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6,171 results for “mutant”
Vesicles clustering around Wdr35-/- cilia lack electron dense decorations although electron-dense clathrin coated vesicles are still observed budding from the mutant plasma membrane (Figure 7- source data 1)
<p>Intraflagellar transport (IFT) is a highly conserved mechanism for motor-driven transport of cargo within cilia, but how this cargo is selectively transported to cilia is unclear. WDR35/IFT121 is a component of the IFT-A complex best known for its role in ciliary retrograde transport. In the absence of WDR35, small mutant cilia form but fail to enrich in diverse classes of ciliary membrane proteins. In <i>Wdr35 </i>mouse mutants, the non-core IFT-A components are degraded and core components accumulate at the ciliary base. We reveal deep sequence homology of WDR35 and other IFT-A subunits to α and ß' COPI coatomer subunits, and demonstrate an accumulation of 'coat-less' vesicles which fail to fuse with <i>Wdr35 </i>mutant cilia. We determine that recombinant non-core IFT-As can bind directly to<u> </u>lipids and provide the first <i>in-situ</i> evidence of a novel coat function for WDR35, likely with other IFT-A proteins, in delivering ciliary membrane cargo necessary for cilia elongation.</p>
Data set - Photosynthetic light harvesting and thylakoid organization in a CRISPR/Cas9 Arabidopsis thaliana LHCB1 knockout mutant.
<p>This data set was produced at the University of Neuchâtel, it cointains the raw data relative to the manuscript entitled "Photosynthetic light harvesting and thylakoid organization in a CRISPR/Cas9 Arabidopsis thaliana LHCB1 knockout mutant."</p> <p>The report presents the difference in terms of protein accumulation, light harvesting, electron transport and thylakoid structure between the WT line (Col0) of <em>Arabidopsis thaliana </em>and a newly generated line that contains multiple mutations in all the genes coding for the light harvesting protein LHCB1, named L1ko.</p> <p>Paper_raw_data.xlsx contains the data utilised to produce the figures presented in the paper.</p> <p>Fluorescence_data.xlsx contains the raw fluorescence traces in excel format for three experiments. The data of the measurments performed with the multispeq are also available here: https://photosynq.org/projects/etr_in_lab_test_protocols</p> <p>Chloroplasts_TEM_WT_L1KO.zip contains all the electron microscopy pictures, at full resolution analysed for the report.</p> <p> </p> <p> </p>
Comparação de ferramentas de análise estática para detecção de defeitos de software usando mutantes
<p>A análise estática de código é uma técnica aplicada na etapa de verificação de um software, com o objetivo de identificar defeitos sem a necessidade da execução da aplicação. Atualmente existem diversas ferramentas de análise estática disponíveis no mercado, onde cada uma possui suas particularidades e diferentes escopos de análise. Portanto, escolher a ferramenta correta a ser usada não é uma atividade trivial. Este estudo tem como objetivo comparar duas ferramentas de análise estática de código sendo elas o SonarQube e o PMD, analisando a sua eficácia na identificação de defeitos em um código de software. Com esta finalidade foram criados mutantes a partir de projetos Open Source, que auxiliaram a verificar a eficácia das ferramentas.</p>
chr2 of mutant genomes used in Rekaik et al. 2022
<p>Fasta file for ch2 of the Del(d1-d4), Del(sub-TAD1) and Ins(2xCBS-d4d8) mutant ES cell lines used in Rekaik et al., 2022. In Del(d1-d4) mutant, the deletion includes bases between mm10:74,719,771 and 74,765,994. The Del(sub-TAD1) chr2 contains the deletion of mm10:74768588 to 75133800. In Ins(2xCBS-d4d8), a 900bp cassette was inserted between bases mm10:74,716,919 and 74,717,063. The insertion contains 2 CTCF binding sites, both cloned from the endogenous CBS1 sequence at the position mm10: 74,715,687-74,716,136 and mm10: 74,715,717-74,716,166, respectively. The fasta files were generated from the chr2 of the mm10 genome (<a href="http://hgdownload.soe.ucsc.edu/goldenPath/mm10/chromosomes/chr2.fa.gz">http://hgdownload.soe.ucsc.edu/goldenPath/mm10/chromosomes/chr2.fa.gz</a>).</p> <p> </p>
Resistance of Dickeya solani strain IPO 2222 to lytic bacteriophage ΦD5 results in fitness tradeoffs for the bacterium during infection - mutants genomes dataset
<p>Raw genome sequence (genomes of the phage-resistant D. solani Tn5 mutants) dataset supporting the manuscript entitled: <strong>Resistance of </strong><em><strong>Dickeya solani</strong></em><strong> strain IPO 2222 to lytic bacteriophage </strong><strong>Φ</strong><strong>D5 results in fitness tradeoffs for the bacterium during infection.</strong></p>
Dataset for: Conformational and Thermodynamic Differences Underlying Wild-type and Mutant YEATS Domain Specificity for Epigenetic Marks
<p>The set of molecular dynamics trajectories generated and analyzed in the paper "Conformational and Thermodynamic Differences Underlying Wild-type and Mutant YEATS Domain Specificity for Epigenetic Marks." <strong>Citations should refer directly to the manuscript. </strong> The preprint version is available at: https://doi.org/10.1101/2022.07.14.500085</p> <p>The uploaded zip file "trajectory_data.zip" contains trajectories for the (1) apo (2) h3k27ac and (3) h3k9ac systems. In each directory is a subdirectory corresponding to the wild-type, deletion, and insertion mutations. In each of those subdirectories are 10 XTC files, which correspond to the trajectories for the 10 different simulations performed for each system, along with an AMBER-formated PRMTOP file. Solvent molecules were removed from each file, and trajectories were strided such that there is one frame per 500 ps. </p>
Do Go Chasing Waterfalls: Enoyl Reductase (FabI) in Complex with Inhibitors Stabilizes the Tetrameric Structure and Opens Water Channels - full trajectories of SaFabI and EcFabI monomers and G112/113V mutants
<p>The following IDs are related to trajectories:</p> <p>v36 = EcFabI apo, monomer<br> v42 = EcFabI + TCL complex, monomer<br> v43 = EcFabI + MUT complex, monomer<br> v44 = EcFabI + AFN complex, monomer<br> v35 = SaFabI apo, monomer<br> v45 = SaFabI + TCL complex, monomer<br> v46 = SaFabI + MUT complex, monomer<br> v47 = SaFabI + AFN complex, monomer<br> v52 = G112V EcFabI apo, tetramer<br> v53 = G112V EcFabI apo, monomer<br> v54 = G113V SaFabI apo, tetramer<br> v55 = G113V SaFabI apo, monomer</p>
Rotational electron diffraction patterns of TIA-1 prion-like domain, A381T mutant
<p>Rotational electron diffraction patterns of TIA-1 prion-like domain, A381T mutant. Collected with a JEOL CRYO ARM 300 electron microscope operated at an accelerating voltage of 300kV on a DirectElectron DE64 detector at RIKEN, SPring-8 Center. The PDB ID associated with this data is 7VI5.The PDB ID associated with this data is 7VI4.</p>
RASTtk annotations of Chromobacterium vaccinii MWU328 and quorum sensing mutant MWU328W
<p>RASTtk genome annotations of Chromobacterium vaccinii MWU328 (wild type) and a spontaneous frameshift mutant in the cviR (quorum sensing autoinducer receptor) gene MWU328W.</p>
Molecular dynamics simulations data of Caspase-3 enzyme with pentapeptide ligand DEVDG and its chiral mutant DEVdG having D-Asp at fourth position
<p>Amino acids in proteins are maintained in one specific L chiral form in the body. D-amino acids are not normally incorporated into proteins and their accumulation has been associated with several conditions including schizophrenia, amyotrophic lateral sclerosis, and other age-related disorders. However, the mechanisms by which the accumulation of D-amino-acids in proteins may lead to pathophysiological consequences remain poorly understood. In this work, we studied a model protease system, caspase-3 that specifically hydrolyses the 4’–5’ peptide bond of the pentapeptide substrate DEVDG. Through extensive molecular dynamics simulations, free energy calculations and distance maps, we reveal that caspase-3 naturally rejects the pentapeptide containing D-Asp substrate, DEVdG and prevents catalytic activity by caspase. The importance of this chiral discriminating capacity is evident from chiral-selective in vivo experimental assays to detect caspase-bound D-Asp in Drosophila where altering the chiral balance created impaired caspase activity and impaired apoptosis, increased tumour formation, and premature death. The modelling data reveals the molecular level charge balancing that enforces the chiral recognition necessary to maintain homeostasis across the cell, tissue, and organ level.</p>
LC-MS/MS data for WT human PANX1 with or without co-expressing Src-Y529F mutant
<p>Protein phosphorylation is one of the major molecular mechanisms regulating protein activity and function throughout the cell. Pannexin 1 (PANX1) is a large-pore channel permeable to ATP and other cellular metabolites. Its tyrosine phosphorylation and subsequent activation have been found to play critical roles in diverse cellular conditions, including neuronal cell death, acute inflammation, and smooth muscle contraction. Specifically, the non-receptor kinase Src has been reported to phosphorylate Tyr198 and Tyr308 of mouse PANX1 (equivalent to Tyr199 and Tyr309 of human PANX1), resulting in channel opening and ATP release. Although the Src-dependent PANX1 activation mechanism has been widely discussed in the literature, independent validation of the tyrosine phosphorylation of PANX1 has been lacking. Here, we show that commercially available antibodies against the two phosphorylation sites mentioned above—which were used to identify endogenous PANX1 phosphorylation at these two sites—are nonspecific and should not be used to interpret results related to PANX1 phosphorylation. We further provide evidence that neither tyrosine residue is a major phosphorylation site for Src kinase in heterologous expression systems. We call on the field to re-examine the existing paradigm of tyrosine phosphorylation-dependent activation of the PANX1 channel.</p>
Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity
<p>Isocitrate Dehydrogenase 1 (IDH1) is the most commonly mutated metabolic gene across human cancers. Mutant IDH1 (mIDH1) generates the oncometabolite (R)-2-hydroxyglutarate, disrupting enzymes involved in epigenetics and other processes. A hallmark of IDH1-mutant solid tumors is T cell exclusion, whereas mIDH1 inhibition in preclinical models restores anti-tumor immunity. Here, we define a cell-autonomous mechanism of mIDH1-driven immune evasion. IDH1-mutant solid tumors show striking, selective hypermethylation and silencing of the cytoplasmic dsDNA sensor, CGAS, compromising innate immune signaling. mIDH1 inhibition restores DNA demethylation, derepressing CGAS and transposable element (TE) subclasses. dsDNA produced by TE-reverse transcriptase activates cGAS, triggering viral mimicry and stimulating anti-tumor immunity. Thus, we demonstrate that mIDH1 epigenetically suppresses innate immunity and link endogenous reverse transcriptase activity to the mechanism of action of an FDA-approved oncology drug.</p>
Data from: Age-specific induction of mutant p53 drives clonal hematopoiesis and acute myeloid leukemia in adult mice
<p>The investigation of the mechanisms behind p53 mutations in acute myeloid leukemia (AML) has been limited by the lack of suitable mouse models, which historically have resulted in lymphoma rather than leukemia. This study introduces two new AML mouse models. One model induces mutant p53 and <em>Mdm2</em> haploinsufficiency in early development, showing the role of Mdm2 in myeloid-biased hematopoiesis and AML predisposition, independent of p53. The second model mimics clonal hematopoiesis by inducing mutant p53 in adult hematopoietic stem cells, demonstrating that the timing of p53 mutation determines AML versus lymphoma development. In this context, age-related changes in hematopoietic stem cells (HSCs), collaborates with mutant p53 to predispose towards myeloid transformation rather than lymphoma development. Our study unveils new insights into the cooperative impact of HSC age, <em>Trp53</em> mutations and <em>Mdm2</em> haploinsufficiency on clonal hematopoiesis and the development of myeloid malignancies.</p>
Data underlying the article: "Excuse me, there is a mutant in my bioactivity soup! A comprehensive analysis of the genetic variability landscape of bioactivity databases and its effect on activity modelling"
<p>This repository contains the data underlying the article: “Excuse me, there is a mutant in my bioactivity soup! A comprehensive analysis of the genetic variability landscape of bioactivity databases and its effect on activity modelling” available as a preprint on ChemRxiv.</p> <p>Main authors: Marina Gorostiola González & Olivier J.M. Béquignon (Leiden University)</p> <p>Senior author: Gerard J.P. van Westen (Leiden University)</p> <p>This analysis was performed using the code available at <a href="https://github.com/CDDLeiden/chembl_variants" target="_blank" rel="noopener">https://github.com/CDDLeiden/chembl_variants</a></p>
HaHB4 promoter mutants GUS histochemistry assays
<p>CORRECTION</p> <p>Manavella PA, Dezar CA, Ariel FD, Chan RL. Two ABREs, two redundant root-specific and one W-box cis-acting elements are functional in the sunflower HAHB4 promoter. Plant Physiol Biochem. 2008 Oct;46(10):860-7. doi: 10.1016/j.plaphy.2008.05.003.</p> <p>During the assembly of Figure 3, the root picture in panel D was accidentally and unintentionally duplicated in panel H. The authors reviewed the original photographs and prepared a corrected version that contains the correct images. The authors apologize for this mistake. The figure legend and main text remain unaltered. This correction does not affect any of the conclusions of this paper.</p> <p>This dataset includes the original photographs of GUS staining of all Arabidopsis transgenic plants shown in Figure 3.</p>
Infection of mice by the enteroaggregative E. coli strain 042 and two mutant derivatives overexpressing virulence factors: impact on disease markers, gut microbiota and concentration of SCFAs in feces
<p>This dataset contains raw sequencing data from the microbiota analysis conducted in the enteroaggregative E. coli strain 042 study. The data includes FASTQ files generated from Illumina sequencing, along with metadata describing the sample collection and processing methods.</p>
Efficacy of inhibitor on wild-type ACVR1 and R206H mutant in C2C12 cells (by DLA)
<p>There are concerns that compounds that are effective in inhibiting ALK2 by occupying its ATP-binding pocket might have reduced efficacy against mutant ALK2. That will be undesirable since the compounds should also target the mutant gain-of-function ALK2 in DIPG cells. The following experiment takes advantage of the fact that ALK2-R206H mutant confers a neofunction of being activated by Activin A (not activating towards wild-type ALK2). Therefore, using Activin A as the stimulation ligand, the effectiveness of inhibition on ALK2-R206H can be specifically determined. BMP6 which activates both wild-type ALK2 and ALK2-R206H is also included.</p>
Scans of leaves dissected in phyllotactic order: complementation of ago7 mutant A. thaliana plants with truncated promoter transgenes
<p>This transgenic complementation experiment is described in a paper by Hoyer et al. (2019): <a href="https://doi.org/10.1002/pld3.102">https://doi.org/10.1002/pld3.102</a></p> <p>Adaxial (ad) and abaxial (ab) surfaces of rosettes were photographed in between removal of leaves, to enable checking that leaves were removed in the correct phyllotactic order.<strong> </strong>A manifest file with file SHA-1 sums is included.</p> <p>Metadata and LeafJ measurements have been made available separately, to facilitate updates -- see <a href="https://github.com/jshoyer/raspi-photo-and-leaf-scan-metadata">https://github.com/jshoyer/raspi-photo-and-leaf-scan-metadata</a>, archived as <a href="https://doi.org/10.5281/zenodo.1340636">https://doi.org/10.5281/zenodo.1340636</a></p> <p>Seed was plated and growth started on 2016-08-26. Leaves were dissected and scanned 33 and 35 days post-stratification (2016-09-28 and 30).</p>
Time-lapse photograph dataset: complementation of ago7 mutant A. thaliana plants with truncated promoter transgenes
<p>This transgenic complementation experiment is described in a paper by Hoyer et al. (2019): <a href="https://doi.org/10.1002/pld3.102">https://doi.org/10.1002/pld3.102</a></p> <p>Time-stamped photographs are provided in twelve directories by camera (twelve overlapping fields of view) and a manifest file with file SHA-1 sums is included.</p> <p>Metadata have been made available separately, to facilitate updates -- see <a href="https://github.com/jshoyer/raspi-photo-and-leaf-scan-metadata">https://github.com/jshoyer/raspi-photo-and-leaf-scan-metadata</a>, archived as <a href="https://doi.org/10.5281/zenodo.1340636">https://doi.org/10.5281/zenodo.1340636</a></p> <p>Seed was plated and growth started on 2016-08-26.</p>
Magnaporthe oryzae polyadenylation sites for wild-type and delta-rbp35 mutant
<p>Magnaporthe oryzae polyadenylation sites for wild-type and delta-rbp35 mutant, in 4 media: CM, MM, MM-N and MM-C</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
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DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
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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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