Mineto Ota

The paper identifies estrogen-modulated SNVs associated with breast cancer risk and shows their interaction with reproductive factors using polygenic risk scores.

Genome-scale CRISPRi perturb-seq in 22 million primary human CD4+ T cells maps stimulation-specific regulators and links perturbation signatures to T cell states and autoimmune genetics.

This paper develops a virus-like particle-based system for CRISPR gene editing and screening in primary human myeloid cells, identifying TNFAIP3 as a key regulator of inflammatory polarization.

The paper identifies a treatment-resistant fibroblast state in RA synovitis that drives chronic inflammation through senescence-associated mechanisms and highlights therapeutic targets beyond cytokine inhibition.

The paper introduces PerturbPair, a platform integrating transcriptomic and optical screens to map macrophage regulatory networks, revealing cross-modal relationships and disease-relevant gene programs.

Circulating miR-1285-3p in SLE promotes ABC differentiation by suppressing OXPHOS and relieving IKZF2-mediated restraint.

The paper uses population-scale Ig genetics to identify genetic associations and map their effects on the human B-cell system, revealing new genes and regulatory mechanisms in humoral immunity.

The paper identifies cis-regulatory elements and transcription factors controlling FOXP3 expression in human Tregs and Tconvs, revealing mechanisms that restrict FOXP3 to Tregs in mice.

The paper integrates genetic associations with Perturb-seq data to build causal graphs linking genes to traits through regulatory programs.

This paper compares how GWAS and rare variant burden tests prioritize genes for 209 traits in the UK Biobank, showing they focus on different genes due to distinct prioritization criteria.

This study uses CRISPR perturbations in CD4+ T cells to infer a gene regulatory network, revealing trans-regulatory mechanisms linking immune GWAS genes to signaling pathways.

This study identifies cell-type-specific transcriptomic signatures associated with SLE disease establishment and exacerbation, highlighting their clinical relevance and potential limitations in capturing genetic risk factors.