M. K. Ghosh

PLGA-based dual-loaded nanoformulation of DIM and TMZ - An advanced clinical strategy for brain cancer treatment in a combinatorial approach

This study develops a PLGA-based nanoformulation combining TMZ and DIM to enhance GBM treatment by improving drug delivery and synergistic cytotoxic effects.

DDX5 (p68) orchestrates β-catenin, RelA and SP1 mediated MGMT gene expression: Implication in TMZ chemoresistance

This study identifies DDX5 (p68) as a master regulator of MGMT gene expression through interactions with β-catenin, RelA, and SP1, contributing to TMZ chemoresistance in colon cancer.

A novel role of USP7 in imparting partial EMT state in colorectal cancer through the DDX3X-β-catenin axis

This study identifies USP7 as a key regulator of partial EMT in colorectal cancer by stabilizing DDX3X and enhancing Wnt/β-catenin signaling.

E3 Ubiquitin Ligase CHIP Drives Monoubiquitination-mediated Nuclear Import of Tumor Suppressor PTEN

This study identifies CHIP as a novel E3 ubiquitin ligase that monoubiquitinates PTEN, promoting its nuclear import and enhancing its tumor suppressive functions.

Identification and validation of E3 ubiquitin ligase XIAP as a novel substrate of deubiquitinase USP7 (HAUSP) - Implication towards oncogenesis

This study identifies XIAP as a novel substrate of USP7, showing that USP7 stabilizes XIAP to promote tumorigenesis by inhibiting apoptosis, and finds that combined inhibition of USP7 and XIAP enhances apoptosis.

Wnt/β-catenin signaling and p68 conjointly regulate CHIP in colorectal cancer

This study identifies a novel mechanism where Wnt/β-catenin signaling and p68 regulate CHIP expression in colorectal cancer, promoting cell proliferation and migration.

Recapitulating the frataxin activation mechanism in an engineered bacterial cysteine desulfurase supports the architectural switch model

The paper engineers a bacterial cysteine desulfurase to recapitulate the frataxin activation mechanism, supporting the architectural switch model by showing FXN compensates for lost subunit interactions.