Auinash Kalsotra

ExPert infers causal perturbations from cell states by learning prototypes across 12 contexts, achieving high recall with low compute and validating findings in disease models.

This study compares stress responses in inbred and outcrossed Drosophila embryos under heat stress, finding that inbred embryos show greater stress response activation and reduced developmental survival.

The paper shows that MALAT1 long noncoding RNA forms condensates with splicing factors to regulate hypoxia-induced alternative splicing near nuclear speckles.

The paper investigates snaR-A, a cancer-associated ncRNA, showing it interacts with splicing factors and disrupts mRNA processing, contributing to cancer progression.

The paper shows that reducing Cofilin dosage in Drosophila embryos enhances stress adaptation and thermotolerance by priming stress response pathways.

The paper identifies dysregulated RNA splicing in alcohol-associated liver disease as a cause of regeneration failure, highlighting ESRP2 deficiency and its impact on key signaling pathways.

The paper identifies PTBP1's role in regulating alternative splicing of actin regulators to control Sertoli cell actin cytoskeleton dynamics during spermatogenesis.

This study identifies the ESRP2-miR-122 axis as critical for postnatal liver polyploidization and maturation through RNA processing and cytokinesis regulation.

This study identifies PTBP1 as essential for intestinal stem cell survival and stemness by regulating gene expression through post-transcriptional mechanisms.

This study shows that DM1 mice have altered drug metabolism and increased fatty liver disease susceptibility due to RNA sequestration and splicing changes.

This study uses single-cell transcriptomics to track liver cell transitions during regeneration, revealing metabolic and proliferative dynamics in mouse liver.

This study identifies cell types and transcriptional heterogeneity in the corneal epithelium of Xenopus larvae through single-cell RNA sequencing, revealing novel genes and regulatory networks involved in differentiation and regeneration.

The paper introduces SimiC, a method for inferring gene regulatory networks per cell phenotype and comparing them across conditions, revealing regulatory dynamics missed by single GRN approaches.

This study identifies overexpression of a non-muscle RBFOX2 isoform as a cause of cardiac conduction defects in myotonic dystrophy by inducing arrhythmia and altering ion channel splicing.