1 ement of patients whose therapy alters renal tubular transport.

2 he study of the physiology of proximal renal tubular transport.

3 nd has a dangling carboxylate group favoring tubular transport.

4 fonate (DMPS) significantly alters the renal tubular transport, accumulation, and toxicity of inorgan

5 thin the ABCC10 gene may influence TFV renal tubular transport and contribute to the development of K

6 excretion, suggesting synergistic actions on tubular transport and vascular smooth muscle cells.

7 J5 in regulation of blood pressure, proximal tubular transport, and afferent arteriolar responsivenes

8  glomerulus in nephrotic syndrome may affect tubular transport by interacting with membrane transport

9 RE VAMP7 mediates fusion of melanosomes with tubular transport carriers that also carry the cargo pro

10        Our findings further reveal that COPI tubular transport complements cisternal maturation in ex

11 OC-2 functions to direct recycling endosomal tubular transport intermediates to maturing melanosomes

12                                              Tubular transport measurements confirmed that BNZ affect

13 ole for these receptors in the regulation of tubular transport mechanisms was indicated by the recent

14 ften complicated by countercurrent exchange, tubular transport or glomerular filtration.

15 enetic model for the study of proximal renal tubular transport pathology.

16   Because of the central nature of sodium in tubular transport physiology, disorders of sodium handli

17 poxyeicosatrienoic acids in modulating renal tubular transport processes, we postulate that CYP2J5 pr

18  increased blood pressure, enhanced proximal tubular transport rates, and exaggerated afferent arteri

19 ated with the lower affinity of MAG3 for the tubular transport receptor, but MAG3 is more highly prot

20 ), an enzyme providing the driving force for tubular transport, were inversely enriched in kidney reg