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1 ement of patients whose therapy alters renal tubular transport.
2 he study of the physiology of proximal renal tubular transport.
3  increased bone resorption, or altered renal tubular transport.
4 ofluorescence revealed alterations in distal tubular transport.
5 nd has a dangling carboxylate group favoring tubular transport.
6 fonate (DMPS) significantly alters the renal tubular transport, accumulation, and toxicity of inorgan
7 thin the ABCC10 gene may influence TFV renal tubular transport and contribute to the development of K
8 excretion, suggesting synergistic actions on tubular transport and vascular smooth muscle cells.
9 J5 in regulation of blood pressure, proximal tubular transport, and afferent arteriolar responsivenes
10  glomerulus in nephrotic syndrome may affect tubular transport by interacting with membrane transport
11 e, we show that Src induces the formation of tubular transport carriers containing GALNTs.
12 RE VAMP7 mediates fusion of melanosomes with tubular transport carriers that also carry the cargo pro
13 requires delivery of melanogenic cargoes via tubular transport carriers that emanate from early endos
14 AMP7, the vSNARE for fusing endosome-derived tubular transport carriers with maturing melanosomes in
15 which are needed for biogenesis of endosomal tubular transport carriers, strongly inhibits the peroxi
16  not influence BLOC-1 function in generating tubular transport carriers.
17        Our findings further reveal that COPI tubular transport complements cisternal maturation in ex
18 t a novel autoimmune cause of specific renal tubular transport disturbances and tubulointerstitial ne
19 OC-2 functions to direct recycling endosomal tubular transport intermediates to maturing melanosomes
20                                              Tubular transport measurements confirmed that BNZ affect
21 ole for these receptors in the regulation of tubular transport mechanisms was indicated by the recent
22 ften complicated by countercurrent exchange, tubular transport or glomerular filtration.
23 enetic model for the study of proximal renal tubular transport pathology.
24   Because of the central nature of sodium in tubular transport physiology, disorders of sodium handli
25 poxyeicosatrienoic acids in modulating renal tubular transport processes, we postulate that CYP2J5 pr
26  increased blood pressure, enhanced proximal tubular transport rates, and exaggerated afferent arteri
27 ated with the lower affinity of MAG3 for the tubular transport receptor, but MAG3 is more highly prot
28 ), an enzyme providing the driving force for tubular transport, were inversely enriched in kidney reg
29 sponse to environmental stressors to support tubular transport, which may ultimately affect regulator