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7,327 results for “pathways”
Data from: Sexual conflict over remating interval is modulated by the sex peptide pathway
Sexual conflict, in which the evolutionary interests of males and females diverge, shapes the evolution of reproductive systems across diverse taxa. Here, we used the fruit fly to study sexual conflict in natural, three-way interactions comprising a female, her current and previous mates. We manipulated the potential for sexual conflict by using sex peptide receptor (SPR) null females and by varying remating from 3 to 48 h, a period during which natural rematings frequently occur. SPR-lacking females do not respond to sex peptide (SP) transferred during mating and maintain virgin levels of high receptivity and low fecundity. In the absence of SPR, there was a convergence of fitness interests, with all individuals gaining highest productivity at 5 h remating. This suggests that the expression of sexual conflict was reduced. We observed an unexpected second male-specific advantage to early remating, resulting from an increase in the efficiency of second male sperm use. This early window of opportunity for exploitation by second males depended on the presence of SPR. The results suggest that the SP pathway can modulate the expression of sexual conflict in this system, and show how variation in the selective forces that shape conflict and cooperation can be maintained.
Data from: Charting the NF-κB pathway interactome map
Inflammation is part of a complex physiological response to harmful stimuli and pathogenic stress. The five components of the Nuclear Factor κB (NF-κB) family are prominent mediators of inflammation, acting as key transcriptional regulators of hundreds of genes. Several signaling pathways activated by diverse stimuli converge on NF-κB activation, resulting in a regulatory system characterized by high complexity. It is increasingly recognized that the number of components that impinges upon phenotypic outcomes of signal transduction pathways may be higher than those taken into consideration from canonical pathway representations. Scope of the present analysis is to provide a wider, systemic picture of the NF-κB signaling system. Data from different sources such as literature, functional enrichment web resources, protein-protein interaction and pathway databases have been gathered, curated, integrated and analyzed in order to reconstruct a single, comprehensive picture of the proteins that interact with, and participate to the NF-κB activation system. Such a reconstruction shows that the NF-κB interactome is substantially different in quantity and quality of components with respect to canonical representations. The analysis highlights that several neglected but topologically central proteins may play a role in the activation of NF-κB mediated responses. Moreover the interactome structure fits with the characteristics of a bow tie architecture. This interactome is intended as an open network resource available for further development, refinement and analysis.
Data from: Differential Expression Analysis for Pathways
Life science technologies generate a deluge of data that hold the keys to unlocking the secrets of important biological functions and disease mechanisms. We present DEAP, Differential Expression Analysis for Pathways, which capitalizes on information about biological pathways to identify important regulatory patterns from differential expression data. DEAP makes significant improvements over existing approaches by including information about pathway structure and discovering the most differentially expressed portion of the pathway. On simulated data, DEAP significantly outperformed traditional methods: with high differential expression, DEAP increased power by two orders of magnitude; with very low differential expression, DEAP doubled the power. DEAP performance was illustrated on two different gene and protein expression studies. DEAP discovered fourteen important pathways related to chronic obstructive pulmonary disease and interferon treatment that existing approaches omitted. On the interferon study, DEAP guided focus towards a four protein path within the 26 protein Notch signalling pathway.
Data from: Health Canada's use of accelerated review pathways and therapeutic innovation, 1995-2016: a cohort study
Objectives: This study examines the use of accelerated approval pathways by Health Canada over the period 1995 to 2016 inclusive and the relationship between the use of these pathways and the therapeutic gain offered by new products. Design: Cohort study. Data sources: Therapeutic Products Directorate, Biologics and Genetic Therapies Directorate, Notice of Compliance database, Notice of Compliance with conditions web site, Patented Medicine Prices Review Board, La revue Prescrire, World Health Organization (WHO) Anatomical Therapeutic Chemical (ATC) classification system. Interventions: None. Primary and secondary outcomes: Percent of new drugs evaluated by Health Canada that went through an accelerated pathway between 1995 and 2016 inclusive. Kappa values comparing the review status to assessments of therapeutic value for individual drugs. Results: 438 (70.3%) drugs went through the standard pathway, 185 (29.7%) an accelerated pathway. Therapeutic evaluations were available for 509 drugs. Health Canada used an accelerated approval pathway for 159 of the 509 drugs whereas only 55 were judged to be therapeutically innovative. The Kappa value for the entire period for all 509 drugs was 0.276 (95% CI 0.194, 0.359) or fair. Conclusion: Health Canada's use of accelerated approvals was stable over the entire time period. Its ability to predict which drugs will offer a major therapeutic gain is relatively poor. The findings in this study should provoke a discussion about whether Health Canada should continue to use these pathways and if so how their use can be improved.
Data from: Fe-S cluster biosynthesis controls uptake of aminoglycosides in a ROS-less death pathway
All bactericidal antibiotics were recently proposed to kill by inducing reactive oxygen species (ROS) production, causing destabilization of iron-sulfur (Fe-S) clusters and generating Fenton chemistry. We find that the ROS response is dispensable upon treatment with bactericidal antibiotics. Furthermore, we demonstrate that Fe-S clusters are required for killing only by aminoglycosides. In contrast to cells, using the major Fe-S cluster biosynthesis machinery, ISC, cells using the alternative machinery, SUF, cannot efficiently mature respiratory complexes I and II, resulting in impendence of the proton motive force (PMF), which is required for bactericidal aminoglycoside uptake. Similarly, during iron limitation, cells become intrinsically resistant to aminoglycosides by switching from ISC to SUF and down-regulating both respiratory complexes. We conclude that Fe-S proteins promote aminoglycoside killing by enabling their uptake.
Data from: Novel evolutionary pathways of sex-determining mechanisms
Evolutionary transitions between sex-determining mechanisms (SDMs) are an enigma. Among vertebrates, individual sex (male or female) is primarily determined by either genes (genotypic sex determination, GSD) or embryonic incubation temperature (temperature-dependent sex determination, TSD), and these mechanisms have undergone repeated evolutionary transitions. Despite this evolutionary lability, transitions from GSD (i.e. from male heterogamety, XX/XY, or female heterogamety, ZZ/ZW) to TSD are an evolutionary conundrum, as they appear to require crossing a fitness valley arising from the production of genotypes with reduced viability owing to being homogametic for degenerated sex chromosomes (YY or WW individuals). Moreover, it is unclear whether alternative (e.g. mixed) forms of sex-determination can persist across evolutionary time. It has previously been suggested that transitions would be easy if temperature-dependent sex-reversal (e.g. XX male or XY female) were asymmetrical, occurring only in the homogametic sex. However, only recently has a mechanistic model of sex determination emerged that may allow such asymmetrical sex-reversal. We demonstrate that selection for TSD in a realistic sex-determining system can readily drive evolutionary transitions from GSD to TSD that do not require the production of YY or WW individuals. In XX /XY systems, sex-reversal (female to male) occurs in a portion of the XX individuals only, leading to the loss of the Y allele (or chromosome) from the population as XX individuals mate with each other. The outcome is a population of XX individuals whose sex is determined by incubation temperature (TSD). Moreover, our model reveals a novel evolutionarily stable state representing a mixed-mechanism system that has not been revealed by previous approaches. This study solves two long-standing puzzles of the evolution of sex-determining mechanisms by illuminating the evolutionary pathways and endpoints.
Data from: Molecular evolution accompanying functional divergence of duplicated genes along the plant starch biosynthesis pathway
Background: Starch is the main source of carbon storage in the Archaeplastida. The Starch Biosynthesis Pathway (SBP) emerged from cytosolic glycogen metabolism shortly after plastid endosymbiosis and was redirected to the plastid stroma during the green lineage divergence. The SBP is a complex network of genes, most of which are members of large multigene families. While some gene duplications occurred in the Archaeplastida ancestor, most were generated during the SBP redirection process, and the remaining few paralogs were generated through compartmentalization or tissue specialization during the evolution of the land plants. In the present study, we tested models of duplicated gene evolution in order to understand the evolutionary forces that have led to the development of SBP in angiosperms. We combined phylogenetic analyses and tests on the rates of evolution along branches emerging from major duplication events in six gene families encoding SBP enzymes. Results: We found evidence of positive selection along branches following cytosolic or plastidial specialization in two starch phosphorylases and identified numerous residues that exhibited changes in volume, polarity or charge. Starch synthases, branching and debranching enzymes functional specializations were also accompanied by accelerated evolution. However, none of the sites targeted by selection corresponded to known functional domains, catalytic or regulatory. Interestingly, among the 13 duplications tested, 7 exhibited evidence of positive selection in both branches emerging from the duplication, 2 in only one branch, and 4 in none of the branches. Conclusions: The majority of duplications were followed by accelerated evolution targeting specific residues along both branches. This pattern was consistent with the optimization of the two sub-functions originally fulfilled by the ancestral gene before duplication. Our results thereby provide strong support to the so-called "Escape from Adaptive Conflict" (EAC) model. Because none of the residues targeted by selection occurred in characterized functional domains, we propose that enzyme specialization has occurred through subtle changes in affinity, activity or interaction with other enzymes in complex formation, while the basic function defined by the catalytic domain has been maintained.
Data from: Stimulation of the salicylic acid pathway aboveground recruits entomopathogenic nematodes belowground
Plant defense pathways play a critical role in mediating tritrophic interactions between plants, herbivores, and natural enemies. While the impact of plant defense pathway stimulation on natural enemies has been extensively explored aboveground, belowground ramifications of plant defense pathway stimulation are equally important in regulating subterranean pests and still require more attention. Here we investigate the effect of aboveground stimulation of the salicylic acid pathway through foliar application of the elicitor methyl salicylate on belowground recruitment of the entomopathogenic nematode, Steinernema diaprepesi. Also, we implicate a specific root-derived volatile that attracts S. diaprepesi belowground following aboveground plant stimulation by an elicitor. In four-choice olfactometer assays, citrus plants treated with foliar applications of methyl salicylate recruited S. diaprepesi in the absence of weevil feeding as compared with negative controls. Additionally, analysis of root volatile profiles of citrus plants receiving foliar application of methyl salicylate revealed production of d-limonene, which was absent in negative controls. The entomopathogenic nematode S. diaprepesi was recruited to d-limonene in two-choice olfactometer trials. These results reinforce the critical role of plant defense pathways in mediating tritrophic interactions, suggest a broad role for plant defense pathway signaling belowground, and hint at sophisticated plant responses to pest complexes.
Data from: Functional diversity and structural disorder in the human ubiquitination pathway
The ubiquitin-proteasome system plays a central role in cellular regulation and protein quality control (PQC). The system is built as a pyramid of increasing complexity, with two E1 (ubiquitin activating), few dozen E2 (ubiquitin conjugating) and several hundred E3 (ubiquitin ligase) enzymes. By collecting and analyzing E3 sequences from the KEGG BRITE database and literature, we assembled a coherent dataset of 563 human E3s and analyzed their various physical features. We found an increase in structural disorder of the system with multiple disorder predictors (IUPred – E1: 5.97%, E2: 17.74%, E3: 20.03%). E3s that can bind E2 and substrate simultaneously (single subunit E3, ssE3) have significantly higher disorder (22.98%) than E3s in which E2 binding (multi RING-finger, mRF, 0.62%), scaffolding (6.01%) and substrate binding (adaptor/substrate recognition subunits, 17.33%) functions are separated. In ssE3s, the disorder was localized in the substrate/adaptor binding domains, whereas the E2-binding RING/HECT-domains were structured. To demonstrate the involvement of disorder in E3 function, we applied normal modes and molecular dynamics analyses to show how a disordered and highly flexible linker in human CBL (an E3 that acts as a regulator of several tyrosine kinase-mediated signalling pathways) facilitates long-range conformational changes bringing substrate and E2-binding domains towards each other and thus assisting in ubiquitin transfer. E3s with multiple interaction partners (as evidenced by data in STRING) also possess elevated levels of disorder (hubs, 22.90% vs. non-hubs, 18.36%). Furthermore, a search in PDB uncovered 21 distinct human E3 interactions, in 7 of which the disordered region of E3s undergoes induced folding (or mutual induced folding) in the presence of the partner. In conclusion, our data highlights the primary role of structural disorder in the functions of E3 ligases that manifests itself in the substrate/adaptor binding functions as well as the mechanism of ubiquitin transfer by long-range conformational transitions.
Technological Pathways for Cost-Effective Steel Decarbonization
<p>The dataset and code were developed as part of research on cost-effective decarbonization of the global iron and steel plants.</p>
Exploring the Molecular Pathways of the Activation Process on PPARγ Recurrent Bladder Cancer Mutants
<p><span>The intricate involvement of Peroxisome Proliferator-Activated Receptor Gamma </span><span>(PPAR</span><span>γ</span><span>) in vital processes such as glucose homeostasis and adipogenesis is well </span><span>established. However, its multifaceted role in cancer, particularly in luminal bladder </span><span>cancer, remains a subject of intense debate. In this context, PPAR</span><span>γ</span><span>’s overexpression </span><span>and activation have been implicated in tumorigenesis. Notably, specific gain-of-function </span><span>mutations (M280I, I290M, and T475M) within PPAR</span><span>γ</span><span>’s ligand-binding domain have </span><span>been pinpointed in bladder cancer, correlating with receptor activation.</span><span> </span><span>Nonethe</span><span>less, the underlying molecular pathways prompted by these mutations remain obscure. <span>Here, we employed a dual-basin structure-based model (db SBM) to unveil the intricate </span><span>conformational dynamics that underlie the transition between PPAR</span><span>γ</span><span>’s inactive and </span><span>active states. Additionally, we explored the effects of the M280I, I290M, and T475M </span><span>mutations on this pivotal process. Our findings concur with existing literature, reveal</span><span>ing heightened ligand-independent transcriptional activity in the I290M and T475M </span><span>mutants compared to other variants.</span><span> </span><span>Importantly, both mutants displayed enhanced </span><span>stabilization of the active state relative to the wild-type receptor, and the I290M mu</span><span>tation promoted a remarkably specific transition route, rendering it a prime candidate </span><span>for further investigation. Electrostatic analysis pinpointed the pivotal role of residues </span><span>K303 and E488 in the activation cascade of I290M. This insight was substantiated by </span><span>biophysical assays, as disruption of the K303-E488 interaction curtailed the thermal </span><span>stabilization characteristic of the I290M mutation. These findings designate K303 and </span><span>E488 as potential targets for inhibitors aimed at modulating PPAR</span><span>γ</span><span> </span><span>activation, with </span><span>promising implications for refining bladder cancer prognosis. In sum, our study high</span><span>lights the remarkable predictive capabilities achieved through the integration of sim</span><span>ulation and cheminformatics methods, validated by biochemical experiments, to gain </span><span>deeper insights into molecular mechanisms of activation and identify target residues </span><span>for protein modulation.</span><br></span></p>
MetSim: Integrated Programmatic Access and Pathway Management for Xenobiotic Metabolism Simulators
<p>Underlying data for manuscript Groff L, Williams A, Shah I, Patlewicz G*. 2024. MetSim: Integrated Programmatic Access and Pathway Management for Xenobiotic Metabolism Simulators. Chem. Res. Toxicol <em>in press</em> <a href="https://doi.org/10.1021/acs.chemrestox.3c00398" rel="nofollow">https://doi.org/10.1021/acs.chemrestox.3c00398</a></p>
Epigenetic regulation of the autonomous pathway mediates the flowering of Arabidopsis thaliana
<p>Studies have shown that plant flowering time is affected by endogenous and exogenous factors, but the role of DNA methylation in flowering still remains unclear. Here, 27 <i>Arabidopsis thaliana</i> populations were used to determine how autonomous pathway gene methylation affects flowering differences by regulating gene expression patterns. DNA methylation analysis, qPCR and transgenic verification were performed. The flowering time of the <i>Arabidopsis</i> populations ranged from 19 to 55 days. Methylation of the coding regions of six upstream genes in the autonomous pathway, <i>FVE</i>,<i> FY</i>,<i> FLD</i>,<i> PEP</i>,<i> HDA5 </i>and<i> PPR 39-1</i>, was significantly correlated with flowering time and relative expression levels (<i>P</i> < 0.05). Expression of <i>FVE</i> and <i>FVE(CS) </i>separately through codon degeneracy substitution (resulting in a reduction in cytosine) led to early flowering (by 8 days and 25 days, respectively). The flowering times of the <i>FVE</i> and <i>FVE(CS)</i> transgenic plants and the Col-0 plants were associated with the number of methylated sites of <i>FVE</i> and <i>FVE(CS)</i>, resulting in the differential expression of <i>FVE</i> and <i>FVE(CS)</i>. Our findings suggest that the methylation of six key upstream transcription factors of the autonomous pathway in <i>Arabidopsis</i> regulates the expression level of these genes, leading to phenotypic differences in flowering.</p>
Dandelion root extracts abolish MAPK pathways to ameliorate experimental mouse ulcerative colitis
<p>Abstract<br> Background. Dextran sodium sulfate (DSS)-triggered ulcerative colitis (UC) model in animals provides<br> a valuable platform to preclinically evaluate the outcome of drug candidates for UC. Dandelion root extracts<br> (DRE) have a particular therapeutic effect on UC. However, the protective mechanism of DRE against UC<br> remains unknown.<br> Objectives. To discover the targeting pathway involved in DRE-induced protection against UC.<br> Materials and methods. The UC model was developed in C57BL/6 mice by oral administration of DSS.<br> Following DSS exposure, sulfasalazine (SASP), low dose of DRE (DRE-L), moderate dose of DRE (DRE-M), high<br> dose of DRE (DRE-H), and DRE-H plus mitogen-activated protein kinases (MAPK) agonist (DRE-H+MA) were<br> administered to the mice. Colon Mucosal Damage Index (CMDI) and histopathological analysis were used<br> to evaluate the colonic mucosal damage. The cytokine levels were detected using commercial enzyme-linked<br> immunosorbent assay (ELISA) kits. The MAPK pathway activation was determined with western blotting.<br> Results. We found that DRE-H attenuated DSS-triggered colonic mucosal damage. The DSS-induced inflammatory responses and oxidative stress in the bloodstream and colon tissues were dramatically inhibited<br> by DRE-H administration. Also, this plant impaired DSS-provoked phosphorylation levels of extracellular<br> signal-regulated kinases (ERK), c-Jun N-terminal kinases (JNK), p38 mitogen-activated protein kinases<br> (p38), p65, and IκB. More importantly, MAPK agonist, BIM-23A760, removed the protective effect of DRE-H<br> on the bloodstream and colon tissues.<br> Conclusions. The DRE-H is capable of relieving DSS-induced UC, and its mechanism links to the MAPK<br> pathways.<br> </p>
Figure 6 from: Wetzel F, Despot Belmonte K, Bingham H, Underwood E, Hoffmann A, Häuser C, Mikolajczyk P, Vohland K (2017) 4th European Biodiversity Observation Network (EU BON) Stakeholder Roundtable: Pathways to sustainability for EU BONs network of collaborators and technical infrastructure. Research Ideas and Outcomes 3: e11875. https://doi.org/10.3897/rio.3.e11875
Figure 6 - Fig. 6: Participants of the 4th EU BON Stakeholder Roundtable (Credits: F. Wetzel).
Endogenous LRRK2 and PINK1 function in a convergent neuroprotective ciliogenesis pathway in the brain
<p>Raw data for Figure 2. Readme file with info regarding the data. Zip file is about 40 GB as contains all raw images used for quantification presented in figure 2 and in supplementary 7</p>
Data for research paper: Social transmission along multiple pathways promotes information fidelity and reduces divisiveness
Open the record for dataset details and reuse information.
Data from: Ergosterol biosynthesis: a fungal pathway for life on land?
Sterols, essential lipids of most eukaryotic cells, ensure important structural and signaling functions. The selection pressure which has led to different dominant sterols in the three eukaryotic kingdoms remains unknown. Here we investigated the influence of the progression in the different steps of the ergosterol biosynthetic pathway (EBP) on the yeast resistance to transitions from aqueous to aerial media, typical perturbations of the higher fungi habitats. Five mutants of the EBP (ergΔ), accumulating different sterol intermediates in the EBP, and the WT strain were exposed to drying under atmospheric air or nitrogen and wetting. Results show that the progression in the EBP parallels an increase in the yeast resistance to air-drying with a maximal survival rate for the WT strain. When drying/wetting was performed under nitrogen, yeast survival was higher, particularly for the earlier mutants of the EBP. Thus, ergosterol, through its protective role against mechanical and oxidative stress, might have been selected by the pressure induced by drying/wetting cycles occurring in the fungi habitats. These results support the Bloch hypothesis, which postulates that the properties of sterols are gradually optimized for function along the biosynthetic pathway and provide a response to the enduring question "why ergosterol in fungi?".
Supporting data to "Sediment source and pathway identification using Sentinel-2 imagery and (kayak-based) lagrangian river profiles on the Vjosa river"
<p>This release contains the supporting data files that are part of the manuscript "Sediment source and pathway identification using Sentinel-2 imagery and (kayak-based) lagrangian river profiles on the Vjosa river."</p>
HAPSTR1 localizes HUWE1 to the nucleus to limit stress signaling pathways_293T_RNAseq
<p>RNA-seq data from 293T cells expressing a doxycycline-induced control shRNA targeting firefly luciferase (FF), or one of two shRNA sequences targeting human HUWE1 for 4 days. sh353155 corresponds to sequence #2, and sh110969 corresponds to sequence #3 in: Monda et al. <em>Cell Reports</em>. 2023. Each sample was collected in triplicate and analyzed with paired-end reads.</p>
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.