arXiv:2607. 13120v1 Announce Type: cross Abstract: Inferring gene regulatory networks (GRNs) from single-cell transcriptomic data is crucial for biological discovery, yet existing approaches suffer from a fundamental misalignment with real-world needs.
arXiv:2606. 14734v1 Announce Type: cross Abstract: Motivation: Gene regulatory network inference from single-cell RNA sequencing (scRNA-seq) data is important for uncovering cell-state-specific transcriptional programs.
arXiv:2607. 16053v1 Announce Type: cross Abstract: Gene regulatory networks (GRNs) link transcription factor (TF) proteins to their target genes, yet reconstructing these networks from genome-wide data remains challenging under practical and methodological constraints.
arXiv:2606. 00685v1 Announce Type: new Abstract: Gene regulatory networks (GRNs) capture transcription factor-target interactions and are central to understanding cell-state regulation and disease.
arXiv:2607. 01627v1 Announce Type: cross Abstract: Accurate protein-protein interaction (PPI) prediction is central to functional genomics, disease mechanism discovery, and drug development.
arXiv:2407. 07357v3 Announce Type: replace Abstract: Predicting signed interactions in biological networks is crucial for understanding drug mechanisms and facilitating drug repurposing.
arXiv:2606. 24940v1 Announce Type: cross Abstract: Predicting transcriptional responses to genetic perturbations could reduce the experimental burden of functional genomics, but extrapolation to genes that were never perturbed during training remains difficult.
arXiv:2607. 04527v1 Announce Type: cross Abstract: Biological systems exhibit a hierarchical structure, characterised by directed flow from upstream regulators to downstream effects.
arXiv:2607. 14097v1 Announce Type: new Abstract: We introduce RegNetAgents, an AI-oriented multi-agent framework for structured, query-driven regulatory candidate identification across heterogeneous gene regulatory networks.
Accurate prediction of patient-specific therapeutic response from pre-treatment transcriptomes is hindered by the scarcity of matched clinical response labels and post-treatment molecular profiles. Preclinical transfer-learning models can simulate drug-induced expression changes but are often hard to interpret and unstable, whereas knowledge-graph methods provide mechanistic context yet remain static and fail to capture drug-induced transcriptomic perturbation dynamics.
Single-cell transcriptomes are sparse observations of coordinated biological programmes, yet most self-supervised models learn by reconstructing individual genes. Here we present BioM-JEPA, a joint-embedding predictive architecture that instead predicts aggregate representations of graph-connected gene blocks defined by protein-association and corpus-derived coexpression evidence.
arXiv:2608. 05928v1 Announce Type: new Abstract: Single-cell transcriptomes are sparse observations of coordinated biological programmes, yet most self-supervised models learn by reconstructing individual genes.
arXiv:2607. 22934v1 Announce Type: cross Abstract: Learning causal graphs from interventional data is a challenging problem with broad applications.