The role of p53 in the aging process of skeletal muscle is likely to be a complex process involving many different cellular effectors.
AKT is involved in the regulation of many cellular processes via various downstream effectors such as mammalian target of the rapamycin (mTOR) in protein synthesis and the transcription factors nuclear factor- κB and FOXO (forkhead box O) in cell survival.
ILK, an integrin β1-subunit binding protein, is an intracellular effector of cell-matrix interactions and regulates many cellular processes, including growth, proliferation, survival, differentiation, migration, invasion, and angiogenesis [ 7, 28, 29].
Many studies focusing either on the signalling pathways controlling PCD or on the cellular effectors, have improved our understanding of this process [1], [3].
PLCγ1 hydrolyzes phosphatidylinositol-4,5-bisphosphate to generate the second messengers inositol-1,4,5-trisphosphate and diacylglycerol which in turn can activate several downstream effectors including specific protein kinase C (PKC) isoforms leading to many cellular responses [18].
83 One of the major effectors downstream of AKT is mTOR complex 1, which integrates many cellular inputs, including growth-factor signaling, metabolic state, cell survival, and proliferation.
Active caspase-8 can then, either directly, or indirectly via the BH3-only protein Bid, activate effector caspases, such as caspase-3, which in turn cleave many cellular substrates resulting in the biochemical and morphological features characteristic of apoptosis [ 11].
ROCK is the main downstream effector of Ras-homologous (Rho) family of GTPases which are involved in many cellular functions, such as cell proliferation, invasion and metastasis.
ROCK is the main downstream effector of Ras-homologous (Rho) family of GTPases which are involved in many cellular functions, such as cell proliferation, apoptosis, invasion and metastasis [ 7].
