![]() p53 also transactivates other genes that may contribute to apoptosis, including PTEN (Phosphatase and Tensin Homolog Deleted On Chromosome-10), APAF1, Perp, p53AIP1 (p53-regulated Apoptosis-Inducing Protein-1), and genes that lead to increases in ROS (Reactive Oxygen Species). Other p53 targets include BAX, Noxa, PUMA (p53-Upregulated Modulator of Apoptosis), and the most recently identified, BID. p53 initiates apoptosis by transcriptionally activating pro-apoptotic Bcl2 family members and repressing anti-apoptotic Bcl2 proteins and CIAPs. When bound to MDM2, p53 can no longer function as an activator of transcription. MDM2 binds p53 and mediates the nuclear export. The DNA checkpoints proteins, ATM (Ataxia Telangiectasia Mutated protein), and Chk2 (Checkpoints Factor-2), directly phosphorylate and stabilize p53 and inhibit MDM2 (Mouse Double Minute-2 Homolog)–mediated ubiquitination of p53. p53 is a sensor of cellular stress and is a critical activator of the intrinsic pathway (See the p53 Pathway for Apoptosis Signaling). Intrinsic stresses such as oncogenes, direct DNA damage, hypoxia, and survival factor deprivation, can activate the intrinsic apoptotic pathway. The intrinsic apoptosis pathway begins when an injury occurs within the cell. Tumoricidal Effects of Hepatic NK Cells.Transendothelial Migration of Leukocytes.IL-2 Gene Expression in Activated and Quiescent T-Cells.Hematopoiesis from Pluripotent Stem Cells.Hematopoiesis from Multipotent Stem Cells.Cytokine, Chemokine, Growth Factor Pathways. ![]() Killer T Cell Mediated Apoptosis Pathway.Intrinsic and Extrinsic Pathways of Apoptosis.Antigen Processing and Presentation by MHCs.
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