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[PMID]:28464239
[Au] Autor:Jumabay M; Zhumabai J; Mansurov N; Niklason KC; Guihard PJ; Cubberly MR; Fogelman AM; Iruela-Arispe L; Yao Y; Saparov A; Boström KI
[Ad] Endereço:Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, California.
[Ti] Título:Combined effects of bone morphogenetic protein 10 and crossveinless-2 on cardiomyocyte differentiation in mouse adipocyte-derived stem cells.
[So] Source:J Cell Physiol;233(3):1812-1822, 2018 Mar.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic protein (BMP) 10, a cardiac-restricted BMP family member, is essential in cardiomyogenesis, especially during trabeculation. Crossveinless-2 (CV2, also known as BMP endothelial cell precursor derived regulator [BMPER]) is a BMP-binding protein that modulates the activity of several BMPs. The objective of this study was to examine the combined effects of BMP10 and CV2 on cardiomyocyte differentiation using mouse dedifferentiated fat (mDFAT) cells, which spontaneously differentiate into cardiomyocyte-like cells, as a model. Our results revealed that CV2 binds directly to BMP10, as determined by co-immunoprecipitation, and inhibits BMP10 from initiating SMAD signaling, as determined by luciferase reporter gene assays. BMP10 treatment induced mDFAT cell proliferation, whereas CV2 modulated the BMP10-induced proliferation. Differentiation of cardiomyocyte-like cells proceeded in a reproducible fashion in mDFAT cells, starting with small round Nkx2.5-positive progenitor cells that progressively formed myotubes of increasing length that assembled into beating colonies and stained strongly for Troponin I and sarcomeric alpha-actinin. BMP10 enhanced proliferation of the small progenitor cells, thereby securing sufficient numbers to support formation of myotubes. CV2, on the other hand, enhanced formation and maturation of large myotubes and myotube-colonies and was expressed by endothelial-like cells in the mDFAT cultures. Thus BMP10 and CV2 have important roles in coordinating cardiomyogenesis in progenitor cells.
[Mh] Termos MeSH primário: Proteínas Morfogenéticas Ósseas/metabolismo
Proteínas de Transporte/metabolismo
Diferenciação Celular/fisiologia
Miócitos Cardíacos/citologia
Células-Tronco/citologia
[Mh] Termos MeSH secundário: Actinina/metabolismo
Adipócitos/citologia
Animais
Proliferação Celular
Células Cultivadas
Proteína Homeobox Nkx-2.5/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Transdução de Sinais/fisiologia
Proteínas Smad/metabolismo
Troponina I/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bmp10 protein, mouse); 0 (Bone Morphogenetic Proteins); 0 (Carrier Proteins); 0 (Homeobox Protein Nkx-2.5); 0 (Nkx2-5 protein, mouse); 0 (Smad Proteins); 0 (Troponin I); 0 (crossveinless 2 protein, mouse); 11003-00-2 (Actinin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171211
[Lr] Data última revisão:
171211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25983


  2 / 2262 MEDLINE  
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[PMID]:28957384
[Au] Autor:Kim SK; Kleimeyer JP; Ahmed MA; Avins AL; Fredericson M; Dragoo JL; Ioannidis JPA
[Ad] Endereço:Dept. Developmental Biology, Stanford University Medical Center, Stanford, CA, United States of America.
[Ti] Título:Two genetic loci associated with ankle injury.
[So] Source:PLoS One;12(9):e0185355, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ankle injuries, including sprains, strains and other joint derangements and instability, are common, especially for athletes involved in indoor court or jumping sports. Identifying genetic loci associated with these ankle injuries could shed light on their etiologies. A genome-wide association screen was performed using publicly available data from the Research Program in Genes, Environment and Health (RPGEH) including 1,694 cases of ankle injury and 97,646 controls. An indel (chr21:47156779:D) that lies close to a collagen gene, COL18A1, showed an association with ankle injury at genome-wide significance (p = 3.8x10-8; OR = 1.99; 95% CI = 1.75-2.23). A second DNA variant (rs13286037 on chromosome 9) that lies within an intron of the transcription factor gene NFIB showed an association that was nearly genome-wide significant (p = 5.1x10-8; OR = 1.63; 95% CI = 1.46-1.80). The ACTN3 R577X mutation was previously reported to show an association with acute ankle sprains, but did not show an association in this cohort. This study is the first genome-wide screen for ankle injury that yields insights regarding the genetic etiology of ankle injuries and provides DNA markers with the potential to inform athletes about their genetic risk for ankle injury.
[Mh] Termos MeSH primário: Traumatismos do Tornozelo/genética
Loci Gênicos
Predisposição Genética para Doença
Estudo de Associação Genômica Ampla
[Mh] Termos MeSH secundário: Actinina/genética
Demografia
Feminino
Seres Humanos
Masculino
Metanálise como Assunto
Meia-Idade
Fenótipo
Polimorfismo de Nucleotídeo Único/genética
Entorses e Distensões/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN3 protein, human); 11003-00-2 (Actinin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170929
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185355


  3 / 2262 MEDLINE  
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[PMID]:28834730
[Au] Autor:Shams H; Mofrad MRK
[Ad] Endereço:Molecular Cell Biomechanics Laboratory, Departments of Bioengineering and Mechanical Engineering, University of California, Berkeley, Berkeley, California.
[Ti] Título:α-Actinin Induces a Kink in the Transmembrane Domain of ß -Integrin and Impairs Activation via Talin.
[So] Source:Biophys J;113(4):948-956, 2017 Aug 22.
[Is] ISSN:1542-0086
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Integrin-mediated signaling is crucial for cell-substrate adhesion and can be triggered from both intra- and extracellular interactions. Although talin binding is sufficient for inside-out activation of integrin, other cytoplasmic proteins such as α-actinin and filamin can directly interfere with talin-mediated integrin activation. Specifically, α-actinin plays distinct roles in regulating α ß versus α ß integrin. It has been shown that α-actinin competes with talin for binding to the cytoplasmic tail of ß -integrin, whereas it cooperates with talin for activating integrin α ß . In this study, molecular dynamics simulations were employed to compare and contrast molecular mechanisms of α ß and α ß activation in the presence and absence of α-actinin. Our results suggest that α-actinin impairs integrin signaling by both undermining talin binding to the ß -integrin cytoplasmic tail and inducing a kink in the transmembrane domain of ß -integrin. Furthermore, we showed that α-actinin promote talin association with ß -integrin by restricting the motion of the cytoplasmic tail and reducing the entropic barrier for talin binding. Taken together, our results showed that the interplay between talin and α-actinin regulates signal transmission via controlling the conformation of the transmembrane domain and altering natural response modes of integrins in a type-specific manner.
[Mh] Termos MeSH primário: Actinina/metabolismo
Membrana Celular/metabolismo
Integrina beta3/química
Integrina beta3/metabolismo
Simulação de Dinâmica Molecular
Talina/metabolismo
[Mh] Termos MeSH secundário: Citoplasma/metabolismo
Integrina alfa5beta1/metabolismo
Cinética
Complexo Glicoproteico GPIIb-IIIa de Plaquetas/metabolismo
Ligação Proteica
Domínios Proteicos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrin alpha5beta1); 0 (Integrin beta3); 0 (Platelet Glycoprotein GPIIb-IIIa Complex); 0 (Talin); 11003-00-2 (Actinin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE


  4 / 2262 MEDLINE  
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[PMID]:28803065
[Au] Autor:Verma D; Bajpai VK; Ye N; Maneshi MM; Jetta D; Andreadis ST; Sachs F; Hua SZ
[Ad] Endereço:Department of Mechanical and Aerospace Engineering, University at Buffalo, Buffalo, NY 14260, USA; Department of Physiology and Biophysics, University at Buffalo, Buffalo, NY 14260, USA.
[Ti] Título:Flow induced adherens junction remodeling driven by cytoskeletal forces.
[So] Source:Exp Cell Res;359(2):327-336, 2017 Oct 15.
[Is] ISSN:1090-2422
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adherens junctions (AJs) are a key structural component for tissue organization and function. Under fluid shear stress, AJs exhibit dynamic assembly/disassembly, but how shear stress couples to AJs is unclear. In MDCK cells we measured simultaneously the forces in cytoskeletal α-actinin and the density and length of AJs using a genetically coded optical force sensor, actinin-sstFRET, and fluorescently labeled E-cadherin (E-cad). We found that shear stress of 0.74dyn/cm for 3h significantly enhanced E-cad expression at cell-cell contacts and this phenomenon has two phases. The initial formation of segregated AJ plaques coincided with a decrease in cytoskeletal tension, but an increase in tension was necessary for expansion of the plaques and the formation of continuous AJs in the later phase. The changes in cytoskeletal tension and reorganization appear to be an upstream process in response to flow since it occurred in both wild type and dominant negative E-cad cells. Disruption of F-actin with a Rho-ROCK inhibitor eliminated AJ growth under flow. These results delineate the shear stress transduction paths in cultured cells, which helps to understand pathology of a range of diseases that involve dysfunction of E-cadherin.
[Mh] Termos MeSH primário: Citoesqueleto de Actina/metabolismo
Junções Aderentes/metabolismo
Mecanotransdução Celular
Estresse Mecânico
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/ultraestrutura
Actinina/genética
Actinina/metabolismo
Actinas/genética
Actinas/metabolismo
Junções Aderentes/ultraestrutura
Amidas/farmacologia
Animais
Fenômenos Biomecânicos
Técnicas Biossensoriais
Caderinas/genética
Caderinas/metabolismo
Cães
Transferência Ressonante de Energia de Fluorescência
Regulação da Expressão Gênica
Células Madin Darby de Rim Canino
Inibidores de Proteínas Quinases/farmacologia
Piridinas/farmacologia
Reologia
Quinases Associadas a rho/antagonistas & inibidores
Quinases Associadas a rho/genética
Quinases Associadas a rho/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Amides); 0 (Cadherins); 0 (Protein Kinase Inhibitors); 0 (Pyridines); 11003-00-2 (Actinin); 138381-45-0 (Y 27632); EC 2.7.11.1 (rho-Associated Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170814
[St] Status:MEDLINE


  5 / 2262 MEDLINE  
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[PMID]:28779483
[Au] Autor:Berania I; Cardin GB; Clément I; Guertin L; Ayad T; Bissada E; Nguyen-Tan PF; Filion E; Guilmette J; Gologan O; Soulieres D; Rodier F; Wong P; Christopoulos A
[Ad] Endereço:CRCHUM and Institut du cancer de Montréal, Montreal, QC, Canada.
[Ti] Título:Four PTEN-targeting co-expressed miRNAs and ACTN4- targeting miR-548b are independent prognostic biomarkers in human squamous cell carcinoma of the oral tongue.
[So] Source:Int J Cancer;141(11):2318-2328, 2017 Dec 01.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The purpose of this study was to determine the prognostic value and oncogenic pathways associated to miRNA expression in squamous cell carcinoma of the oral tongue and to link these miRNA candidates with potential gene targets. We performed a miRNA screening within our institutional cohort (n = 58 patients) and reported five prognostic targets including a cluster of four co-expressed miRNAs (miR-18a, miR-92a, miR-103, and miR-205). Multivariate analysis showed that expression of miR-548b (p = 0.007) and miR-18a (p = 0.004, representative of co-expressed miRNAs) are independent prognostic markers for squamous cell carcinoma of the oral tongue. These findings were validated in The Cancer Genome Atlas (TCGA) cohort (n = 131) for both miRNAs (miR-548b: p = 0.027; miR-18a: p = 0.001). Bioinformatics analysis identified PTEN and ACTN4 as direct targets of the four co-expressed miRNAs and miR-548b, respectively. Correlations between the five identified miRNAs and their respective targeted genes were validated in the two merged cohorts and were concordantly significant (miR-18a/PTEN: p < 0.0001; miR-92a/PTEN: p = 0.0008; miR-103/PTEN: p = 0.008; miR-203/PTEN: p = 0.019; miR-548b/ACTN4: p = 0.009).
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Carcinoma de Células Escamosas/patologia
Regulação Neoplásica da Expressão Gênica/genética
Neoplasias de Cabeça e Pescoço/patologia
MicroRNAs/genética
Neoplasias da Língua/patologia
[Mh] Termos MeSH secundário: Actinina/metabolismo
Idoso
Área Sob a Curva
Biomarcadores Tumorais/análise
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/mortalidade
Feminino
Imunofluorescência
Neoplasias de Cabeça e Pescoço/genética
Neoplasias de Cabeça e Pescoço/mortalidade
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
PTEN Fosfo-Hidrolase/metabolismo
Prognóstico
Curva ROC
Reação em Cadeia da Polimerase em Tempo Real
Neoplasias da Língua/genética
Neoplasias da Língua/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN4 protein, human); 0 (Biomarkers, Tumor); 0 (MIRN548 microRNA, human); 0 (MicroRNAs); 11003-00-2 (Actinin); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.30915


  6 / 2262 MEDLINE  
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[PMID]:28664914
[Au] Autor:Liao Q; Li R; Zhou R; Pan Z; Xu L; Ding Y; Zhao L
[Ad] Endereço:Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
[Ti] Título:LIM kinase 1 interacts with myosin-9 and alpha-actinin-4 and promotes colorectal cancer progression.
[So] Source:Br J Cancer;117(4):563-571, 2017 Aug 08.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: LIM kinase 1 (LIMK1) is a key regulator of the cytoskeletal organisation involved in cell proliferation and migration. Even though LIMK1 is frequently dysregulated in epithelial cancers, the role and mechanisms of LIMK1 in colorectal cancer (CRC) remains unclear. METHODS: Immunohistochemical analysis was performed to examine the expression and clinical significance of LIMK1 in CRC samples. Loss- and gain-of-function assay was performed to investigate the effects of aberrant expression on cellular biological behaviour of CRC cells in vitro and in vivo. Immunoblotting and immunoprecipitation was used to screen LIMK1-related signalling pathways and downstream factors. RESULTS: In this study, our results showed that LIMK1 was upregulated in CRC tissues and localised in both the cytoplasm and the nucleus of CRC cells. Overexpression of LIMK1 in cytoplasmic and nuclear subcellular compartments was closely related to tumour metastasis and poor prognosis of CRC patients. Enhanced expression of cytoplasmic and nuclear LIMK1 significantly increased cell proliferation and migration by driving epithelial-mesenchymal transition and activating the PI3K/Akt signal pathway in vitro as well as promoting growth and metastasis of CRC xenografts, whereas opposite effects were achieved in LIMK1-silenced cells. Furthermore, we identified two tumour metastasis-associated proteins, MYH9 and ACTN4, as direct targets of LIMK1, which were required for a LIMK1-mediated aggressive phenotype. CONCLUSIONS: These findings indicate that LIMK1 plays a critical role in promoting CRC progression at subcellular level. Our findings provide new insights into the metastasis of CRC and advocate for the development of clinical intervention strategies against advanced CRC.
[Mh] Termos MeSH primário: Actinina/metabolismo
Neoplasias Colorretais/metabolismo
Neoplasias Colorretais/patologia
Quinases Lim/metabolismo
Proteínas Motores Moleculares/metabolismo
Cadeias Pesadas de Miosina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular
Núcleo Celular/química
Proliferação Celular
Neoplasias Colorretais/química
Neoplasias Colorretais/genética
Citoplasma/química
Progressão da Doença
Transição Epitelial-Mesenquimal
Inativação Gênica
Seres Humanos
Quinases Lim/análise
Quinases Lim/genética
Camundongos
Camundongos Nus
Transplante de Neoplasias
Fenótipo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN4 protein, human); 0 (MYH9 protein, human); 0 (Molecular Motor Proteins); 11003-00-2 (Actinin); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (LIMK1 protein, human); EC 2.7.11.1 (Lim Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170701
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.193


  7 / 2262 MEDLINE  
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[PMID]:28613835
[Au] Autor:Tseng PY; Henderson PB; Hergarden AC; Patriarchi T; Coleman AM; Lillya MW; Montagut-Bordas C; Lee B; Hell JW; Horne MC
[Ad] Endereço:Department of Pharmacology, School of Medicine, University of California , Davis, California 95615-8636, United States.
[Ti] Título:α-Actinin Promotes Surface Localization and Current Density of the Ca Channel Ca 1.2 by Binding to the IQ Region of the α1 Subunit.
[So] Source:Biochemistry;56(28):3669-3681, 2017 Jul 18.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The voltage-gated L-type Ca channel Ca 1.2 is crucial for initiating heartbeat and control of a number of neuronal functions such as neuronal excitability and long-term potentiation. Mutations of Ca 1.2 subunits result in serious health problems, including arrhythmia, autism spectrum disorders, immunodeficiency, and hypoglycemia. Thus, precise control of Ca 1.2 surface expression and localization is essential. We previously reported that α-actinin associates and colocalizes with neuronal Ca 1.2 channels and that shRNA-mediated depletion of α-actinin significantly reduces localization of endogenous Ca 1.2 in dendritic spines in hippocampal neurons. Here we investigated the hypothesis that direct binding of α-actinin to Ca 1.2 supports its surface expression. Using two-hybrid screens and pull-down assays, we identified three point mutations (K1647A, Y1649A, and I1654A) in the central, pore-forming α 1.2 subunit of Ca 1.2 that individually impaired α-actinin binding. Surface biotinylation and flow cytometry assays revealed that Ca 1.2 channels composed of the corresponding α-actinin-binding-deficient mutants result in a 35-40% reduction in surface expression compared to that of wild-type channels. Moreover, the mutant Ca 1.2 channels expressed in HEK293 cells exhibit a 60-75% decrease in current density. The larger decrease in current density as compared to surface expression imparted by these α 1.2 subunit mutations hints at the possibility that α-actinin not only stabilizes surface localization of Ca 1.2 but also augments its ion conducting activity.
[Mh] Termos MeSH primário: Actinina/metabolismo
Canais de Cálcio Tipo L/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Canais de Cálcio Tipo L/análise
Células HEK293
Seres Humanos
Ligação Proteica
Subunidades Proteicas/análise
Subunidades Proteicas/metabolismo
Transporte Proteico
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels, L-Type); 0 (L-type calcium channel alpha(1C)); 0 (Protein Subunits); 11003-00-2 (Actinin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00359


  8 / 2262 MEDLINE  
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[PMID]:28592635
[Au] Autor:Owen LM; Adhikari AS; Patel M; Grimmer P; Leijnse N; Kim MC; Notbohm J; Franck C; Dunn AR
[Ad] Endereço:Biophysics, Stanford University, Stanford, CA 94305.
[Ti] Título:A cytoskeletal clutch mediates cellular force transmission in a soft, three-dimensional extracellular matrix.
[So] Source:Mol Biol Cell;28(14):1959-1974, 2017 Jul 07.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The ability of cells to impart forces and deformations on their surroundings underlies cell migration and extracellular matrix (ECM) remodeling and is thus an essential aspect of complex, metazoan life. Previous work has resulted in a refined understanding, commonly termed the molecular clutch model, of how cells adhering to flat surfaces such as a microscope coverslip transmit cytoskeletally generated forces to their surroundings. Comparatively less is known about how cells adhere to and exert forces in soft, three-dimensional (3D), and structurally heterogeneous ECM environments such as occur in vivo. We used time-lapse 3D imaging and quantitative image analysis to determine how the actin cytoskeleton is mechanically coupled to the surrounding matrix for primary dermal fibroblasts embedded in a 3D fibrin matrix. Under these circumstances, the cytoskeletal architecture is dominated by contractile actin bundles attached at their ends to large, stable, integrin-based adhesions. Time-lapse imaging reveals that α-actinin-1 puncta within actomyosin bundles move more quickly than the paxillin-rich adhesion plaques, which in turn move more quickly than the local matrix, an observation reminiscent of the molecular clutch model. However, closer examination did not reveal a continuous rearward flow of the actin cytoskeleton over slower moving adhesions. Instead, we found that a subset of stress fibers continuously elongated at their attachment points to integrin adhesions, providing stable, yet structurally dynamic coupling to the ECM. Analytical modeling and numerical simulation provide a plausible physical explanation for this result and support a picture in which cells respond to the effective stiffness of local matrix attachment points. The resulting dynamic equilibrium can explain how cells maintain stable, contractile connections to discrete points within ECM during cell migration, and provides a plausible means by which fibroblasts contract provisional matrices during wound healing.
[Mh] Termos MeSH primário: Adesões Focais/metabolismo
Adesões Focais/fisiologia
Fibras de Estresse/fisiologia
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/metabolismo
Actinina/metabolismo
Actinas/metabolismo
Actomiosina/metabolismo
Fenômenos Biomecânicos/fisiologia
Adesão Celular
Movimento Celular
Citoesqueleto/metabolismo
Matriz Extracelular/metabolismo
Matriz Extracelular/fisiologia
Fibroblastos/metabolismo
Seres Humanos
Integrinas/metabolismo
Paxilina/metabolismo
Fibras de Estresse/metabolismo
Imagem com Lapso de Tempo/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN1 protein, human); 0 (Actins); 0 (Integrins); 0 (Paxillin); 11003-00-2 (Actinin); 9013-26-7 (Actomyosin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E17-02-0102


  9 / 2262 MEDLINE  
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[PMID]:28581489
[Au] Autor:Liu X; Chu KM
[Ad] Endereço:Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong.
[Ti] Título:α-Actinin-4 promotes metastasis in gastric cancer.
[So] Source:Lab Invest;97(9):1084-1094, 2017 Sep.
[Is] ISSN:1530-0307
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Metastasis increases the mortality rate of gastric cancer, which is the third leading cause of cancer-associated deaths worldwide. This study aims to identify the genes promoting metastasis of gastric cancer (GC). A human cell motility PCR array was used to analyze a pair of tumor and non-tumor tissue samples from a patient with stage IV GC (T3N3M1). Expression of the dysregulated genes was then evaluated in GC tissue samples (n=10) and cell lines (n=6) via qPCR. Expression of α-actinin-4 (ACTN4) was validated in a larger sample size (n=47) by qPCR, western blot and immunohistochemistry. Knockdown of ACTN4 with specific siRNAs was performed in GC cells, and adhesion assays, transwell invasion assays and migration assays were used to evaluate the function of these cells. Expression of potential targets of ACTN4 were then evaluated by qPCR. Thirty upregulated genes (greater than twofold) were revealed by the PCR array. We focused on ACTN4 because it was upregulated in 6 out of 10 pairs of tissue samples and 5 out of 6 GC cell lines. Further study indicated that ACTN4 was upregulated in 22/32 pairs of tissue samples at stage III &IV (P=0.0069). Knockdown of ACTN4 in GC cells showed no significant effect on cell proliferation, but significantly increased cell-matrix adhesion, as well as reduced migration and invasion of AGS, MKN7 and NCI-N87 cells. We found that NF-κB was downregulated in GC with the knockdown of ACTN4. In conclusion, this is the first study to indicate that ACTN4 is significantly upregulated in patients with metastatic GC. ACTN4 reduces cell adhesion and enhances migration and invasion of GC cells and may therefore be a novel therapeutic target for GC.
[Mh] Termos MeSH primário: Actinina/análise
Actinina/metabolismo
Neoplasias Gástricas/metabolismo
Neoplasias Gástricas/patologia
Estômago/metabolismo
[Mh] Termos MeSH secundário: Actinina/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Linhagem Celular Tumoral
Movimento Celular/genética
Estudos de Coortes
Feminino
Perfilação da Expressão Gênica
Técnicas de Silenciamento de Genes
Seres Humanos
Masculino
Meia-Idade
NF-kappa B/análise
NF-kappa B/metabolismo
Estômago/química
Neoplasias Gástricas/química
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN4 protein, human); 0 (NF-kappa B); 11003-00-2 (Actinin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1038/labinvest.2017.28


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[PMID]:28562514
[Au] Autor:Boutroux H; David B; Guéguen P; Frange P; Vincenot A; Leverger G; Favier R
[Ad] Endereço:*Department of pediatric Hematology and Oncology #Haematological Laboratory **French Reference Center for Inherited Platelet Disorders, Trousseau Hospital (AP-HP) ∥Department of Immunology and Hematology, Necker Hospital (AP-HP) ¶Haematological Laboratory, Robert Debré Hospital (AP-HP) †UPMC Univ Paris 06, UMR_S938, Sorbonne University, Paris ‡Department of General Pediatrics, Kremlin-Bicêtre Hospital (AP-HP), Kremlin-Bicêtre §Molecular Genetic Laboratory, INSERM, U1078, CHRU de Brest, Brest, France.
[Ti] Título:ACTN1-related Macrothrombocytopenia: A Novel Entity in the Progressing Field of Pediatric Thrombocytopenia.
[So] Source:J Pediatr Hematol Oncol;39(8):e515-e518, 2017 Nov.
[Is] ISSN:1536-3678
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The most common cause of thrombocytopenia in children is immune thrombocytopenia. Nevertheless, some atypical cases should evoke the hypothesis of genetic thrombocytopenia. Indeed, in the past years, 30 new genes had been described in the field of inherited thrombocytopenia. We report a series of 11 cases of a newly diagnosed entity: ACTN1-related macrothrombocytopenia. Mutations in the gene ACTN1 cause mild macrothrombocytopenia characterized by elevated mean platelet volume and elevated immature platelet fraction, and low bleeding tendency. Its transmission is autosomal dominant. Molecular diagnosis is made by sequencing the ACTN1 gene. Its potential role in hematological malignancy predisposition remains unclear and should be clarified. CONCLUSION: We identified 11 patients with ACTN1-related macrothrombocytopenia diagnosed through pediatric probands. The aim was to underline the specificities of this entity, especially in children, and bring it to the knowledge of pediatricians.
[Mh] Termos MeSH primário: Actinina/genética
Mutação
Trombocitopenia/diagnóstico
Trombocitopenia/genética
[Mh] Termos MeSH secundário: Adolescente
Alelos
Substituição de Aminoácidos
Biomarcadores
Contagem de Células Sanguíneas
Criança
Feminino
Genótipo
Seres Humanos
Imunofenotipagem
Recém-Nascido
Masculino
Linhagem
Análise de Sequência de DNA
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTN1 protein, human); 0 (Biomarkers); 11003-00-2 (Actinin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170601
[St] Status:MEDLINE
[do] DOI:10.1097/MPH.0000000000000885



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