Find research datasets worth reusing

Dataset related to article "Evaluation of cell metabolic adaptation in wound and tumour by fluorescence Lifetime imaging Microscopy"

This record contains data related to article "Evaluation of cell metabolic adaptation in wound and tumour by fluorescence Lifetime imaging Microscopy" Abstract Acidic pH occurs in acute wounds progressing to healing as consequence of a cell metabolic adaptation in response to injury-induced tissue hypoperfusion. In tumours, high metabolic rate leads to acidosis affecting cancer progression. Acidic pH affects activities of remodelling cells in vitro. The pH measurement predicts healing in pathological wounds and success of surgical treatment of burns and chronic ulcers. However, current methods are limited to skin surface or based on detection of fluorescence intensity of specific sensitive probes that suffer of microenvironment factors. Herein, we ascertained relevance in vivo of cell metabolic adaptation in skin repair by interfering with anaerobic glycolysis. Moreover, a custom-designed skin imaging chamber, 2-Photon microscopy (2PM), fluorescence lifetime imaging (FLIM) and data mapping analyses were used to correlate maps of glycolytic activity in vivo as measurement of NADH intrinsic lifetime with areas of hypoxia and acidification in models of skin injury and cancer. The method was challenged by measuring the NADH profile by interfering with anaerobic glycolysis and oxidative phosphorylation in the mitochondrial respiratory chain. Therefore, intravital NADH FLIM represents a tool for investigating cell metabolic adaptation occurring in wounds, as well as the relationship between cell metabolism and cancer.

openother-openJan 2021View details →

Input data of manuscript "CACTUS: integrating clonal architecture with genomic clustering and transcriptome profiling of single tumor cells"

This is the directory containing input data necessary to reproduce analyses presented in the manuscript: <blockquote> CACTUS: integrating clonal architecture with genomic clustering and transcriptome profiling of single tumor cells Shadi Darvish Shafighi, Szymon M Kiełbasa, Julieta Sepúlveda Yáñez, Ramin Monajemi, Davy Cats, Hailiang Mei, Roberta Menafra, Susan Kloet, Hendrik Veelken, Cornelis A.M. van Bergen, Ewa Szczurek </blockquote>

opencc-zeroJan 2021View details →

Improved small-angle x-ray scattering of nanoparticle self-assembly using a cell with a flat liquid surface

One important way of forming nanostructures entails the assembly of nanoparticle (NP) monolayers at a liquid surface. Probing this assembly of 11.8-nm-diameter iron oxide NPs by small-angle x-ray scattering (SAXS) is studied using cells with walls at angles designed to significantly reduce the size of the meniscus. This enables the collection of much larger signals in the SAXS images of ordered arrays of NPs at liquid/gas interfaces, as is needed for kinetics studies and x-ray exposure minimization, along with the observation of extremely high degrees of order. Meniscus flattening and improved signal collection are demonstrated for the assembly of ordered arrays of iron oxide NP monolayers at a diethylene glycol surface.

opencc-by-4.0Sep 2020View details →

AnnData files for "Human dermal fibroblast subpopulations are conserved across single-cell RNA sequencing studies"

AnnData files for "Human dermal fibroblast subpopulations are conserved across single-cell RNA sequencing studies".  Includes Joined dataset with all four datasets at once.

opencc-zeroJan 2021View details →

Data from: Egg mass polymorphism in Ambystoma maculatum is not associated with larval performance or survival, or with cell density of the algal symbiont Oophila amblystomatis

These data are from a 2018 study of larval morphology, performance, and survival in the spotted salamander (Ambystoma maculatum). We examined larvae of two egg mass color morphs: clear and white. We also quantified the density of algal (Oophila amblystomatis) cells on the egg capsules of embryos. The data correspond to our publication in Evolutionary Ecology.

opencc-zeroDec 2021View details →

Data from: Shape matters: The relationship between cell geometry and diversity in phytoplankton

We compiled the most comprehensive data set of phytoplankton and other marine protists in terms of sizes, shapes, genus, and species names. Samples were obtained from seven globally distributed marine areas: Baltic Sea, North Atlantic (Scotland), Mediterranean Sea (Greece and Turkey), Indo-Pacific (the Maldives), South-western Pacific (Australia), Southern Atlantic (Brazil). See details in Ryabov et al Ecology Letters 'Shape matters: the relationship between cell geometry and diversity in phytoplankton'

opencc-by-4.0Mar 2021View details →

Prioritization of cell types responsive to biological perturbations in single-cell data with Augur

Processed and analysis-ready input data discussed in our Augur procedures.

The Influence of the Extremely Low Frequency Electromagnetic Field on Clear Cell Renal Carcinoma

Abstract:   The development of new technologies and industry is conducive to the increase in the number and variety of electromagnetic field (EMF) sources in our environment. The main sources of EMF are high-voltage lines, household appliances, audio/video devices, mobile phones, radio stations, and radar devices. In the growing use of electronic devices, scientists are increasingly interested in the effects of EMF on human health. Even though many studies on the effects of EMF have already been carried out, none of them has shown a significant effect on mammals, including humans. Moreover, it is not entirely clear how EMF influences cell behavior. The International Agency for Research on Cancer on May 31, 2011, classified PEM as a possible carcinogenic factor. This study aimed to investigate the effect of the electromagnetic field on morphological and functional changes in clear cell renal carcinoma. The research was carried out on in vitro cultures of four cell lines: HEK293, 786-O 769-P, and Caki1. The results of the research showed that the EMF of low frequency had a slight effect on the viability of cells. EMF, which induced cell arrest in the G1 phase, increased the number of early apoptotic cells and decreased the number of viable cells in the 786-O line. EMF did not affect the proliferation and viability of HEK293 cells. Extreme low-frequency EMF (ELF-EMF) also showed an inhibitory effect on the migration and metastatic properties of clear cell kidney cancer cells. Moreover, shortly after the end of ELF-EMF exposure, significant increases in ROS levels were observed in all tested cell lines. As part of the work, it was shown that low-frequency EMF shows an inhibitory effect on the proliferation of primary cancer cells, diminishing their migratory, invasive, and metastatic abilities. It also increases the apoptosis of cancer cells and the amount of reactive oxygen species. Based on the results of our research, we want to point up that the effect of ELF-EMF depends on a specific metabolic state or at a specific stage in the cell cycle of the cells under study.

Kinesin-1 activity recorded in living cells with a precipitating dye FIB-SEM data 1

Kinesin-1 activity recorded in living cells with a precipitating dye FIB-SEM dataset 1 - QPDTf precipitating dye with HeLa cells

Classification of pseudocalcium visual responses from mouse retinal ganglion cells

The dataset includes spike data of 9 different recordings from mouse retina ganglion cells and the Pseudocalcium traces after convolving spikes with OGB kernel.

opencc-zeroJan 2021View details →

Data from: Intrinsic growth heterogeneity of mouse leukemia cells underlies differential susceptibility to a growth-inhibiting anticancer drug

Cancer cell populations consist of phenotypically heterogeneous cells. Growing evidence suggests that pre-existing phenotypic differences among cancer cells correlate with differential susceptibility to anticancer drugs and eventually lead to a relapse. Such phenotypic differences can arise not only externally driven by the environmental heterogeneity around individual cells but also internally by the intrinsic fluctuation of cells. However, the quantitative characteristics of intrinsic phenotypic heterogeneity emerging even under constant environments and their relevance to drug susceptibility remain elusive. Here we employed a microfluidic device, mammalian mother machine, for studying the intrinsic heterogeneity of growth dynamics of mouse lymphocytic leukemia cells (L1210) across tens of generations. The generation time of this cancer cell line had a distribution with a long tail and a heritability across generations. We determined that a minority of cell lineages exist in a slow-cycling state for multiple generations. These slow-cycling cell lineages had a higher chance of survival than the fast-cycling lineages under continuous exposure to the anticancer drug Mitomycin C. This result suggests that heritable heterogeneity in cancer cells' growth in a population influences their susceptibility to anticancer drugs.

opencc-zeroJun 2021View details →

The cell adhesion molecule Sdk1 shapes assembly of a retinal circuit that detects localized edges

Nearly 50 different mouse retinal ganglion cell (RGC) types sample the visual scene for distinct features. RGC feature selectivity arises from its synapses with a specific subset of amacrine (AC) and bipolar cell (BC) types, but how RGC dendrites arborize and collect input from these specific subsets remains poorly understood. Here we examine the hypothesis that RGCs employ molecular recognition systems to meet this challenge. By combining calcium imaging and type-specific histological stains we define a family of circuits that express the recognition molecule Sidekick 1 (Sdk1) which include a novel RGC type (S1-RGC) that responds to local edges. Genetic and physiological studies revealed that Sdk1 loss selectively disrupts S1-RGC visual responses which result from a loss of excitatory and inhibitory inputs and selective dendritic deficits on this neuron. We conclude that Sdk1 shapes dendrite growth and wiring to help S1-RGCs become feature selective.

opencc-zeroJun 2021View details →

Phosphotyrosine peptide abundance in control and Cul5-deficient MCF10A cells

The Cullin 5 RING ligase complex inhibits Src activity and Src-dependent transformation of MCF10A epithelial cells, in part by targeting pY proteins such as pYCas for degradation by the ubiquitin-proteasome system (Teckchandani et al., 2014). Because overexpression of Cas alone did not phenocopy CRL5 inhibition (Teckchandani et al., 2014), we infer that CRL5 down-regulates additional pY proteins that become limiting when Cas is over-expressed. We sought to identify such pY proteins by screening for pY peptides whose abundance increases when Cul5 is inhibited. To this end, control and Cul5-deficient MCF10A cells were lysed under denaturing conditions, proteins were digested with trypsin, and peptides were labeled with isobaric TMT tags for quantitative pY proteomics (Zhang et al., 2007). In one experiment, samples were prepared from control and Cul5-deficient cells that were starved for epidermal growth factor (EGF) for 0, 24 or 72 hr. Starvation time had no systematic effect on peptide abundance, so, in a second experiment, we prepared biological triplicate samples from growing control and Cul5-deficient cells. Sixteen pY peptides increased significantly in Cul5-deficient cells in both experiments, including pY128 from Cas and pY117 and pY266 from BCAR3.

opencc-zeroDec 2019View details →

Spectrum of mutational signatures in T-cell lymphoma reveals a key role for UV radiation in mycosis fungoides and Sezary syndrome

T-cell non-Hodgkin's lymphomas (NHL) develop following transformation of tissue resident T-cells. We performed a meta-analysis of mutational catalogues derived from whole exome sequencing data from 403 patients with eight subtypes of T-cell NHL to identify mutational signatures and recurrent gene mutations associated with specific causal peaks within these signatures. Signature 1, indicative of age-related deamination, was prevalent across all T-cell NHL subtypes, reflecting the derivation of these malignancies from memory T-cell subsets. Adult T-cell leukemia-lymphoma (ATLL) was specifically associated with signature 17, which was found to strongly correlate with the IRF4 K59R mutation that is exclusive to ATLL. Signature 7, implicating UV exposure as a potential initiating factor was uniquely identified in cutaneous T-cell lymphoma, contributing 52% of the mutational burden in mycosis fungoides and 23% in Sezary syndrome. Importantly this UV signature was observed in CD4+ T-cells isolated from blood suggesting extensive re-circulation of these T-cells through both skin and blood and strongly implicating a role for UV in the pathogenesis of cutaneous T-cell lymphoma.

opencc-zeroMar 2020View details →

Data from Native adiponectin in serum binds to mammalian cells expressing T-cadherin, but not AdipoRs or calreticulin

Adiponectin is an adipocyte-derived atypically abundant circulating factor that protects various organs and tissues through its receptors, AdipoRs, calreticulin, and T-cadherin. To identify the major binding partner of circulating native adiponectin, we expressed these receptors on the surface of HEK293 cells. Adiponectin, either that in mouse or human serum, purified from serum, or produced by mammalian cells, bound to cells expressing T-cadherin, but not to those expressing AdipoR1 or calreticulin. The stable introduction of T-cadherin and AdipoR1 into CHO cells resulted in the cell surface localization of these receptors. Native adiponectin in serum bound to cells expressing T-cadherin, not to those expressing AdipoR1. The knockdown of T-cadherin, but not AdipoRs resulted in the significant attenuation of native adiponectin binding to C2C12 myotubes. Therefore, native adiponectin binding depended on the amount of T-cadherin expressed in HEK293 cells, CHO cells, and C2C12 myotubes. Collectively, our mammalian cell-based studies suggest that T-cadherin is the major binding partner of native adiponectin in serum.

opencc-zeroDec 2017View details →

Data from: Of puzzles and pavements: a quantitative exploration of leaf epidermal cell shape

Epidermal cells of leaves are diverse: tabular pavement cells, trichomes, and stomatal complexes. Pavement cells from the monocot Zea mays (maize) and the eudicot Arabidopsis thaliana (Arabidopsis) have highly undulate anticlinal walls. The molecular basis for generating these undulating margins has been extensively investigated in these species. This has led to two assumptions: first, that particular plant lineages are characterized by particular pavement cell shapes; and second, that undulatory cell shapes are common enough to be model shapes. To test these assumptions, we quantified pavement cell shape in epidermides from the leaves of 278 vascular plant taxa. We found that monocot pavement cells tended to have weakly undulating margins, fern cells had strongly undulating margins, and eudicot cells showed no particular undulation degree. Cells with highly undulating margins, like those of Arabidopsis and maize, were in the minority. We also found a trend towards more undulating cell margins on abaxial leaf surfaces; and that highly elongated leaves in ferns, monocots and gymnosperms tended to have highly elongated cells. Our results reveal the diversity of pavement cell shapes, and lays the quantitative groundwork for testing hypotheses about pavement cell form and function within a phylogenetic context.

opencc-zeroDec 2017View details →

Data from: Response to persistent er stress in plants: a multiphasic process that transitions cells from prosurvival activities to cell death

The unfolded protein response (UPR) is a highly conserved response that protects plants from adverse environmental conditions. The UPR is elicited by endoplasmic reticulum (ER) stress, in which unfolded and misfolded proteins accumulate within the ER. Here, we induced the UPR in maize (Zea mays) seedlings to characterize the molecular events that occur over time during persistent ER stress. We found that a multiphasic program of gene expression was interwoven among other cellular events, including the induction of autophagy. One of the earliest phases involved the degradation by regulated IRE1-dependent RNA degradation (RIDD) of RNA transcripts derived from a family of peroxidase genes. RIDD resulted from the activation of ZmIRE1 for promiscuous ribonuclease activity that attacks the mRNAs of secreted proteins. This was followed by an upsurge in expression of the canonical UPR genes indirectly driven by ZmIRE1 due to its splicing of Zmbzip60 to make an active transcription factor that directly upregulates many of the UPR genes. At the peak of UPR gene expression, a global wave of alternative RNA processing led to the production of many aberrant UPR gene transcripts, likely tempering the ER stress response. During later stages of ER stress, ZmIRE1's activity declined as did the expression of survival modulating genes, Bax inhibitor1 and Bcl-2-associated athanogene7, amidst a rising tide of cell death. Thus, in response to persistent ER stress, maize seedlings embark on a course of gene expression and cellular events progressing from adaptive responses to cell death.

opencc-zeroFeb 2020View details →

Somatic copy number and structural variation in RPE-1 cells with induced chromosomal instability

The chromosome breakage-fusion-bridge (BFB) cycle is a mutational process that produces gene amplification and genome instability. Signatures of BFB cycles can be observed in cancer genomes alongside chromothripsis, another catastrophic mutational phenomenon. Here, we explain this association by elucidating a mutational cascade, downstream of <a>th</a>e single cell division error of chromosome bridge formation, that rapidly generates extreme genomic complexity. We show that actomyosin forces are required for initial bridge breakage and mutagenesis, following which chromothripsis accumulates with aberrant interphase replication of bridge DNA. This is then followed by an unexpected burst of DNA replication in the next mitosis, generating extensive DNA damage. During this second cell division, broken bridge chromosomes frequently mis-segregate and form micronuclei, promoting additional chromothripsis. We <a>fu</a>rther show that this mutational cascade generates the continuing evolution and sub-clonal heterogeneity characteristic of many human cancers.

openother-openJun 2021View details →

broadinstitute/lincs-cell-painting: Full release of LINCS Cell Painting dataset

Summary This release contains finalized profile and metadata information for the CellProfiler-derived features from the LINCS Cell Painting dataset. We assayed two batches of data and applied an image analysis pipeline using CellProfiler to segment cells and extract morphology features. Using the CellProfiler output, we applied an image-based profiling pipeline to process the morphology profiles into an analysis-ready form. In this repository, we provide the full image-based profiling pipeline we used to process the data, as well as most of the intermediate data. Data counts <ul> <li>Two batches ("2016_04_01_a549_48hr_batch1" and "2017_12_05_Batch2")</li> <li>159,717,488 unique cells total</li> </ul> 2016_04_01_a549_48hr_batch1 <ul> <li>52,223 profiles (batch corrected)</li> <li>10,752 unique perturbations</li> <li>1,571 unique compounds</li> <li>1 time point (48 hour)</li> <li>7 doses</li> <li>1 cell line (A549)</li> <li>110,012,425 unique cells</li> </ul> 2017_12_05_Batch2 <ul> <li>51,447 profiles (batch corrected)</li> <li>10,368 unique perturbations</li> <li>349 unique compounds</li> <li>3 time points (6 hour, 24 hour, 48 hour)</li> <li>6 doses</li> <li>3 cell lines (A549, MCF7, U2OS)</li> <li>49,705,063 unique cells</li> </ul>