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Castiblanco, D.

Publications and source records attributed to Castiblanco, D..

2 recordsLinked to original sources

A ML-framework for the discovery of next-generation IBD targets using a harmonized single-cell atlas of patient tissue

Target discovery for IBD has traditionally relied on genetic associations, which lack the cellular resolution needed to identify novel, actionable, cell type-specific disease pathways. Here, we describe an integrated analytical and experimental framework that leverages harmonized single-cell data to systematically discover novel therapeutic strategies for IBD. We used AMICA DBTM, Immunais harmonized database of single-cell RNA datasets to construct a harmonized 1 million single-cell atlas of the human intestine. We applied a machine learning framework (Immune Patient Representation, IPR) to identify disease-associated transcriptional programs and cell type-specific gene targets. Candidate targets were prioritized using atlas-derived metrics, refined using custom criteria emphasizing translational actionability, and validated across independent clinical cohorts. Select candidates were evaluated in human primary-cell models reflecting the targets cell-type context. The IPR framework identified 85 disease-associated transcriptional programs and ranked 400 cell type-specific target genes across immune and stromal lineages. Disease-associated programs were interpreted using a structured AI-assisted reasoning framework for structured biological reasoning, linking them to IBD-relevant pathways and guiding the identification of novel, promising gene targets. Functional validation of two cell-type-specific candidates, PTGIR in myeloid cells and IL6ST in fibroblasts, confirmed the reduction of inflammatory and fibrotic pathways linked to IBD pathology. Multi-omic profiling and projection of in vitro phenotypes to patient datasets demonstrated the reversal of disease-associated programs via mechanisms distinct from those of existing biologics. Our single-cell anchored, machine-learning framework integrates in silico discovery with experimental validation, revealing new cell type-specific therapeutic opportunities and supporting a scalable approach for precision target discovery in IBD and other immune-mediated diseases.

bioinformatics↗

Stalling of elongating Pol II triggers Ser7 phosphorylation in trans to drive transcription recovery

DNA is scattered with obstacles that stall RNA polymerase II (Pol II) and block the production of full-length transcripts. Two mechanisms are known to resolve stalled Pol II: transcription-coupled nucleotide excision repair (TC-NER) and the "last resort" Pol II ubiquitylation-degradation pathway. Here, we uncover a third, distinct mechanism that alerts incoming Pol II molecules to roadblocks ahead and primes them for efficient elongation. We show that transcription stalling triggers GSK3-mediated phosphorylation of Ser7 residues (Ser7P) on the Pol II C-terminal domain. Unexpectedly, this phosphorylation occurs in trans: obstacles in gene bodies induce Ser7P on Pol II complexes at gene beginnings. This modification enables processive transcription while restraining excessive Pol II degradation by the "last resort" pathway. Our findings reveal an adaptive system that preserves transcriptional homeostasis by coordinating polymerase behavior across the gene in response to elongation stress.

molecular biology↗