Quantitative metabolomics services for biomarker discovery and validation.
Specializing in ready to use metabolomics kits.
Your source for quantitative metabolomics technologies and bioinformatics.
Loader

Loading Pathway...

Serine/threonine- protein kinase Chk2 Cellular tumor antigen p53 Serine/threonine- protein kinase Chk1 E3 ubiquitin-protein ligase Mdm2 Protein Mdm4 Caspase-8 BH3-interacting domain death agonist BH3-interacting domain death agonist Apoptosis regulator BAX Bcl-2 homologous antagonist/killer Tumor necrosis factor receptor superfamily member 6 FAS-associated death domain protein Cellular tumor antigen p53 Tumor necrosis factor receptor superfamily member 6 Metalloreductase STEAP3 DNA damage-binding protein 2 Cyclin-dependent kinase inhibitor 1 Protein reprimo Caspase-9 Cytochrome c Cytochrome c Cytochrome c Serine-protein kinase ATM Serine/threonine- protein kinase ATR Apoptotic protease- activating factor 1 Apoptotic protease- activating factor 1 Pi Pi Deoxyadenosine triphosphate dADP Apoptosis Signaling MDM2 and p53 together generate negative feedback loop to maintain p53 levels under normal cellular conditions UV, gamma-irradiation, genotoxic drugs, heat/cold shock, stress signals, etc. DNA Damage MDM2 and MDM4 generate a negative feedback loop to regulate p53 expression A truncated BH3-Interacting domain death agonist translocates to integrate into the mitochondrial membrane p53 acts as a transcription factor that regulates the expression of genes involved in cell cycle arrest, apoptosis, DNA repair, and senescence The altered mitochondrial membrane permeability results in the release of cytochrome c into the cytosol, it then can bind to Apaf-1 to accelerate apoptosis Mitochondria Damaged mitochondria Exosome mediated secretion DNA repair G1 arrest G2 arrest Extracellular Space Cytosol Nucleus