Ras oncogene is regulated by GTP binding and GTP hydrolysis, which is associated with Ras-dependent signal transduction. Several factors affect Ras GTP binding and hydrolysis, including T-cell receptors, GPCR receptors, Growth factors and calcium.
Retinoblastoma protein is acetylated by p300 protein acetylase and deacetylated by HDAC and SIRT1. Acetylation causes Rb activation and E2F sequestration and deacetylation reverses this process.
EGFR-HER2 receptor complex is an important trigger of the oncogenic process. The process of tyrosine phosphorylation upon receptor activation undergoes a sequence of molecular steps that ultimately lead to signal transduction in cancer.
Retinoblastoma protein can have both pro- and anti-apoptotic functions in DNA damage response, depending on the particular cell type and activation state.
Stem cells have been increasingly viewed as potential therapeutic modalities in several diseases. In this respect both embrional and adult stem cells showed therapeutic potential.
PTEN phosphorylation regulates protein stability and activity through altering PTEN subcellular localization and conformation.
p53 tumor suppressor protein is under complex regulation through protein phosphorylation, acetylation, ubiquitination, neddylation, sumoylation and methylation. These modification affect both protein activity and stability.
IP3R calcium channel is regulated by several signaling pathways, including T-cell receptor, GPCR receptors, etc. These signaling pathways converge on cAMP and PKA, G proteins beta and gamma, CDK1, BCL-2, BCL-xL IRBIT, PKG/IRAG and other signaling proteins.