Nitin Khandelwal

This paper shows that SB431542, a TGF-β inhibitor, suppresses SARS-CoV-2 replication through three mechanisms: disrupting ORF3a function, inhibiting lysosomal biogenesis, and blocking TGF-β-induced apoptosis, with no resistance observed after 50 generations of exposure.

This study investigates the cell type-specific roles of FOXP1 in mouse neocortical development, revealing its impact on neurogenesis, gene expression, and cortical layering, with implications for ASD and FOXP1 syndrome.

This study shows that p38-MAPK is essential for SARS-CoV-2 replication, as its inhibition reduces viral growth and its activation supports RNA/protein synthesis without affecting viral entry or budding.

This study shows FOXP1 regulates glutamatergic input development in striatal neurons, with potential therapeutic implications for FOXP1 syndrome.

The paper shows that Foxp1 and Foxp2 compensate for each other in D1-SPNs, and their loss causes motor and social deficits, which can be reversed by re-expressing Foxp1.

This study shows that human CLOCK has extra-circadian functions in the neocortex, enhancing cognitive flexibility and neural connectivity through altered gene expression in excitatory neurons.

The paper shows that FOXP1 reduces intrinsic excitability in D2 striatal projection neurons by increasing potassium currents through transcriptional activation of KIR and KLeak channels.

This study shows that knocking down Piwil1 and Piwil2 in the mouse hippocampus enhances contextual fear memory without affecting anxiety.

This study shows that ING1 regulates activity-induced gene expression in cortical neurons by interacting with other epigenetic factors and affecting synaptic plasticity-related genes.