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Dataset results
18 results for “Actomyosin”
Myosin turnover controls actomyosin contractile instability
<p>Simulation and experimental data related to the preprint "Myosin turnover controls actomyosin contractile instability" (https://www.biorxiv.org/content/10.1101/2021.03.18.436017). </p>
Single molecule dataset for article: Multistep orthophosphate release tunes actomyosin energy transduction
<table> <tbody> <tr> <td> <p>Dataset (single molecule movies) that is behind the results in the article's Figure 2 and Figure 3.</p> <p>MATLAB scripts used to analyze the dataset. </p> </td> </tr> </tbody> </table> <p> </p>
Microscopic images and schematics illustrating processes of microenvironment sensing and cortical actomyosin partitioning in T cells
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Epithelial cell chirality emerges through the dynamic concentric pattern of actomyosin cytoskeleton
<p>Supporting Information for</p> <p>Epithelial cell chirality emerges through the dynamic concentric pattern of actomyosin cytoskeleton</p> <p>Takaki Yamamoto, Tomoki Ishibashi, Yuko Mimori-Kiyosue, Sylvain Hiver, Naoko Tokushige, Mitsusuke Tarama, Masatoshi Takeichi, Tatsuo Shibata</p> <p>Tatsuo Shibata<br>Email: tatsuo.shibata@riken.jp</p> <p>Numerical data used for Figs. 1B, and C: </p> <p>Fig1B.csv,<br>Fig1C.csv</p> <p>Numerical data used for Fig. 1 figure supplement 1:</p> <p>Fig1S1_Collagen.csv,<br>Fig1S1_Fibronectin.csv,<br>Fig1S1_Non-coated.csv,<br>Fig1S1_PLL.csv</p> <p>Numerical data used for Figs. 2B, C and D: </p> <p>Fig2B.csv,<br>Fig2C_Blebbistatin.csv,<br>Fig2C_CK666.csv,<br>Fig2C_DMSO.csv,<br>Fig2C_Nocodazole.csv,<br>Fig2C_SMIFH2.csv,<br>Fig2D_DMSO.csv,<br>Fig2D_SMIFH2.csv</p> <p>Numerical data used for Fig. 2 figure supplement 2 A, D:</p> <p>Fig2S2A.csv,<br>Fig2S2D_NC.csv,<br>Fig2S2D_DAAM1_siRNA.csv,<br>Fig2S2D_DIAPH2_siRNA.csv</p> <p>Numerical data used for Fig. 2 figure supplement 3:</p> <p>Fig2S3A_NC.csv,<br>Fig2S3A_Myo2A_siRNA.csv,<br>Fig2S3A_Myo2B_siRNA.csv,<br>Fig2S3A_Myo2A_B_siRNA.csv,<br>Fig2S3B.csv</p> <p>Numerical data used for Fig. 2 figure supplement 4:</p> <p>Fig2S4A_NC.csv,<br>Fig2S4A_VCL_siRNA.csv,<br>Fig2S4B.csv</p> <p>Note: Fig2S2D_NC.csv, Fig2S3A_NC.csv and Fig2S4A_NC.csv represent data from the same control experiment.</p> <p>Numerical data used for Figs. 6C and D:<br>Fig6C.xls,<br>Fig6D_1.xls,<br>Fig6D_2.xls</p> <p>Numerical data used for Figs. 6 figure supplement 1:<br>Fig6S1I.xls,<br>Fig6S1J.xls</p> <p>Note: these data were also used in Figure 7 figure supplement 2A-H.</p> <p>Numerical data used for Figs. 8D and E:<br>Fig8DE.csv: </p> <p>FreeFEM++ script to perform the numerical computation used in Fig. 7 and matlab script for Fig 7 BCDFGH, and Fig. 7 figure supplement 2I: </p> <p>caco2ActiveChiralModel.edp,<br>PlotSimulationResults.m</p>
A B cell actomyosin arc network couples integrin co-stimulation to mechanical force-dependent immune synapse formation
<p>B-cell activation and immune synapse (IS) formation with membrane-bound antigens are actin-dependent processes that scale positively with the strength of antigen-induced signals. Importantly, ligating the B-cell integrin, LFA-1, with ICAM-1 promotes IS formation when antigen is limiting. Whether the actin cytoskeleton plays a specific role in integrin-dependent IS formation is unknown. Here we show using super-resolution imaging of mouse primary B cells that LFA-1: ICAM-1 interactions promote the formation of an actomyosin network that dominates the B-cell IS. This network is created by the formin mDia1, organized into concentric, contractile arcs by myosin 2A, and flows inward at the same rate as B-cell receptor (BCR): antigen clusters. Consistently, individual BCR microclusters are swept inward by individual actomyosin arcs. Under conditions where integrin is required for synapse formation, inhibiting myosin impairs synapse formation, as evidenced by reduced antigen centralization, diminished BCR signaling, and defective signaling protein distribution at the synapse. Together, these results argue that a contractile actomyosin arc network plays a key role in the mechanism by which LFA-1 co-stimulation promotes B-cell activation and IS formation.</p>
Mitochondrial MICOS complex genes, implicated in hypoplastic left heart syndrome, maintain cardiac contractility and actomyosin integrity
<p>Hypoplastic left heart syndrome (HLHS) is a severe congenital heart disease (CHD) with a likely oligogenic etiology, but our understanding of the genetic complexities and pathogenic mechanisms leading to HLHS is limited. We therefore performed whole genome sequencing (WGS) on a large cohort of HLHS patients and their families to identify candidate genes that were then tested in <em>Drosophila</em> heart model for functional and structural requirements. Bioinformatic analysis of WGS data from an index family comprised of a HLHS proband born to consanguineous parents and postulated to have a homozygous recessive disease etiology, prioritized 9 candidate genes with rare, predicted damaging homozygous variants. Of the candidate HLHS gene homologs tested, cardiac-specific knockdown (KD) of mitochondrial MICOS complex subunit dCHCHD3/6 resulted in drastically compromised heart contractility, diminished levels of sarcomeric actin and myosin, reduced cardiac ATP levels, and mitochondrial fission-fusion defects. Interestingly, these heart defects were similar to those inflicted by cardiac KD of ATP synthase subunits of the electron transport chain (ETC), consistent with the MICOS complex's role in maintaining cristae morphology and ETC complex assembly. Analysis of 183 genomes of HLHS patient-parent trios revealed five additional HLHS probands with rare, predicted damaging variants in CHCHD3 or CHCHD6. Hypothesizing an oligogenic basis for HLHS, we tested 60 additional prioritized candidate genes in these cases for genetic interactions with CHCHD3/6 in sensitized fly hearts. Moderate KD of CHCHD3/6 in combination with Cdk12 (activator of RNA polymerase II), RNF149 (E3 ubiquitin ligase), or SPTBN1 (scaffolding protein) caused synergistic heart defects, suggesting the potential involvement of a diverse set of pathways in HLHS. Further elucidation of novel candidate genes and genetic interactions of potentially-disease-contributing pathways is expected to lead to a better understanding of HLHS and other CHDs.</p>
A B cell actomyosin arc network couples integrin co-stimulation to mechanical force-dependent immune synapse formation
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Mitochondrial MICOS complex genes, implicated in hypoplastic left heart syndrome, maintain cardiac contractility and actomyosin integrity
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The role of the Arp2/3 complex in shaping the dynamics and structures of branched actomyosin networks
<p>Actomyosin networks give cells the ability to move and divide. These networks contract and expand while being driven by active energy-consuming processes such as motor protein walking and actin polymerization. Actin dynamics is also regulated by actin-binding proteins, such as the actin-related protein 2/3 (Arp2/3) complex. This complex generates branched filaments thereby changing the overall organization of the network. In this work, the spatiotemporal patterns of dynamical actin assembly accompanying the branching-induced reorganization caused by Arp2/3 were studied using a computational model (MEDYAN); this model simulates actomyosin network dynamics as a result of chemical reactions whose rates are modulated by rapid mechanical equilibration. We show that branched actomyosin networks relax significantly more slowly than do unbranched networks. Also, branched networks undergo rare convulsive movements, “avalanches”, that release strain in the network. These avalanches are associated with the more heterogeneous distribution of mechanically-linked filaments displayed by branched networks. These far-from equilibrium events arising from the marginal stability of growing actomyosin networks provide a possible mechanism of the “cytoquakes” recently seen in experiments.</p>
Cell size regulates human endoderm specification through actomyosin-dependent AMOT-YAP signaling
GEO Series GSE232608. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
MYBPH, a novel transcriptional target of NKX2-1/TTF-1, inhibits ROCK1 and actomyosin assembly, and reduces cell motility and tumor metastasis
GEO Series GSE26721. Homo sapiens. 2 samples. Type: Expression profiling by array.
Stem cell specification and niche formation in developing incisor depend on actomyosin forces
GEO Series GSE299463. Mus musculus. 10 samples. Type: Expression profiling by high throughput sequencing.
Secretion of interleukin-1 by dedifferentiated melanoma cells inhibits JAK1-STAT3-driven actomyosin contractility of lymph node fibroblastic reticular cells
GEO Series GSE157355. Homo sapiens. 8 samples. Type: Expression profiling by array.
Actomyosin-mediated tension orchestrates uncoupled respiration in adipose tissues
GEO Series GSE109829. Mus musculus. 14 samples. Type: Expression profiling by high throughput sequencing.
miRNA-mediated inhibition of an actomyosin network in hippocampal pyramidal neurons restricts sociability in adult male mice
GEO Series GSE247439. Mus musculus. 12 samples. Type: Expression profiling by high throughput sequencing.
Expression data from actomyosin contractility regulated genes
GEO Series GSE23764. Homo sapiens. 18 samples. Type: Expression profiling by array.
Age-associated Tissue Organization Shifts Retinal Pigmented Epithelium Actomyosin Plasticity in Phagocytosis
GEO Series GSE297557. Homo sapiens. 8 samples. Type: Expression profiling by high throughput sequencing.
Afadin and Zyxin contribute to coupling between cell junctions and contracting actomyosin networks during apical constriction
GEO Series GSE205061. Caenorhabditis elegans. 65 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
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DANDI Archive for NWB datasets
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The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
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