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At least 739 records · Page 41Linked to original sources
PubMed2005

New directions in incidence-dose modeling.

Many cellular responses are quantal; that is, they either take place or they do not. Examples of "either-or" responses include cell replication, differentiation and apoptosis. Surprisingly, induction of suites of genes and coordinated phenotypic changes in cells are also often quantal, where embedded molecular circuitry creates on-off switches. Mechanistic incidence-dose (ID) models need to account for the quantal characteristics of cellular switches that contribute, in turn, to dose thresholds and to the incidence of biological responses in individuals. Interdisciplinary systems biology approaches create mechanistic ID models based on: (i) detailed knowledge of the cellular circuitry controlling signal transduction; (ii) evolving biological modeling tools describing cellular circuits and their perturbations by chemicals and (iii) high throughput, high coverage "omic" screens for examining cell signaling pathways and biological responses. These interdisciplinary approaches should produce novel, quantitative ID models for biological responses and greatly improve the biological basis of safety and risk assessments.

Incidence↗
PubMed2005

Systems biotechnology for strain improvement.

Various high-throughput experimental techniques are routinely used for generating large amounts of omics data. In parallel, in silico modelling and simulation approaches are being developed for quantitatively analyzing cellular metabolism at the systems level. Thus informative high-throughput analysis and predictive computational modelling or simulation can be combined to generate new knowledge through iterative modification of an in silico model and experimental design. On the basis of such global cellular information we can design cells that have improved metabolic properties for industrial applications. This article highlights the recent developments in these systems approaches, which we call systems biotechnology, and discusses future prospects.

Genome↗
PubMed2005

Reconstructing the metabolic network of a bacterium from its genome.

The prospect of understanding the relationship between the genome and the physiology of an organism is an important incentive to reconstruct metabolic networks. The first steps in the process can be automated and it does not take much effort to obtain an initial metabolic reconstruction from a genome sequence. However, such a reconstruction is certainly not flawless and correction of the many imperfections is laborious. It requires the combined analysis of the available information on protein sequence, phylogeny, gene-context and co-occurrence but is also aided by high-throughput experimental data. Simultaneously, the reconstructed network provides the opportunity to visualize the "omics" data within a relevant biological functional context and thus aids the interpretation of those data.

Bacteria↗
PubMed2006

The nature of systems biology.

The advent of functional genomics has enabled the molecular biosciences to come a long way towards characterizing the molecular constituents of life. Yet, the challenge for biology overall is to understand how organisms function. By discovering how function arises in dynamic interactions, systems biology addresses the missing links between molecules and physiology. Top-down systems biology identifies molecular interaction networks on the basis of correlated molecular behavior observed in genome-wide "omics" studies. Bottom-up systems biology examines the mechanisms through which functional properties arise in the interactions of known components. Here, we outline the challenges faced by systems biology and discuss limitations of the top-down and bottom-up approaches, which, despite these limitations, have already led to the discovery of mechanisms and principles that underlie cell function.

Cell Physiological Phenomena↗
PubMed2006

Cytomics: A multiparametric, dynamic approach to cell research.

Cytomics aims to determine the molecular phenotype of single cells. Within the context of the -omics, cytomics allows the investigation of multiple biochemical features of the heterogeneous cellular systems known as the cytomes. Cytomics can be considered as the science of single cell-based analyses that links genomics and proteomics with the dynamics of cell and tissue function, as modulated by external influences. Inherent to cytomics are the use of sensitive, scarcely invasive, fluorescence-based multiparametric methods and the event-integrating concept of individual cells to understand the complexity and behaviour of tissues and organisms. Among cytomic technologies, flow cytometry, confocal laser scanning microscopy and laser capture microdissection are of great relevance. Other recent technologies based on single cell bioimaging and bioinformatic tools become important in drug discovery and toxicity testing, because of both high-content and high-troughput. The multiparametric capacity of cytomics is very useful for the identification, characterization and isolation of stem cell populations. In our experience, flow cytometry is a powerful and versatile tool that allows quantitative analysis of single molecules, prokaryotic and eukaryotic cells for basic, biotechnological, environmental and clinical studies. The dynamic nature of cytomic assays leads to a real-time kinetic approach based on sequential examination of different single cells from a population undergoing a dynamic process, the in fluxo level. Finally, cytomic technologies may provide in vitro methods alternative to laboratory animals for toxicity assessment.

Animals↗
PubMed2004

Interaction networks: coordinating responses to xenobiotic exposure.

In the last decade the increased usage of '-omic' technologies, plus the sequencing of over 800 complete genomes has led to a vast increase in the amount of information available to the researcher for examining cellular responses to xenobiotics. Much effort has been put into the identification and analysis of expression profiles associated with pathobiological conditions and/or xenobiotic exposure. These profiles are commonly used in two applications. Firstly, comparative profile experiments are used to classify pathobiological states and for the screening of novel chemical entities to predict their action(s) on the body. Secondly, mechanistic investigations will gain information on the molecular mechanisms underlying toxic responses/pathobiological states. During the course of such analysis it has become increasingly clear that a series of highly refined interaction networks exist within the body, regulating both the sensitivity and selectivity of the body's response to pathobiological states/xenobiotic exposure. These interaction networks exist at several levels: Firstly, within individual cells, the interaction between factors that transmit xenobiotics signals will determine the overall cellular response. Secondly, intraorgan communication occurs between the different cell types/sub-types which makes up an organ, coordinating the overall organ response. Finally, interorgan interactions provide axes of response through the body.

Animals↗
PubMed2026

The Brazilian contribution to ant toxinology: challenges and perspectives.

Ant toxinology in Brazil is a small but growing field that has revealed wide biochemical diversity and clear potential for bioprospecting therapeutic molecules. This review compiles the Brazilian contribution, focusing on advances in the characterization of venoms from medically and ecologically important species of Dinoponera, Solenopsis, Paraponera, Pachycondyla, Neoponera, and Ectatomma. Brazilian groups applied omics approaches, including transcriptomics and proteomics, to resolve the composition of these venoms and identified peptide-rich arsenals with antimicrobial, antiparasitic, antitumor, and neuroactive activity. Studies of venom phenotypic plasticity showed ecological factors such as diet and seasonality shape venom composition. Two challenges persist: assigning function to still unidentified components and obtaining venom in the quantities that broad analysis requires. The near-term prospects are the rational design of peptide analogues with improved activity and continued bioprospecting of new species, which together position Brazil as a central contributor to ant toxinology.

Animals↗
PubMed2026

The genomic alchemist's arsenal: A comprehensive review of gene recruitment, regulatory rewiring, and the evolutionary arms race in snake envenomation.

Snake venom represents a striking example of evolutionary innovation, in which ancestral physiological gene networks have been co-opted into potent biochemical weapons. Advances in multi-omics, single-cell genomics, and structural bioinformatics have catalyzed a conceptual shift from descriptive toxin cataloging to a systems-level understanding of venom evolution, regulation, and function. This Review integrates genomic, cellular, and structural perspectives to delineate the molecular architecture underpinning venom diversification and target-site co-evolution. Emphasis is placed on regulatory mechanisms driving rapid expression plasticity, including super-enhancer activity, transposable element insertion, spatial heterogeneity within the venom gland, and non-coding RNA-mediated modulation. At the protein level, the review examines how hypervariable toxins engage in structural arms races with prey targets, and how multi-toxin complex formation, functional synergy, and molecular dynamics simulations inform models of lethality and resistance. A comparative framework is provided by contrasting high-potency predatory snake venoms with low-potency defensive venoms of hymenopterans such as bees and wasps, revealing how ecological selective pressures shape toxin potency, composition, and target specificity across taxa. Finally, current translational strategies are evaluated, with a focus on the relative merits of recombinant human monoclonal antibodies versus catalytic-site small-molecule inhibitors as deployable interventions for snakebite. By synthesizing evolutionary genomics, structural biology, comparative toxinology, and synthetic antivenomics, this Review outlines a predictive framework for anticipating venom evolutionary trajectories and for designing broad-spectrum, next-generation therapeutics.

Animals↗
PubMed2026

Phytolacca acinosa Roxb. induces intestinal toxicity through the histamine-MLCK-tight junction axis: Integrated evidence from proteomics, metabolomics, intestinal organoids and epithelial barrier validation.

Phytolacca acinosa Roxb. (PR) is a saponin-rich medicinal plant associated with gastrointestinal toxicity, but the mechanisms underlying PR-induced intestinal barrier injury remain unclear. In this study, raw PR extract was analytically characterized by UPLC-ZenoTOF-MS/MS, confirming triterpenoid saponins as the predominant constituents. C57BL/6 J mice were orally exposed to characterized PR extract (1.20 or 12.0 g/kg for 5 h), and Caco-2 cells and mouse intestinal organoids were used to assess epithelial toxicity and barrier disruption. Histopathology, ELISA, FITC-dextran permeability assays, immunofluorescence, CCK-8, LDH release, western blotting, DIA-based proteomics and untargeted metabolomics were integrated to define toxicological mechanisms. PR induced dose-dependent intestinal inflammation and barrier dysfunction, with the ileum as the most sensitive target. PR increased serum DAO and D-lactate and intestinal TNF-α and IL-1β, disrupted organoid morphology, enhanced epithelial permeability, and reduced ZO-1 expression. Proteomics revealed changes in inflammatory, lipid-metabolic, cytoskeletal and tight-junction pathways, including upregulation of MLCK3 and phospholipase-related proteins and downregulation of ZO-1 and ZO-2. Metabolomics identified histidine metabolism disturbance and histamine accumulation. Integrated multi-omics and pharmacological validation indicated that histamine activated the PLC/IP₃/Ca²⁺/CaM/MLCK cascade, promoting MLC phosphorylation, tight-junction disassembly and epithelial leakiness. MLCK inhibition partially restored ZO-1/ZO-2 expression and attenuated PR-induced epithelial injury. These findings identify the histamine-MLCK-tight junction axis as a key mechanism of PR-induced intestinal toxicity and support hazard identification of saponin-rich PR exposure.

Animals↗
PubMed2026

Have we entered a 'post-model' era in plant biology?

Models such as arabidopsis (Arabidopsis thaliana) have underpinned genomic and physiological research in plant science. Advances in genome sequencing, pangenomics, and genome editing have prompted claims of a 'post-model' era, with model-crops and crops such as rice and bread wheat combining agricultural relevance with experimental tractability. We argue that the 'simplicity-to-complexity' approach remains valid, although model systems have evolved. Arabidopsis remains indispensable for interpreting multi-omics data, testing developmental hypotheses, and generating mechanistic insights difficult to obtain in crops. Linking these strengths to model-crops adds translational value by bridging discovery and breeding, while niche models such as Brachypodium distachyon and legumes address grass cell wall biology and nitrogen fixation. Future progress depends on diverse species with complementary strengths across fundamental and applied plant biology.

arabidopsis↗
PubMed2026

The pseudouridine epitranscriptomic landscape of advanced prostate cancer therapeutic resistance identifies TIMM17A as a key player.

BACKGROUND: Resistance to androgen receptor signaling inhibitors (ARSIs) remains a major barrier of advanced prostate cancer (PCa) treatment. While RNA epitranscriptomic modifications are increasingly recognized as key regulators of tumor biology, the role of pseudouridine (Ψ) in therapeutic resistance is largely unexplored. METHODS: A darolutamide-resistant PCa cell model was established and subjected to integrated multi-omics profiling using bulk RNA sequencing and photo-crosslinking-assisted Ψ sequencing (PA-Ψ-seq). Differential expression and pseudouridylation analyses were combined to identify Ψ-associated genes. Public datasets validated expression and prognosis. Functional assays including RNA knockdown, cell proliferation, colony formation, and xenograft models were conducted. Single-cell RNA sequencing investigated tumor microenvironment (TME) interactions. RESULTS: We identified extensive transcriptomic and pseudouridylation alterations associated with ARSI resistance, with a significant positive correlation between Ψ modification and mRNA expression. Integrated analysis highlighted a subset of "hyper-up" genes enriched in resistance-related pathways. Thus, TIMM17A was identified as a novel candidate. TIMM17A expression was significantly elevated in PCa and correlated with disease progression and poor prognosis. Experimental validations demonstrated that TIMM17A promoted tumor growth and resistance, while its knockdown restored sensitivity to darolutamide both in vitro and in vivo. Mechanistically, TIMM17A expression may be regulated by PUS1‑mediated pseudouridylation. Single-cell analysis further revealed that TIMM17A is enriched in malignant epithelial cells and associated with enhanced cell-cell communication within the TME. CONCLUSIONS: This study delineates the pseudouridine epitranscriptomic landscape in advanced PCa and identifies TIMM17A as a key mediator of therapeutic resistance. Targeting the Ψ-TIMM17A axis may offer a novel strategy to overcome ARSI resistance.

Advanced prostate cancer↗
PubMed2005

Stable isotopes, mass spectrometry, and molecular fluxes: applications to toxicology.

In order to meet the increasing demands for safe and affordable drugs, improvements in the efficiency and accuracy of every step in drug development are required. Accordingly, new approaches for assessing drug toxicity that are faster and more precise are in demand. Numerous approaches using -omics and systems biology are being developed to meet this demand and, while promising, they have not yet provided the improvements in toxicology promised. Other innovative methodologies for predicting and assessing toxicities should therefore be explored. Here we present a novel approach for directly measuring the in vivo response of specific metabolic pathways to toxic agents. Using stable isotopes and ultra sensitive mass spectrometry, the effect of an agent on myelin synthesis, protein synthesis, or cell proliferation can be directly measured. Examples are presented where this approach is used to detect toxicity in the liver, brain, peripheral neurons, breast, and skin. Collagen synthesis, microglia proliferation, myelin synthesis, tubulin synthesis, hepatic cell proliferation, epidermal cell proliferation and mammary epithelial cell proliferation are quantitatively determined in vivo, in a high throughput manner. This approach avoids the computationally complex approach of systems biology and allows the user to observe the emergent properties of the system directly and quantitatively.

Animals↗
PubMed2026

Can host genetics transform the sustainable control of tropical theileriosis? Insights from the Tick-Theileria interface.

Tropical theileriosis, caused by the tick-transmitted apicomplexan parasite Theileria annulata, remains a major constraint on cattle production across North Africa, the Mediterranean basin, the Middle East and South Asia. Current control depends on acaricides, the theilericidal drug buparvaquone and live attenuated schizont vaccines, but acaricide resistance, buparvaquone-resistance mutations and the logistical demands of vaccination are eroding the sustainability of these tools. Host genetics offers a complementary and durable alternative. Indigenous Bos indicus breeds are consistently more resistant to ticks and tolerate T. annulata infection better than exotic Bos taurus cattle, and this advantage has a measurable heritable component. Unlike previous reviews, which treat tick resistance, T. annulata immunobiology and livestock genomic selection as separate subjects, we integrate all three and assess host genetics specifically against the failure modes of current control. We review the tick, parasite and host interface, the evidence for natural resistance, and the genetic and immunological mechanisms involved, including signal-regulatory protein, bovine major histocompatibility complex class II and inflammatory pathway genes. We then assess whether genomic selection, multi-omics, machine learning and gene editing can translate these mechanisms into resistant cattle, and we weigh the biological, economic and infrastructural barriers to implementation. The evidence indicates that host genetics will not replace existing control but could reduce reliance on acaricides and chemotherapy. That contribution remains prospective rather than demonstrated: no resistance marker for T. annulata has yet been validated, prediction accuracies are moderate and transfer poorly between breeds, and no endemic production system has implemented selection for resistance.

Animals↗
PubMed2026

First-line fecal microbiota transplantation for the management of immune checkpoint inhibitor-mediated diarrhea and colitis.

Immune checkpoint inhibitor (ICI) therapy commonly leads to adverse events such as ICI-mediated diarrhea and colitis (IMDC). Fecal microbiota transplantation (FMT) remains an option for patients with refractory colitis. We report a multi-omics profiling of patients receiving first-line FMT for IMDC. In our preliminary analysis, 10 (76.9%) patients achieve clinical response, with a median time to clinical improvement of 1.5 (1-10.5) days. Among responder patients with baseline and follow-up samples, 6 (75%) show an increase in alpha-diversity post-FMT. Pre-FMT samples show an increase in the abundance scores of plasma cells, neutrophils, macrophages (M1 and M2), memory activated and resting memory CD4+ T cells, CD8+ T cells, T follicular helper (Tfh) cells, and regulatory T cells (Tregs), all of which decrease post-FMT. In a small cohort of patients, we identify potential mechanisms for FMT response and demonstrate that first-line FMT in patients with IMDC (NCT04038619) can be effective.

FMT↗
PubMed2026

De novo Genes in Plants: Origins, Mechanisms, and Functional Implications.

De novo genes originate from previously non-coding genomic regions. They provide an important source of lineage-specific innovation. In plants, these genes may contribute to adaptation, trait diversity and crop evolution. This review summarizes recent progress in plant de novo gene research. It first discusses major routes of gene birth, including transcription-first, open reading frame (ORF)-first and concurrent models. It also examines how nascent loci acquire regulatory control and enter existing biological networks. The review then summarizes their evolutionary features, including weak early constraint, rapid molecular change, restricted expression and structural refinement. It further discusses plant de novo genes involved in stress responses, seed germination, kernel dehydration, subspecies divergence, reproductive isolation and floral scent diversification. Current methods for identifying de novo genes remain limited by rapid sequence evolution, genome annotation quality, polyploidy and transposable elements. Whole-genome synteny alignment, multi-omics evidence and machine-learning approaches can improve candidate discovery. However, each method has important limitations. Finally, this review highlights key future questions in functional validation, latent coding potential in long non-coding RNAs, epigenetic activation, regulatory-network integration and crop improvement. These perspectives clarify how de novo genes shape plant adaptation and how they may be used in precision breeding and synthetic biology.

adaptive evolution↗
PubMed2026

Pan-cancer analysis identifies GPRIN1 as a prognostic biomarker and promoter of cell proliferation in pancreatic cancer.

BACKGROUND: G protein-regulated inducer of neurite outgrowth 1 (GPRIN1), an emerging modulator of GPCR signaling, has been implicated in oncogenesis. However, its comprehensive role across human cancers, particularly in reshaping the tumor microenvironment (TME), remains poorly characterized. We aimed to elucidate the pan-cancer significance of GPRIN1 in TME modulation and its therapeutic implications. METHODS: We analyzed multi-omics data from TCGA and other public databases, performing a systematic analysis of GPRIN1 regarding expression, prognosis, immune infiltration, and genomic instability across 33 cancer types. To validate these bioinformatic findings, we performed lentiviral shRNA-mediated knockdown in pancreatic (PANC-1) and hepatic (HepG2) cancer cells to assess proliferation and migration. Crucially, the clinical relevance of GPRIN1 was further validated in an independent cohort of pancreatic cancer patients (N&#xa0;=&#xa0;17) using immunohistochemistry (IHC). RESULTS: The analysis identified a lineage-dependent expression pattern. Epithelial tumors exhibited upregulation, whereas glioblastoma samples displayed downregulation. GPRIN1 expression consistently correlated with immune subtypes and CD8+ T cell abundance. In vitro assays demonstrated that GPRIN1 depletion significantly inhibited cell proliferation and migration (P&#xa0;<&#xa0;0.0001). In the clinical validation cohort, multivariate Cox regression analysis identified high GPRIN1 protein levels as an independent predictor of post-operative recurrence. These patients also showed a trend toward extended overall survival. CONCLUSIONS: These findings define GPRIN1 as a context-dependent regulator of the TME. By integrating computational and experimental data, this study supports GPRIN1 as a potential biomarker for risk assessment in pancreatic cancer.

Humans↗
PubMed2005

Assessment and integration of publicly available SAGE, cDNA microarray, and oligonucleotide microarray expression data for global coexpression analyses.

Large amounts of gene expression data from several different technologies are becoming available to the scientific community. A common practice is to use these data to calculate global gene coexpression for validation or integration of other "omic" data. To assess the utility of publicly available datasets for this purpose we have analyzed Homo sapiens data from 1202 cDNA microarray experiments, 242 SAGE libraries, and 667 Affymetrix oligonucleotide microarray experiments. The three datasets compared demonstrate significant but low levels of global concordance (rc<0.11). Assessment against Gene Ontology (GO) revealed that all three platforms identify more coexpressed gene pairs with common biological processes than expected by chance. As the Pearson correlation for a gene pair increased it was more likely to be confirmed by GO. The Affymetrix dataset performed best individually with gene pairs of correlation 0.9-1.0 confirmed by GO in 74% of cases. However, in all cases, gene pairs confirmed by multiple platforms were more likely to be confirmed by GO. We show that combining results from different expression platforms increases reliability of coexpression. A comparison with other recently published coexpression studies found similar results in terms of performance against GO but with each method producing distinctly different gene pair lists.

Gene Expression Profiling↗
PubMed2026

Integrating transcriptomics and metabolomics reveals the molecular landscape of sperm maturation driven by regional differentiation in the epididymis of Guizhou-Guiqian semi-fine wool sheep.

Epididymal regionalized differentiation is crucial for sperm maturation. However, little is known about the synergistic remodeling mechanisms of different epididymal segments at the transcriptional and metabolic levels during sexual maturation in ruminants (especially sheep). We investigated the caput, corpus, and cauda epididymidis of pre-pubertal (2-month-old) and post-pubertal (7-month-old) Guizhou-Guiqian semi-fine wool sheep using histology, RNA sequencing, and metabolomics. Post-pubertal tissues exhibited increased luminal diameters, cilia lengths, and abundant cauda spermatozoa. Transcriptomic analysis revealed increasing differentially expressed genes (DEGs) along the caput-corpus-cauda axis (4642, 6103, and 7698 DEGs, respectively). Metabolomics detected 786 unique differentially accumulated metabolites (DAMs). Region-specific analysis showed that in the caput, up-regulated pathways (fructose/mannose metabolism; HK2, ALDOA, HKDC1) provide energy and substrates for initial sperm motility. In the corpus, down-regulated genes associated with extracellular matrix and tight junctions suggested epithelial barrier remodeling to establish an immune-tolerant microenvironment. The cauda specifically up-regulated the pentose phosphate pathway (FBP1, GPI) and glutathione metabolism, maintaining redox homeostasis for long-term sperm storage. Additionally, glycerophospholipid metabolism was enriched across all segments, where PEMT, AGPAT5, and LCAT likely regulate sperm plasma membrane fluidity. In conclusion, during sexual maturation, the caput drives energy metabolism and glycosylation, the corpus establishes immune tolerance, and the cauda maintains antioxidant homeostasis. The glycerophospholipid network throughout the across all epididymal segments synergistically remodels sperm membrane. This study reveals the underlying multi-omics regulatory mechanisms of epididymal functional differentiation, providing a theoretical basis for elucidating the molecular mechanisms of sperm maturation in this breed and for the molecular breeding of early reproductive performance in rams.

Animals↗