Browse reusable Agent Skills, each with a clear purpose and practical guidance.
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.
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.
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.
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.
Interpret hits from CRISPR-KO/CRISPRi/shRNA screens by integrating DepMap essentiality, gnomAD constraint scores, pathway context (Reactome, STRING), druggability (DGIdb), and clinical evidence (CIViC, COSMIC). Use for screen-hit prioritization, essentiality ranking, and turning a list of screen hits into a prioritized target shortlist.
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.
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.
Transform GWAS signals into drug targets and repurposing opportunities. Connects GWAS-significant loci to causal genes via fine-mapping/eQTL, then to druggable proteins via DGIdb/OpenTargets, then to existing drugs via ChEMBL. Use for GWAS-to-target hypothesis generation, druggable-fraction analysis of disease loci, and human-genetics-validated drug-repurposing prioritization.
Statistical fine-mapping of GWAS loci using credible sets (SuSiE, FINEMAP) and locus-to-gene scoring (Open Targets L2G). Identifies likely causal variants and target genes — distinct from positional 'nearest gene' which is often wrong. Use for prioritizing causal variants at GWAS hits, comparing fine-mapping methods, and converting lead SNPs to target genes.
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.