Cell communication – Cell-cell contact
Local signal transduction channels are through cell-cell contact. There are 4 types of cell-cell contacts in mammalian cells: tight junctions, adheren’s junctions, gap junctions and desmosomes.
Cell communication - Paracrine signal vs. Endocrine signal
Cell signals can be local signal (paracrine signal) which is communicated through cell-cell contacts, or endocrine signal which is mostly hormones secreted by glands and transported via blood.
Cell signals are chemicals. Signal reception is a process of ligand binding to the receptors; mimic a lock and key model. There are three major types of signal receptors: receptor tyrosine kinases (RTKs), G protein-coupled receptors (GCPRs) and intracellular receptors. Ligand binding activates RTKs via dimerization and phosphorylation; Ligand binding activates GCPRs by activating G protein (replacing GDP by GTP) which can then phosphorylate the downstream targets. Intracellular receptors can be translocated into nucleus upon signal binding and activate gene expression directly.
Signal transduction is often achieved by phosphorylation and de-phosphorylation, and therefore involves kinase and phosphotases. Protein kinases are often involved in cell proliferation and phosphotases play antagonized roles.
Second messenger and signal amplification
Cell signals can be amplified during transduction because one kinase can phosphorylate multiple copies of downstream targets. Second messengers also play important roles in signal amplification. There are three major types of second messengers: cAMP/cGMP, IP3 and DAG, calcium ions. cAMP activates gene expression via CREB or PKA which further activates downstream targets. IP3 and DAG activate PKC and releases calcium ions. Calcium ions can also activate PKC which further activates the downstream targets. Calcium ions play multiple roles in cells in addition to second messenger.
Proliferating cells undergo cell cycle which is composed of G1, S, G2 and M phases. Resting cells are in G0. Cell cycle is controlled by cyclins and CDKs, when circumstances are not right, cell cycle checkpoints can be activated to restrain cell cycle. There are 4 major cell cycle checkpoints: G1 checkpoint, intra-S phase checkpoints, G2 checkpoints and spindle checkpoints. When cell cycle checkpoints are broken or cell cycle goes wrong, cells may undergo apoptosis or become cancerous.