Gourisankar Ghosh

This paper uses cryo-EM to show that IKK2/β adopts distinct dimeric conformations that regulate its activation through structural plasticity and interactions with NEMO and polyubiquitin.

This paper identifies the PFKFB3-F2,6BP metabolic axis as a key driver of Alzheimer's disease by linking metabolic dysregulation to genomic stability and Tau proteostasis, showing that F2,6BP supplementation rescues AD phenotypes across multiple models.

This study shows that fructose-2,6-bisphosphate (F2,6BP) restores genome repair and motor function in TDP-43 pathology-driven motor neuron diseases.

This paper shows that F2,6BP restores mitochondrial genome integrity in Huntington's Disease by rescuing PNKP activity and mitochondrial function.

This study identifies NME1 as a cofactor that enhances RelA's DNA binding to κB sites, promoting gene expression and suggesting that κB site clustering is necessary for transcription complex assembly.

This study shows phosphorylation at Ser366 enhances Bcl3's transcriptional activity by increasing C-terminal flexibility, enabling better DNA binding with p52:p52 complexes, and linking structural changes to cancer-related mutations.

This study shows that CgA deficiency reduces tau pathology and improves cognitive function in tauopathy models by modulating epinephrine-alpha-adrenergic receptor signaling.

The paper shows that phosphorylated IκB binds chromatin via acetylated H4 and that proteolytic cleavage of H4 inhibits this binding, affecting intestinal cell differentiation.