Science & Research for Claude Code

Perform pairwise sequence alignment using Biopython Bio.Align.PairwiseAligner. Use when comparing two sequences, finding optimal alignments, scoring similarity, and identifying local or global matches between DNA, RNA, or protein sequences.

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Call accessible chromatin regions from ATAC-seq data using MACS3 with ATAC-specific parameters. Use when identifying open chromatin regions from aligned ATAC-seq BAM files, different from ChIP-seq peak calling.

Quality control metrics for ATAC-seq data including fragment size distribution, TSS enrichment, FRiP, and library complexity. Use when assessing ATAC-seq library quality before or after peak calling to identify problematic samples.

Find differentially accessible chromatin regions between conditions using DiffBind or DESeq2. Use when comparing chromatin accessibility between treatment groups, cell types, or developmental stages in ATAC-seq experiments.

Detect transcription factor binding sites through footprinting analysis in ATAC-seq data using TOBIAS. Use when identifying TF occupancy patterns within accessible regions, as TF binding protects DNA from Tn5 cutting.

Analyze transcription factor motif accessibility variability using chromVAR. Use when identifying which TF motifs show variable accessibility across samples or conditions in ATAC-seq data.

Extract nucleosome positions from ATAC-seq data using NucleoATAC, ATACseqQC, and fragment analysis. Use when analyzing chromatin organization, identifying nucleosome-free regions at promoters, or characterizing nucleosome occupancy patterns from ATAC-seq fragment size distributions.

Convert raw Nanopore signal data (FAST5/POD5) to nucleotide sequences using Dorado basecaller. Covers model selection, GPU acceleration, modified base detection, and quality filtering. Use when processing raw Nanopore data before alignment. Guppy is deprecated; use Dorado for all new analyses.

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Process multiple sequence files in batch using Biopython. Use when working with many files, merging/splitting sequences, or automating file operations across directories.

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<!-- COPYRIGHT NOTICE This file is part of the "Universal Biomedical Skills" project. Copyright c 2026 MD BABU MIA, PhD <md.babu.mia@mssm.edu All Rights Reserved. This code is proprietary and confidential. Unauthorized copying of this file, via any medium is strictly prohibited. Provenance:

Test whether two traits share a causal variant at a genomic locus using Bayesian colocalization with coloc. Computes posterior probabilities for shared vs distinct causal variants between GWAS and eQTL signals. Use when determining if a GWAS signal and an eQTL share the same causal variant.

Identify likely causal variants within GWAS loci using SuSiE for sum of single effects regression and FINEMAP for shotgun stochastic search. Computes posterior inclusion probabilities and credible sets to prioritize variants for functional follow-up. Use when narrowing GWAS association signals to candidate causal variants or building credible sets for functional validation.

Decompose genetic effects into direct and indirect paths through mediating variables using the mediation R package. Tests whether gene expression, methylation, or other molecular phenotypes mediate the effect of genetic variants on disease. Use when testing whether a molecular phenotype mediates the genotype-to-phenotype relationship.

Estimate causal effects between exposures and outcomes using genetic variants as instrumental variables with TwoSampleMR. Implements IVW, MR-Egger, weighted median, and MR-PRESSO methods for robust causal inference from GWAS summary statistics. Use when testing whether an exposure causally affects an outcome using genetic instruments.

Detect and correct for horizontal pleiotropy in Mendelian randomization analyses using MR-PRESSO for outlier removal, MR-Egger regression for directional pleiotropy, and Steiger filtering for variant directionality. Use when validating MR results, detecting pleiotropic instruments, or running sensitivity analyses for causal inference.

Preprocesses cell-free DNA sequencing data including adapter trimming, alignment optimized for short fragments, and UMI-aware duplicate removal using fgbio. Applies cfDNA-specific quality thresholds and fragment length filtering. Use when processing plasma cfDNA sequencing data before downstream analysis.

Differential binding analysis using DiffBind. Compare ChIP-seq peaks between conditions with statistical rigor. Requires replicate samples. Outputs differentially bound regions with fold changes and p-values. Use when comparing ChIP-seq binding between conditions.

De novo motif discovery and known motif enrichment analysis using HOMER and MEME-ChIP. Identify transcription factor binding motifs in ChIP-seq, ATAC-seq, or other genomic peak data. Use when finding enriched DNA motifs in peak sequences.

Annotate ChIP-seq peaks to genomic features and genes using ChIPseeker. Assign peaks to promoters, exons, introns, and intergenic regions. Find nearest genes and calculate distance to TSS. Generate annotation plots and statistics. Use when annotating ChIP-seq peaks to genomic features.

ChIP-seq peak calling using MACS3 (or MACS2). Call narrow peaks for transcription factors or broad peaks for histone modifications. Supports input control, fragment size modeling, and various output formats including narrowPeak and broadPeak BED files. Use when calling peaks from ChIP-seq alignments.

ChIP-seq quality control metrics including FRiP (Fraction of Reads in Peaks), cross-correlation analysis (NSC/RSC), library complexity, and IDR (Irreproducibility Discovery Rate) for replicate concordance. Use to assess experiment quality before downstream analysis. Use when assessing ChIP-seq data quality metrics.

Identifies super-enhancers from H3K27ac ChIP-seq data using ROSE and related tools. Use when studying cell identity genes, cancer-associated regulatory elements, or master transcription factor binding regions that cluster into large enhancer domains.

Visualize ChIP-seq data using deepTools, Gviz, and ChIPseeker. Create heatmaps, profile plots, and genome browser tracks. Visualize signal around peaks, TSS, or custom regions. Use when visualizing ChIP-seq signal and peaks.

Query ClinVar for variant pathogenicity classifications, review status, and disease associations via REST API or local VCF. Use when determining clinical significance of variants for diagnostic or research purposes.

Query dbSNP for rsID lookups, variant annotations, and cross-references to other databases. Use when mapping between rsIDs and genomic coordinates or retrieving basic variant information.

Query gnomAD for population allele frequencies to assess variant rarity. Use when filtering variants by population frequency for rare disease analysis or determining if a variant is common in the general population.

Call HLA alleles from NGS data using OptiType, HLA-HD, or arcasHLA for immunogenomics applications. Use when determining HLA genotype for transplant matching, neoantigen prediction, or pharmacogenomic screening.

Query myvariant.info API for aggregated variant annotations from multiple databases (ClinVar, gnomAD, dbSNP, COSMIC, etc.) in a single request. Use when annotating variants with clinical and population data from multiple sources simultaneously.

Query PharmGKB and CPIC for drug-gene interactions, pharmacogenomic annotations, and dosing guidelines. Use when predicting drug response from genetic variants or implementing clinical pharmacogenomics.

Calculate polygenic risk scores using PRSice-2, LDpred2, or PRS-CS from GWAS summary statistics. Use when predicting disease risk from genome-wide genetic variants.

Extract and analyze mutational signatures from somatic variants using SigProfiler or MutationalPatterns to characterize mutagenic processes. Use when identifying DNA damage mechanisms or etiology in cancer genomes.

Calculate tumor mutational burden from panel or WES data with proper normalization and clinical thresholds. Use when assessing immunotherapy eligibility or characterizing tumor immunogenicity.

Filter and prioritize variants by pathogenicity, population frequency, and clinical evidence for rare disease analysis. Use when identifying candidate disease-causing variants from exome or genome sequencing.

<!-- COPYRIGHT NOTICE This file is part of the "Universal Biomedical Skills" project. Copyright c 2026 MD BABU MIA, PhD <md.babu.mia@mssm.edu All Rights Reserved. This code is proprietary and confidential. Unauthorized copying of this file, via any medium is strictly prohibited. Provenance:

<!-- COPYRIGHT NOTICE This file is part of the "Universal Biomedical Skills" project. Copyright c 2026 MD BABU MIA, PhD <md.babu.mia@mssm.edu All Rights Reserved. This code is proprietary and confidential. Unauthorized copying of this file, via any medium is strictly prohibited. Provenance:

<!-- COPYRIGHT NOTICE This file is part of the "Universal Biomedical Skills" project. Copyright c 2026 MD BABU MIA, PhD <md.babu.mia@mssm.edu All Rights Reserved. This code is proprietary and confidential. Unauthorized copying of this file, via any medium is strictly prohibited. Provenance: