The transport of solutes across the cell membrane is essential for metabolic processes, like maintaining cell size and volume, generating the action potential, exchanging nutrients and gases, etc. Membrane transport can be either passive or active. It can be simple diffusion, facilitated, or mediated transport aided by transport proteins such as transporters and channels.
Transporters facilitate either an active or passive movement of solutes. They can allow a single-molecule transport down its concentration or electrochemical gradient. At the same time, some transporters can also transport two different molecules simultaneously, in the same or opposite direction. A transporter may utilize energy from ATP hydrolysis to move a solute against its concentration or electrochemical gradient. Transporters are especially involved in maintaining cell homeostasis, transcellular transport of solutes like amino acids, monosaccharides, ions, etc.
Channels form transmembrane pores that enable passive transport of solutes. Gated channels open only under specific conditions, whereas non-gated channels are always open, allowing ions to pass through them continuously down their concentration gradient. Channels serve numerous functions like signal transduction, transepithelial transport, pH regulation, etc.
Channels act faster than transporters. For example, when we touch a hot surface or pat on the back, the receptors that detect this action are cation-gated channels that open in response to these stimuli and help us react within seconds.
Clinical effect of non-functional transport proteins
Many diseases are caused due to mutations or defects in the regulation of the membrane transport proteins. Cystic fibrosis is caused due to the non-functional chloride ion transport proteins in the epithelial cells, which leads to excessive mucus build-up in the lungs. Some members of the ABC (ATP-binding cassette) family of membrane transporters contribute to cancer cells’ resistance to chemotherapy, limiting treatment efficacy. Glucose intolerance in type 2 diabetes mellitus is mainly due to the defective glucose transporters in the muscle and adipose tissues.
