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12,455 results for “Promoters”
Growth monitoring and promotion_Riskofbias2
<p>Presents the risk of bias assessments for the Cochrane review: "impact of growth monitoring and promotion on health indicators in children under 5 in low - and middle- income countries"</p>
Data from: HIV-1 capsid stability enables inositol phosphate-independent infection of target cells and promotes integration into genes
<p>The mature HIV-1 capsid is stabilized by host and viral determinants. The capsid protein CA binds to the cellular metabolites inositol hexakisphosphate (IP6) and its precursor inositol (1, 3, 4, 5, 6) pentakisphosphate (IP5) to stabilize the mature capsid. In target cells, capsid destabilization by the antiviral compounds lenacapavir and PF74 reveals an HIV-1 infectivity defect due to IP5/IP6 (IP5/6) depletion. To test whether intrinsic HIV-1 capsid stability and/ or host factor binding determines HIV-1 insensitivity to IP5/6 depletion, a panel of CA mutants was assayed for infection of IP5/6-depleted T cells and wildtype cells. Four CA mutants with unstable capsids exhibited dependence on host IP5/6 for infection and reverse transcription (RTN). Adaptation of one such mutant, Q219A, by spread in culture resulted in Vpu truncation and a capsid three-fold interface mutation, T200I. T200I increased intrinsic capsid stability as determined by <em>in vitro</em> uncoating of purified cores and partially reversed the IP5/6-dependence in target cells for each of the four CA mutants. T200I further rescued the changes to lenacapavir sensitivity associated with the parental mutation. The premature dissolution of the capsid caused by the IP5/6-dependent mutations imparted a unique defect in integration targeting that was rescued by T200I. Collectively, these results demonstrate that T200I restored other capsid functions after RTN for the panel of mutants. Thus, the hyperstable T200I mutation stabilized the instability defects imparted by the parental IP5/6-dependent CA mutation. The contribution of Vpu truncation to mutant adaptation was linked to BST-2 antagonization, suggesting that cell-to-cell transfer promoted replication of the mutants. We conclude that interactions at the three-fold interface are adaptable, key mediators of capsid stability in target cells and are able to antagonize even severe capsid instability to promote infection.</p>
[Data S10] Microbiota dictate T cell clonal selection to promote graft-vs-host disease after stem cell transplantation
<p>Data S10. 10x genomics sequencing data files for Figure 5. Matrix file "sample_filtered_feature_bc_matrix.h5" and V(D)J annotations "filtered_contig_annotations.csv" are included below. Accompanying code can be found at https://github.com/acyeh-lab/2023/tree/main/scseq.</p>
Transient acetaldehyde production by SO2 producing S. cerevisiae promotes survival of Oenococcus oeni during co-fermentation
<p>Stuck or sluggish malolactic fermentation (MLF) can be problematic in limiting wine conditions, particularly white and sparkling base musts / wines. In these cases, knowledge of yeast-bacteria strain compatibility and the amount of sulfur dioxide (SO<sub>2</sub>) a yeast strain produces are important considerations for successful MLF.</p> <p>Here, the effects of yeast-derived SO<sub>2</sub> production on <em>O. oeni</em> survival was investigated in laboratory- and pilot-scale co-fermentations in Chardonnay. Further to the <em>S</em>. <em>cerevisiae</em> strain affecting <em>O. oeni</em> survival and MLF, we show that SO<sub>2</sub> production by yeast (to approximately 65 mg/L) can be uncoupled from <em>O. oeni </em>survival in early stages of co-fermentation. Bacterial survival with certain SO<sub>2</sub>-producing yeast strains was correlated with early, transient formation of a high concentration of acetaldehyde. Upon co-inoculation, an extremely low concentration range (approximately 1–44 µg/L) of calculated molecular SO<sub>2</sub> is indicated to regulate <em>O</em>. <em>oeni</em> survival. <span>Possible strain-dependent sensitivity of <em>O. oeni</em> to bound SO<sub>2</sub> may also occur, although the extent and nature of such inhibition by the SO<sub>2</sub> adduct itself during co-fermentation remains unclear. </span></p> <p><span>Choice of co-inoculation yeast strain also influenced wine diacetyl concentration, </span>which was only detected in wines co-inoculated with high-SO<sub>2</sub>-producing <em>S. cerevisiae </em>strains. <span>These wines also had comparatively high citation frequency for a buttery sensory attribute. </span>Both the SO<sub>2</sub> and acetaldehyde production capacity of yeasts are therefore seen as meaningful co-inoculation selection criteria. <span>The range of yeast strains suitable for MLF induction by co-inoculation could be widened to include SO<sub>2</sub>-producing strains which transiently produce an early, high concentration of acetaldehyde. Reliance on total / bound SO<sub>2</sub> concentration may also potentially provide an inaccurate measure of SO<sub>2</sub> toxicity towards <em>O. oeni</em>, particularly for co-inoculation, and the impact of low, equilibrium concentrations of molecular SO<sub>2</sub> should also be considered. </span></p>
Data from: Multi-locus homozygosity promotes actuarial senescence in a wild mammal
<ol> <li>Genome-wide homozygosity, caused for example by inbreeding, is expected to have deleterious effects on survival and/or reproduction. Evolutionary theory predicts that any fitness costs are likely to be detected in late life because natural selection will filter out negative impacts on younger individuals with greater reproductive value.</li> <li>Here we infer associations between multi-locus homozygosity, sex, disease, and age-dependent mortality risks using Bayesian analysis of the life histories of wild European badgers (<em>Meles</em> <em>meles</em>) in a population naturally infected with <em>Mycobacterium</em> <em>bovis</em> (the causative agent of bovine tuberculosis).</li> <li>We find important effects of multi-locus homozygosity on all parameters of the Gompertz-Makeham mortality hazard function, but particularly in later-life.</li> <li>Our findings confirm the predicted association between genomic homozygosity and actuarial senescence. Increased homozygosity is particularly associated with an earlier onset, and greater rates of actuarial senescence, regardless of sex. The association between homozygosity and actuarial senescence is further amplified among badgers putatively infected with bovine tuberculosis.</li> <li>These results recommend further investigation into the ecological and behavioural processes that result in genome-wide homozygosity, and focused work on whether homozygosity is harmful or beneficial during early life-stages.</li> </ol>
Intrinsically Disordered Regions Promote Protein Refoldability and Facilitate Retrieval from Biomolecular Condensates–Peptide Quantifications
<p>Many eukaryotic proteins contain intrinsically disordered regions (IDRs) that intersperse globular folded domains, in contrast with bacterial proteins which are typically highly globular. Recent years have seen great progress in identifying biological functions associated with these elusive protein sequence: in specific cases, they mediate liquid- liquid phase separation, perform molecular recognition, or act as sensors to changes in the environment. Nevertheless, only a small number of IDRs have annotated functions despite their presence in 64% of yeast proteins, stimulating some to question what ‘general purpose’ they may serve. Here, by interrogating the refoldability of two fungal proteomes (Saccharomyces cerevisiae and Neurosporra crassa), we show that IDRs render their host proteins more refoldable from the denatured state, allowing them to cohere more closely to Anfinsen’s thermodynamic hypothesis. The data provide an exceptionally clear picture of which biophysical and topological characteristics enable refoldability. Moreover, we find that almost all yeast proteins that partition into stress granules during heat shock are refoldable, a finding that holds for other condensates such as P-bodies and the nucleolus. Finally, we find that the Hsp104 unfoldase is the principal actor in mediating disassembly of heat stress granules and that the efficiency with which condensed proteins are returned to the soluble phase is also well explained by refoldability. Hence, these studies establish spontaneous refoldability as an adaptive trait that endows proteins with the capacity to reform their native soluble structures following their extraction from condensates. Altogether, our results provide an intuitive model for the function of IDRs in many multidomain proteins and clarifies their relationship to the phenomenon of biomolecular condensation.</p> <p>This dataset provides peptide quantifications (and their respective P-values) from three separate types of experiments used to support the claims in this study.</p> <p>1. Peptide quantifications from global refolding reactions, assessed with limited-proteolysis mass spectrometry (LiP-MS), carried out on two fungal organisms (S. cerevisiae [yeast] & N. crassa), at three refolding times, repeated on three separate iterations (for yeast).</p> <p>2. Peptide quantifications from LiP-MS experiments conducted on yeast extracts during heat shock or recovery from heat shock</p> <p>3. Annotations for peptides in #1 that are associated with linker regions between folded domains.</p>
Matrix N, TEs vs promoters, weighted with L = 2.5e5kb, hg19
<p>Regulatory susceptibility matrix N, with rows as hg19 protein coding genes and columns as TE subfamilies. For any given gene, regulatory TEs are strictly out of any promoter and any exon belonging to that gene. The contribution of each single TE is weighted by a gaussian kernel centered on the closest promoter of that gene, with a bandwidth L = 2.5e5kb</p>
Dataset - ExperDF-Onto: an Ontology for Promoting Controlled Experimentation in Digital Forensics
<p>Dataset - ExperDF-Onto: an Ontology for Promoting Controlled Experimentation in Digital Forensics</p>
Data from: Shifts in mutation bias promote mutators by altering the distribution of fitness effects
<p>Recent experimental evidence demonstrates that shifts in mutational biases, for example increases in transversion frequency, can change the distribution of fitness effects of mutations (DFE). In particular, reducing or reversing a prevailing bias can increase the probability that a <em>de novo</em> mutation is beneficial. It has also been shown that mutator bacteria are more likely to emerge if the beneficial mutations they generate have a larger effect-size than observed in the wildtype. Here, we connect these two results, demonstrating that mutator strains that reduce or reverse a prevailing bias have a positively-shifted DFE, which in turn can dramatically increase their emergence probability. Since changes in mutation rate and bias are often coupled through the gain and loss of DNA repair enzymes, our results predict that the invasion of mutator strains will be facilitated by shifts in mutation bias that offer improved access to previously under-sampled beneficial mutations.</p>
Embedded machine learning to promote detection of unsafe environments
<p>Datasets used to train and validate the devices and model described in the paper "<strong>Embedded machine learning of IoT streams to promote early detection of unsafe environments</strong>"</p>
Data Set: Promoting Open Science in Test-Driven Software Experiments
<p>Data set for reproduction purposes (tabular data is stored using Apache's Parqet format).</p>
Data and code for: Somatostatin peptide signaling dampens cortical circuits and promotes exploratory behavior
<p>Our dataset reflects the data and code used in Brockway et al., Cell Reports. We sought to characterize the unique role of somatostatin (SST) in the prelimbic (PL) cortex. We perform slice electrophysiology in pyramidal and GABAergic neurons to characterize the pharmacological mechanism of SST signaling, and fiber photometry of GCaMP6f fluorescent calcium signals from SST neurons to characterize the activity profile of SST neurons during exploration of an elevated plus maze (EPM) and open field test (OFT). We used local delivery of a broad SST receptor (SSTR) agonist and antagonist to test causal effects of SST signaling. SSTR activation hyperpolarizes layer 2/3 pyramidal neurons, an effect that is recapitulated with optogenetic stimulation of SST neurons. SST neurons in PL are activated during EPM and OFT exploration, and SSTR agonist administration directly into the PL enhances open-arm exploration in the EPM. This work describes a broad ability for SST peptide signaling to modulate microcircuits within the prefrontal cortex and related exploratory behaviors.</p>
TKS5 mediates the formation of podosome rosettes in pulmonary fibroblasts and promotes fibrosis.
<p>Data and code for recreation of computationally-created figures of the paper: Barbayianni I., Kanellopoulou P. et al. <strong><em>SRC and TKS5-mediated podosome formation promotes Extracellular matrix invasion and pulmonary fibrosis</em></strong>. 2023</p> <p>Raw QuantSeq and re-analyzed single cell RNA-seq data can be found at GSE220982 and GSE122960, respectively.</p>
Human OPRM1 and murine Oprm1 promoter driven viral constructs for genetic access to μ-opioidergic cell-types
<p>With concurrent global epidemics of chronic pain and opioid use disorders, there is a critical need to identify, target and manipulate specific cell populations expressing the mu-opioid receptor (MOR). However, available tools and transgenic models for gaining long-term genetic access to MOR+ neural cell-types and circuits involved in modulating pain, analgesia and addiction across species are limited. To address this, we developed a catalog of MOR promoter (<em>MORp</em>) based constructs packaged into adeno-associated viral vectors that drive transgene expression in MOR+ cells. <em>MORp</em> constructs designed from promoter regions upstream of the mouse <em>Oprm1</em> gene (<em>mMORp</em>) were validated for transduction efficiency and selectivity in endogenous MOR+ neurons in the brain, spinal cord, and periphery of mice, with additional studies revealing robust expression in rats, shrews, and human induced pluripotent stem cell (iPSC)-derived nociceptors. The use of <em>mMORp</em> for <em>in vivo</em> fiber photometry, behavioral chemogenetics, and intersectional genetic strategies is also demonstrated. Lastly, a human designed <em>MORp</em> (<em>hMORp</em>) efficiently transduced macaque cortical <em>OPRM1</em>+ cells. Together, our <em>MORp</em> toolkit provides researchers cell-type specific genetic access to target and functionally manipulate mu-opioidergic neurons across a range of vertebrate species and translational models for pain, addiction, and neuropsychiatric disorders.</p>
Ether lipid biosynthesis promotes lifespan extension and enables diverse prolongevity paradigms in Caenorhabditis elegans
<p class="MsoNormal">Biguanides, including the world's most prescribed drug for type 2 diabetes, metformin, not only lower blood sugar but also promote longevity in preclinical models. Epidemiologic studies in humans parallel these findings, indicating favorable effects of metformin on longevity and on reducing the incidence and morbidity associated with aging-related diseases. Despite this promise, the full spectrum of molecular effectors responsible for these health benefits remains elusive. Through unbiased screening in <em>C. elegans</em>, we uncovered a role for genes necessary for ether lipid biosynthesis in the favorable effects of biguanides. We demonstrate that biguanides prompt lifespan extension by stimulating ether lipid biogenesis. Loss of the ether lipid biosynthetic machinery also mitigates lifespan extension attributable to dietary restriction, target of rapamycin (TOR) inhibition, and mitochondrial electron transport chain inhibition. A possible mechanistic explanation for this finding is that ether lipids are required for activation of longevity-promoting, metabolic stress defenses downstream of the conserved transcription factor <em>skn-1/</em>Nrf. In alignment with these findings, overexpression of a single, key, ether lipid biosynthetic enzyme, <em>fard-1</em>/FAR1, is sufficient to promote lifespan extension. These findings illuminate the ether lipid biosynthetic machinery as a novel therapeutic target to promote healthy aging.</p>
Data from: A comparative analysis of stably expressed genes across diverse angiosperms exposes flexibility in underlying promoter architecture
<p><span>Promoters regulate both the amplitude and pattern of gene expression—key factors needed for optimization of many synthetic biology applications. Previous work in <em>Arabidopsis</em> found that promoters that contain a TATA-box element tend to be expressed only under specific conditions or in particular tissues, while promoters which lack any known promoter elements, thus designated as Coreless, tend to be expressed more ubiquitously. To test whether this trend represents a conserved promoter design rule, we identified stably expressed genes across multiple angiosperm species using publicly available RNA-seq data. Comparisons between core promoter architectures and gene expression stability revealed differences in core promoter usage in monocots and eudicots. Furthermore, when tracing the evolution of a given promoter across species, we found that core promoter type was not a strong predictor of expression stability. Our analysis suggests that core promoter types are correlative rather than causative in promoter expression patterns and highlights the challenges in finding or building constitutive promoters that will work across diverse plant species.</span></p>
Spatial sorting promotes rapid (mal)adaptation in the red-shouldered soapberry bug after hurricane-driven local extinctions
<p>Predicting future evolutionary change is a critical challenge in the Anthropocene as geographic range shifts and local extinction emerge as hallmarks of planetary change. Hence, spatial sorting – a driver of rapid evolution in which dispersal-associated traits accumulate along expanding range edges and within recolonized habitats – might be of growing importance in ecology and conservation. We report on the results of a natural experiment that monitored re-colonization of host plants by the seed-feeding, red-shouldered soapberry bug, <em>Jadera</em> <em>haematoloma</em>, after local extinctions from catastrophic flooding in an extreme hurricane. We tested the contribution of spatial sorting to generate rapid and persistent evolution in dispersal traits, as well as in feeding traits unrelated to dispersal. Long-winged dispersal forms accumulated in re-colonized habitats, and due to genetic correlation, mouthparts also became longer, and this shift persisted across generations. Those longer mouthparts were likely adaptive on one host plant species but maladaptive on two others based on matching the optimum depth of seeds within their host fruits. Moreover, spatial sorting eroded recently evolved adaptive divergence in mouthpart length among all host-associated biotypes, an outcome pointing to profound practical consequences of the extreme weather event for local adaptation, population resilience, and evolutionary futures.</p>
Anisogamy does not always promote the evolution of mating competition traits in males
<p>Anisogamy has evolved in most sexually reproducing multicellular organisms allowing the definition of the male and female sexes, producing small and large gametes. Anisogamy, as the initial sexual dimorphism, is a good starting point to understand the evolution of further sexual dimorphisms. For instance, it is generally accepted that anisogamy sets the stage for more intense mating competition in males than in females. We argue that this idea stems from a restrictive assumption on the conditions under which anisogamy evolved in the first place: the absence of sperm limitation (assuming that all female gametes are fertilized). Here, we relax this assumption and present a model that considers the coevolution of gamete size with a mating competition trait, starting in a population without dimorphism. We vary gamete density to produce different scenarios of gamete limitation. We show that, while at high gamete density the evolution of anisogamy always results in male investment in competition, gamete limitation at intermediate gamete densities allows for either females or males to invest more into mating competition. Our results thus suggest that anisogamy does not always promote mating competition among males. The conditions under which anisogamy evolves matter, as well as the competition trait.</p>
Airway environment drives the selection of quorum sensing mutants and promote Staphylococcus aureus chronic lifestyle
<p>Sequence data linked to the manuscript "Airway environment drives the selection of quorum sensing mutants and promote <em>Staph</em><em>ylococcus</em><em> aureus</em> chronic lifestyle"</p> <p>- Shotgun metagenomic from sputa of Patients A B C H J</p> <p>- 10 hemolytic and 10 non-hemolytic isolates from competition assays at day 5</p>
PHRF1 promotes the class switch recombination of IgA in CH12F3-2A cells-Dataset
<p><span> PHRF1 is an E3 ligase that promotes TGF-</span><span>B</span><span> signaling by ubiquitinating a homeodomain repressor TG-interacting factor (TGIF). The suppression of PHRF1 activity by PML-RAR</span><span> facilitates the progression of acute promyelocytic leukemia (APL). PHRF1 also contributes to non-homologous end-joining in response to DNA damage by linking H3K36me3 and NBS1 with DNA repair machinery. However, its role in class switch recombination (CSR) is not well understood. In this study, we report the importance of PHRF1 in IgA switching in CH12F3-2A cells and CD19-Cre mice. Our studies revealed that Crispr-Cas9 mediated PHRF1 knockout and shRNA-silenced CH12F3-2A cells reduced IgA production, as well as decreased the amounts of PARP1, NELF-A, and NELF-D. The introduction of PARP1 could partially restore IgA production in PHRF1 knockout cells. Intriguingly, IgA, as well as IgG1, IgG2a, and IgG3, switchings were not significantly decreased in PHRF1 deficient splenic B lymphocytes isolated from CD19-Cre mice. The levels of PARP1 and NELF-D were not decreased in PHRF1-depleted primary splenic B cells. Overall, our findings suggest that PHRF1 may modulate IgA switching in CH12F3-2A cells.</span></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.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
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.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.