-G13 de Proteínas de Ligação ao GTP/genética
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Mutação
Proteínas do Tecido Nervoso/química
Proteínas do Tecido Nervoso/genética
Neuritos/enzimologia
Neurônios/citologia
Neurônios/enzimologia
Fragmentos de Peptídeos/química
Fragmentos de Peptídeos/genética
Fragmentos de Peptídeos/metabolismo
Domínios e Motivos de Interação entre Proteínas
Multimerização Proteica
Proteínas RGS/química
Proteínas RGS/genética
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Carrier Proteins); 0 (Nerve Tissue Proteins); 0 (Peptide Fragments); 0 (R7BP protein, human); 0 (R7BP protein, mouse); 0 (RGS Proteins); 0 (RGS7 protein, human); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (Rgs7 protein, mouse); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, G12-G13)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170423
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.771923


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[PMID]:28237701
[Au] Autor:Li Q; Jin W; Cai Y; Yang F; Chen E; Ye D; Wang Q; Guan X
[Ad] Endereço:Department of Medical Oncology, Jinling Hospital, School of Medicine, Southern Medical University, Guangzhou, 510282, China; Department of Oncological Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
[Ti] Título:Regulator of G protein signaling 20 correlates with clinicopathological features and prognosis in triple-negative breast cancer.
[So] Source:Biochem Biophys Res Commun;485(3):693-697, 2017 Apr 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Triple-negative breast cancer (TNBC) is a highly aggressive tumor subtype lacking effective prognostic indicators or therapeutic targets. Therefore, finding a novel molecular biomarker for TNBC to achieve target therapy and predict its prognosis is crucial in preventing inappropriate treatment. Regulator of G-protein signaling (RGS) families of protein can negatively regulate signaling of heterotrimeric G proteins and are known to be upregulated in various tumors. In this study, we demonstrated that RGS20 was more highly expressed in TNBC tumor tissue than in adjacent normal tissue by analyzing the cancer genome atlas (TCGA) database. However, RGS20 expression was low in all breast cancer and luminal breast cancer patients. Validated by the TCGA cohort, RGS20 was upregulated in lymph node-positive TNBC compared with that in lymph node-negative breast cancer. High expression of RGS20 had a risk of lymph node metastasis, ki-67 > 14%, poor N stage, and poor clinical stage in the immunohistochemistry of tissue microarrays. Moreover, K-M plot analysis showed that TNBC patients with high RGS20 expression had poor relapse-free survival. In summary, the findings revealed that RGS20 was a special TNBC oncogene that promoted tumor progression and influenced TNBC prognosis. This study is the first to show that RGS20 was a special oncogene, and its high expression was significantly associated with the progression and prognosis of TNBC. RGS20 may be a novel molecular biomarker for the targeted therapy and prognosis of TNBC.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteínas RGS/biossíntese
Neoplasias de Mama Triplo Negativas/metabolismo
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Intervalo Livre de Doença
Feminino
Seres Humanos
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Metástase Linfática
Meia-Idade
Recidiva Local de Neoplasia
Estadiamento de Neoplasias
Prognóstico
Neoplasias de Mama Triplo Negativas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (RGS Proteins); 0 (RGS20 protein, human)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170612
[Lr] Data última revisão:
170612
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE



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