Antiporter

About: Antiporter is a research topic. Over the lifetime, 3687 publications have been published within this topic receiving 172648 citations. The topic is also known as: antiporter.

Enzymatic basis for active transport of na+ and k+ across cell membrane.

Abstract: Afhnity for Monovalent Cations. 597 Relationship of Enzyme System to ATP. 598 Isolation of Enzyme System from Other Cells with Active Transport of Na+ and K+ 602 Location of Enzyme System in the Cell. 604 Effect of Cardiac Glycosides. 605 Quantitative Relation between Effect of Na+ + K+ on Enzyme System and Active Transport in Intact Cell. 606 Nature of Enzyme System. 607 Relation of (Na + + K+)-Activated Enzyme System to Active Transport of Cations. 6 10 Conclusion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6’4

Salt Tolerance Conferred by Overexpression of a Vacuolar Na+/H+ Antiport in Arabidopsis

Abstract: Agricultural productivity is severely affected by soil salinity. One possible mechanism by which plants could survive salt stress is to compartmentalize sodium ions away from the cytosol. Overexpression of a vacuolar Na+/H+antiport from Arabidopsis thaliana in Arabidopsisplants promotes sustained growth and development in soil watered with up to 200 millimolar sodium chloride. This salinity tolerance was correlated with higher-than-normal levels of AtNHX1transcripts, protein, and vacuolar Na+/H+(sodium/proton) antiport activity. These results demonstrate the feasibility of engineering salt tolerance in plants.

Acid pH in Tumors and Its Potential for Therapeutic Exploitation

Abstract: Measurement of pH in tissue has shown that the microenvironment in tumors is generally more acidic than in normal tissues. Major mechanisms which lead to tumor acidity probably include the production of lactic acid and hydrolysis of ATP in hypoxic regions of tumors. Further reduction in pH may be achieved in some tumors by administration of glucose (+/- insulin) and by drugs such as hydralazine which modify the relative blood flow to tumors and normal tissues. Cells have evolved mechanisms for regulating their intracellular pH. The amiloride-sensitive Na+/H+ antiport and the DIDS-sensitive Na+-dependent HCO3-/Cl- exchanger appear to be the major mechanisms for regulating pHi under conditions of acid loading, although additional mechanisms may contribute to acid extrusion. Mitogen-induced initiation of proliferation in some cells is preceded by cytoplasmic alkalinization, usually triggered by stimulation of Na+/H+ exchange; proliferation of other cells can be induced without prior alkalinization. Mutant cells which lack Na+/H+ exchange activity have reduced or absent ability to generate solid tumors; a plausible explanation is the failure of such mutant cells to withstand acidic conditions that are generated during tumor growth. Studies in tissue culture have demonstrated that the combination of hypoxia and acid pHe is toxic to mammalian cells, whereas short exposures to either factor alone are not very toxic. This interaction may contribute to cell death and necrosis in solid tumors. Acidic pH may influence the outcome of tumor therapy. There are rather small effects of pHe on the response of cells to ionizing radiation but acute exposure to acid pHe causes a marked increase in response to hyperthermia; this effect is decreased in cells that are adapted to low pHe. Acidity may have varying effects on the response of cells to conventional anticancer drugs. Ionophores such as nigericin or CCCP cause acid loading of cells in culture and are toxic only at low pHc; this toxicity is enhanced by agents such as amiloride or DIDS which impair mechanisms involved in regulation of pHi. It is suggested that acid conditions in tumors might allow the development of new and relatively specific types of therapy which are directed against mechanisms which regulate pHi under acid conditions.

Understanding and Improving Salt Tolerance in Plants

Abstract: One-fifth of irrigated agriculture is adversely affected by soil salinity. Hence, developing salt-tolerant crops is essential for sustaining food production. Progress in breeding for salt-tolerant crops has been hampered by the lack of understanding of the molecular basis of salt tolerance and lack of availability of genes that confer salt tolerance. Genetic evidence suggests that perception of salt stress leads to a cytosolic calcium-signal that activates the calcium sensor protein SOS3. SOS3 binds to and activates a ser/thr protein kinase SOS2. The activated SOS2 kinase regulates activities of SOS1, a plasma membrane Na + /H + antiporter, and NHX1, a tonoplast Na + /H + anti-porter. This results in Na + efflux and vacuolar compartmentation. A putative osmosensory histidine kinase (AtHKI)-MAPK cascade probably regulates osmotic homeostasis and ROS scavenging. Osmotic stress and ABA (abscisic acid)-mediated regulation of LEA (late-embryogenesis-abundant)-type proteins also play important roles in plant salt tolerance. Genetic engineering of ion transporters and their regulators, and of the CBF (C-repeat-binding factor) regulons, holds promise for future development of salt-tolerant crops.