ToolUniverse

Metabolomics research — metabolite identification, study analysis, and database searches across HMDB, MetaboLights, Metabolomics Workbench, KEGG. Use for annotating mass-spec features to known metabolites, finding metabolomics studies of a disease, and structured metabolomics research reports with metabolite-pathway mapping.

Metabolomics pathway analysis — metabolite identification (HMDB, KEGG, ChEBI), pathway mapping (Reactome, KEGG, MetaCyc), disease associations, enzyme/gene linkage. Use for metabolite-to-pathway-to-disease connections, BridgeDb-based ID conversion, and integrating metabolomics with gene-level pathway analyses.

Meta-analysis / evidence synthesis — pool effect sizes across studies (odds ratios, risk ratios, hazard ratios, mean differences, correlations, GWAS betas) with fixed- or random-effects models, quantify heterogeneity (Q, I², τ²), and build a forest plot. Use when you have results from MULTIPLE studies and need a single pooled estimate, or to synthesize evidence from a systematic review / multiple GWAS / replicated experiments. Handles the error-prone effect-size + standard-error preparation (converting OR/HR/CI, two-group means±SD, proportions, and correlations into the (effect, SE) the pooling step needs).

Lipid analysis and lipid-disease associations using LIPID MAPS classification, HMDB metabolite data, KEGG/Reactome lipid pathways (sphingolipid, eicosanoid, steroid, fatty acid), and PubChem chemical info. Use for lipid identification, lipid metabolism pathway mapping, and lipid-associated disease analysis (cardiovascular, diabetes, NAFLD).

KEGG-based disease-drug-variant network research. Connects diseases to causal genes, drugs to molecular targets, and variants to pathways using KEGG's editorially curated databases (KEGG Disease, Drug, Network, Variant, Pathway). Use for drug repurposing via shared pathways, mechanistic disease-gene-drug networks, and pathway-based target discovery. Distinguishes direct (binding) vs indirect (pathway co-membership) drug-target relationships.

Inorganic chemistry, physical chemistry, and materials science — crystal structures, coordination chemistry, lattice parameters, thermodynamic properties, electronic structure. Use for unit cell volume calculations, coordination geometry, materials property estimation, and inorganic-mechanism reasoning. Complementary to tooluniverse-organic-chemistry.

Predict patient response to immune checkpoint inhibitors (ICIs) by integrating tumor mutational burden (TMB), microsatellite instability (MSI), PD-L1 expression, HLA status, and immune-related gene expression. Outputs ICI Response Score with drug-specific recommendations and resistance-risk assessment. Use for melanoma/NSCLC/RCC immunotherapy decision support.

Immunology research workflows: antibody-antigen interactions, T/B cell repertoire, MHC/HLA binding prediction, autoimmune disease genetics, vaccine epitope mapping. Uses IEDB, IMGT, SAbDab, UniProt. Use for adaptive immunity questions, immune response analysis, antibody/TCR/BCR characterization, immunogenicity prediction, and immune-pathway-to-disease mapping.

Microscopy and quantitative imaging analysis — colony morphometry, fluorescence intensity quantification, cell-count statistics, dose-response curves, and ANOVA/Dunnett on image-derived measurements. Uses pandas/numpy/scipy/scikit-image. Use for analyzing tabular outputs from CellProfiler/ImageJ, image-derived measurement statistics, and image-based assay quantification.

HLA gene-family analysis and MHC-peptide binding for transplant compatibility, vaccine epitope coverage, and cancer immunotherapy. Uses IMGT (HLA polymorphism), IEDB (epitope-MHC binding), UniProt (annotation), DGIdb (druggability). Use for HLA typing/imputation review, vaccine HLA coverage, and immunotherapy prediction biomarkers (HLA-LOH, neoantigen presentation).

Compare GWAS studies, perform meta-analyses across cohorts, and assess signal replication. Uses GWAS Catalog metadata, study-level statistics, and cross-cohort comparison. Use for evaluating GWAS reproducibility for a trait, meta-analysis sample size and effect-size aggregation, and detecting study heterogeneity (population, design, ancestry).

Interpret a single GWAS SNP across multiple databases — GWAS Catalog hits, LD/haplotype context, eQTL evidence, regulatory annotation, ClinVar pathogenicity, gnomAD frequency. Use for 'what does this SNP do', SNP-to-mechanism tracing, and resolving lead-SNP-vs-causal-variant ambiguity. Always considers LD structure before claiming a SNP is mechanistically responsible.

GPCR receptor pharmacology — agonist/antagonist/inverse-agonist/biased-agonist classification, GPCRdb structural data, receptor-ligand binding analysis, antibody-target interface (SAbDab). Use for GPCR drug discovery, biased-agonism analysis, receptor subtype selectivity questions, and orthosteric vs allosteric pocket characterization.

Gene regulatory network analysis — TF-target inference (JASPAR motifs, ChIP-seq), motif scanning, eQTL integration, perturbation evidence (knockout/overexpression). Use for 'which TF regulates gene X', 'which genes does TF Y target', regulatory pathway reconstruction. Distinguishes direct (binding) vs indirect (co-expression) regulatory evidence.

Gene-disease association analysis across DisGeNET, OpenTargets, Monarch, OMIM, GenCC, Orphanet. Cross-references multiple sources for evidence-graded association reports with concordance scoring (5/5 sources agree → strong, 1/5 → weak). Use for 'which diseases is gene X associated with' or 'which genes cause disease Y' queries with quantitative confidence.

Histone-modification ChIP-seq, ATAC-seq accessibility, chromatin state, and TF binding analysis from ENCODE, Roadmap Epigenomics, ChIP-Atlas. Use for chromatin-state-by-tissue queries, TF-binding-by-region, regulatory landscape mapping, and ENCODE-cCRE annotations. For DNA methylation use tooluniverse-epigenomics; for RNA-seq use tooluniverse-rnaseq-deseq2.

End-to-end observational epidemiology analysis — from research question (PECO Population/Exposure/Comparator/Outcome) to publication-ready statistical report. Covers cohort/case-control/cross-sectional design, regression with confounders, propensity scoring, sensitivity analysis. Writes Python code for every step. Use for epidemiology study analysis, NHANES/UK-Biobank-style analyses.

Enzyme kinetics — Michaelis-Menten Km, Vmax, kcat (turnover), and kcat/Km (catalytic efficiency / specificity constant) from substrate-velocity data, plus inhibition-mechanism analysis (competitive / uncompetitive / non-competitive, Ki). Fits the MM equation by nonlinear regression (and reports Lineweaver-Burk for reference). Use when you have substrate concentrations and initial reaction velocities and need kinetic parameters or to classify an inhibitor. NOT for BRENDA database lookups of published constants (use the BRENDA tools).

Search and analyze electron microscopy data — cryo-EM density maps (EMDB), fitted atomic models (PDB), raw micrograph datasets (EMPIAR), and cryo-electron tomography volumes (CryoET Data Portal). Use for finding 3D structural data on a protein/complex, comparing experimental EM resolution to AlphaFold confidence, and accessing raw EM data for re-processing.

Ecology, biodiversity, and conservation biology research — species identification (GBIF, NCBI Taxonomy), invasive species impact, ecosystem dynamics, conservation status (IUCN), niche ecology. Use for biodiversity questions, species comparison, invasion biology, conservation prioritization, and ecology-related literature search.

Drug-combination synergy analysis — quantify whether two drugs together are synergistic, additive, or antagonistic using the standard reference models (Bliss independence, HSA / highest single agent, Loewe additivity, ZIP, and the Chou-Talalay Combination Index). Use when you have measured single-drug and combination effects (inhibition/viability) and need a synergy score. Explains which model to use, what data each one needs, and how to read the score. NOT for looking up pre-computed synergy in a database (use the SYNERGxDB tool / cell-line-profiling skill).

Comprehensive drug profiling — mechanism, primary/secondary targets, drug interactions, clinical-trial status, adverse events (FAERS), pharmacogenomics, and approval history. Use for full drug investigation reports, 'tell me about drug X' queries, and assembling drug profiles for clinicians, researchers, or regulatory work.

Identify drug repurposing candidates via target-based, compound-based, and disease-based strategies. Combines drug-target-disease network reasoning with mechanism rationale, clinical-trial precedent, and patent/regulatory feasibility. Use for hypothesis-generating repurposing for orphan diseases, finding existing drugs for new indications, and prioritizing candidates by evidence and feasibility.

Drug regulatory and approval research — FDA substance registry, ATC/EPC classification, EMA decisions, generic-drug status, FDA Orange Book exclusivity, NDA/BLA pathways. Use for jurisdiction-aware approval status (FDA vs EMA), generic vs brand availability, exclusivity expiry tracking, and regulatory pathway selection. Always specifies the market when reporting status.

Trace drug mechanism of action — primary target → downstream signaling → pathway perturbation → tissue/organ effect → clinical outcome. Uses DrugBank, ChEMBL, KEGG, Reactome, STRING. Use for understanding how a drug works, identifying off-target effects, mechanism-based combination therapy design, and writing mechanism sections of reports.