o Illustrate the basic transport mechanisms that were discussed in class -glucos
ID: 209260 • Letter: O
Question
o Illustrate the basic transport mechanisms that were discussed in class -glucose carrier, Na+/K+ antiporter and Na+/glucose symporter. Relate allosteric regulation/conformational change to the function of these transporters and identify major differences in function. Relate the HCO3-/Cl- antiporter to gas transport in the blood Describe the “ping-pong" mechanism for this transport system Make predictions about the effect of changing/mutating a transport mechanism if given a description of the model/mechanism.Explanation / Answer
1) Glucose transporters are membrane proteins facilitating transport of glucose across plasma membrane. GLUT or SLC2A family of transporters are found in mammals. 14 GLUTS are encoded by human genome. GLUT is a type of uniporter transporter protein. GLUTs are integral membrane proteins containing 12 membrane-spanning helices with both the amino and carboxyl termini exposed on the cytoplasmic side of the plasma membrane. Glucose is transported by GLUT proteins according to a model of alternate conformation. Binding of glucose to one site provokes a conformational change associated with transport, and releases glucose to the other side of the membrane.
Sodium–potassium pump is an enzyme found in the plasma membrane of all animal cells. It pumps sodium out of cells while pumping potassium into cells, both against their concentration gradients. This pumping utilises energy in the form of ATP. For every ATP molecule that the pump uses, three sodium ions are exported and two potassium ions are imported; there is hence a net export of a single positive charge per pump cycle.
Sodium-glucose symporter is a transmembrane protein. It is found on the apical membrane of the epithelial cells of the small intestines and is an example of sodium-driven Secondary active transport. The sodium and glucose bind to the symporter and are simultaneously both co-transported into the epithelial cells. The sodium driven-glucose symporter uses the potential free energy stored in the sodium electrochemical gradient i.e. low sodium concentration inside the epithelial cells, established by Sodium-potassium pump. Therefore, the sodium influx from the lumen to the epithelial cell is coupled with glucose transport.
2) Bicarbonate transporter proteins are proteins which transport bicarbonate and regulate pH in cells which plays a vital role in acid-base movements in the stomach, pancreas, intestine, kidney, reproductive organs and the central nervous system. When Carbon dioxide (CO2) is generated in tissues as a byproduct of normal metabolism, it dissolves in blood plasma and enters into red blood cells (RBC), where carbonic anhydrase catalyzes its hydration to carbonic acid (H2CO3). Carbonic acid then spontaneously dissociates to form bicarbonate (HCO3) and a hydrogen ion (H+). In response to the decrease in intracellular pCO2, more CO2 passively diffuses into the cell.However, cell membranes are impermeable to charged ions (i.e. H+, HCO3 ) but RBCs are able to exchange bicarbonate for chloride using the anion exchanger protein. Thus, the rise in intracellular bicarbonate leads to bicarbonate export and chloride intake.
Chloride concentration is lower in systemic venous blood than in systemic arterial blood. High venous pCO2 leads to bicarbonate production in RBCs, which then leaves the RBC in exchange for chloride entering.
The opposite of this occurs in the pulmonary capillaries of the lungs when the PO2 rises and PCO2 falls. This releases hydrogen ions from hemoglobin, increases free H+ concentration within RBCs, and shifts the equilibrium towards CO2 and water formation from bicarbonate. The subsequent decrease in intracellular bicarbonate concentration reverses chloride-bicarbonate exchange: bicarbonate moves into the cell in exchange for chloride moving out.
3) Na+/H+ antiporters are crucial for survival in all living organisms because they control the intracellular sodium and proton concentration. Any kind of change or mutation in the cellular transport mechanism can cause the complete phenotype of a disease. For example, mutations in the cystic fibrosis transmembrane conductance regulator (CFTR)—a chloride channel—were identified as initiators of cystic fibrosis. Besides, the Na+,K+-ATPase—a member of the P-type ATPase family—is an essential ion transporter in all animal cells. It exists in several isoforms to manage the specific metabolic needs of each cell type. However, for decades, several clinical conditions have been correlated with modified Na+,K+-ATPase activity which are mainly caused by alteration of endogenous or xenobiotic factors.
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