Avtar Roopra

This study shows that tofacitinib, a JAK inhibitor, reduces seizures and improves cognition in a mouse model of drug-resistant epilepsy when used as an add-on therapy to carbamazepine.

This study uses Motion Sequencing combined with a novel analysis pipeline to identify repetitive behaviors in epileptic mice and shows that carbamazepine partially rescues these behaviors.

In mice 4 days after kainate-induced status epilepticus, H3K27me3 gains coincide with repression of excitability genes; EZH2 inhibition with UNC1999 lowers seizure threshold acutely and increases chronic seizure frequency.

The paper uses autofluorescence imaging to identify and track neural stem cell activation states in vitro and in vivo, linking it to transcriptional features and cell behavior.

The paper shows that brief tofacitinib treatment suppresses seizures and reverses cognitive deficits in chronic epilepsy by targeting a resurgent JAK/STAT pathway activation.

This study shows that maternal sleep apnea during pregnancy in rats leads to long-term respiratory deficits and neuroinflammation in male offspring due to microglia changes, while female offspring are unaffected.

The paper introduces exclusion-based immunoprecipitation methods to identify RNA binding partners of CRD-BP in mammary epithelial cells, showing enrichment in mRNAs related to mitochondrial function and oxidative stress.

This study investigates the effects of TCF19 overexpression in pancreatic beta-cells, revealing increased DNA damage response and inflammatory gene expression.

This study shows that prior hypoxia exposure increases microglial inflammatory gene expression in response to LPS without increasing H3K4me3 at these genes.

MAGIC predicts transcription factors and cofactors driving gene sets by analyzing ENCODE ChIP-seq data, outperforming existing tools in three biological contexts.

This paper identifies EZH2 as a protective factor in epilepsy using a systems approach to analyze transcriptomic data from rodent and human samples.

This study shows that the γ2R43Q GABAA receptor mutation abolishes tonic inhibition in mice, leading to absence epilepsy and febrile seizures.