Publications by authors named "Shrikant Babanrao Kokate"
Helicobacter pylori infection is one of the leading factors that promotes, among other diseases, gastric cancer (GC). Infection of gastric epithelial cells (GECs) by H. pylori enhances the expression as well as acetylation of the E3 ubiquitin ligase SIAH2 which promotes GC progression.
View Article and Find Full Text PDFHelicobacter pylori-mediated gastric carcinogenesis involves upregulation of the E3 ubiquitin ligase Siah2 and its phosphorylation-mediated stabilization. This study elucidates a novel mechanism of oxidative stress regulation by phosphorylated Siah2 in H. pylori-infected gastric epithelial cancer cells (GECs).
View Article and Find Full Text PDFHelicobacter pylori is the strongest known risk-factor for gastric cancer. However, its role in gastric cancer metastasis remains unclear. Previously we have reported that H.
View Article and Find Full Text PDFGastric epithelial cells infected with Helicobacter pylori acquire highly invasive and metastatic characteristics. The seven in absentia homolog (Siah)2, an E3 ubiquitin ligase, is one of the major proteins that induces invasiveness of infected gastric epithelial cells. We find that p300-driven acetylation of Siah2 at lysine 139 residue stabilizes the molecule in infected cells, thereby substantially increasing its efficiency to degrade prolyl hydroxylase (PHD)3 in the gastric epithelium.
View Article and Find Full Text PDFArticle Synopsis
- The study investigates how hypoxia, a condition of low oxygen, enhances the aggressive characteristics of solid tumors, particularly gastric cancer cells (GCCs).
- Researchers tested the effects of a compound called CTK7A, which inhibits a specific enzyme involved in histone acetylation, to see if it could trigger cell death (apoptosis) in GCCs under hypoxic conditions.
- Results indicated that CTK7A caused increased production of hydrogen peroxide in GCCs, leading to activation of a specific cell death pathway, making hypoxic and invasive GCCs more susceptible to apoptosis compared to normal cells.
Article Synopsis
- Helicobacter pylori is a key factor in causing stomach cancer, and the protein Siah2 may play a crucial role in this process.
- Research showed that H. pylori infection boosts Siah2 levels in gastric cancer cells, leading to increased cell movement and invasiveness.
- The study also found that two specific proteins, ETS2 and Twist1, activate Siah2 expression, suggesting potential for these factors to be used in diagnosing or treating gastric cancer.
Helicobacter pylori induces the antiapoptotic protein myeloid cell leukemia 1 (Mcl1) in human gastric epithelial cells (GECs). Apoptosis of oncogenic protein Mcl1-expressing cells is mainly regulated by Noxa-mediated degradation of Mcl1. We wanted to elucidate the status of Noxa in H.
View Article and Find Full Text PDF