Core Engines
Scientific Diligence
Institutional
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© 2026 Nilus Lab · Institute of Computation
Nilus Lab combines 12 public cardiac datasets (11 human, 1 mouse) with human genetics to identify candidate targets for heart failure and myocardial ageing. All candidates are at the computational identification stage.
6 single-cell atlases · 3 bulk RNA · 3 proteomes (2 human, 1 mouse).
FDR q < 0.05 concordance across Reichart 2022 SC & MAGNet LV myocardium (451 genes of 5,677).
Blind recovery of the positive control: #3 of 11 genes passing DCM, ageing and protein filters (#76 of 5,677 by DCM Z alone).
PPP1R12C q = 0.037 in the Malecki LV proteome (main test): the only one of the tested candidates to pass FDR (15 proteins pass in that screen).
Each target was found by a computational screen of human heart data: single-cell and tissue RNA from failing and healthy hearts, two human heart proteomes and heart-failure genetics. None has been tested in the lab yet. Open a target to see its evidence.
A separate audit tested eight candidates against GTEx data from 11 tissues and two human heart proteomes, and removed five. In GTEx left ventricle none of these four changes significantly with age. Only PPP1R12C changes at protein level with age, and that result passes correction for multiple testing in one of three tests. No target has been tested in the lab.
Three sequential mathematical gates eliminate false positives, ambient single-cell RNA contamination, and compensatory stress traps.
Donor-level pseudobulk regressions across 6 cardiac lineages (Cardiomyocytes, Fibroblasts, Mural/Pericytes, Endothelial, Myeloid, Lymphoid) enforcing ≥10% detection and ≥0.5× intrinsic specificity to eliminate ambient RNA artifacts.
Cross-validates 451 concordant transcriptomic genes against three mass-spectrometry cohorts: Malecki 2025 (25 human left-ventricle hearts by protein; RNA-seq on 16 of them), GTEx TMT proteomics, and Takasugi 2024 mouse heart proteomics.
Enforces cis-colocalised Heart Failure GWAS priors (H4 ≥ 0.80) where genetic risk and disease expression move in the exact same direction, while automatically screening out protective compensatory stress responses via mouse knockout phenotyping.
Full bioinformatic specification of 451 concordant genes, cross-tissue specificity indices, and mass spectrometry tables.
Interactive 3D structure visualization and coordinates viewer.
Full data provenance, statistical methodology, and intended-use boundaries for institutional due diligence.