High impact information on LOC508734

• In that case, addition of either NPPB or flufenamic acid did not produce further inhibition [1].
• Hypotonic cell swelling stimulated outwardly rectifying I(Cl,swell), which was reversibly inhibited by the Cl(-) channel blockers, phloretin (300 microM) or 5-nitro-2-(phenylpropylamino)-benzoate (NPPB, 100 microM) [2].
• 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB; 0.1 mM), a chloride channel blocker in the nonpigmented cells, produced a 25% reduction when applied to the aqueous side [3].
• Intercellular gap junctions between the two cell layers and the NPPB-sensitive Cl channels at the basolateral surface in nonpigmented epithelial cells also play a crucial role in regulating the Cl movement across the functional syncytium [4].
• Bilateral heptanol (3.5 mM) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB; 0.1 mM) on the aqueous side also inhibited the Cl transport by 80% and 92%, respectively [4].

Biological context of LOC508734

• Chloride uptake was inhibited by both NPPB and IAA94/95 with apparent IC50 values of around 10 microM under optimal conditions (i.e., 4 min uptake at 4 degrees C) [5].
• In addition, both NPPB and, to a lesser extent, IAA94/95 were found to have other effects on the vesicles, in that, when added at a concentration of 100 microM, they induced a leakage of pre-accumulated 36Cl-. This was probably caused by either dissipation of membrane potential or damage to the vesicle membranes [5].

Anatomical context of LOC508734

• The Cl(-) channel blocker 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB; 10(-4) M), previously shown to inhibit SR Cl(-) channels, significantly reduced the magnitude of successive acetylcholine-induced contractions of airway smooth muscle (ASM), suggesting a "run down" of sequestered Ca(2+) within the SR [6].
• The effects of the Cl- channel blockers, NPPB, IAA94/95 and a number of related compounds on 36Cl- transport in membrane vesicles from bovine kidney cortex and rabbit ileum mucosa brush borders have been studied [5].

Associations of LOC508734 with chemical compounds

• 4. Hypertonic cell shrinkage inhibited an outwardly rectifying Cl- current, which was also efficiently blocked by 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB; 100 microM), quinine (500 microM) and quinidine (500 microM) [7].
• FSK (50 microM) increased apical HCO permeability by twofold, which was inhibited 42% by NPPB and 65% by glibenclamide [8].
• Furthermore, NPPB significantly reduced caffeine-induced contraction and increases in intracellular Ca(2+) concentration ([Ca(2+)](i)) [6].
• FSK-activated basolateral Cl(-) permeability was insensitive to NPPB, glibenclamide, or furosemide but was inhibited 80% by H(2)DIDS [8].
• ER, for the NO3-/I-anion-pair, was significantly reduced by DIDS (100% at 500 microm), NPPB ( approximately 80% at 100 microm) and tamoxifen (approximately 85% at 12 microm) [9].

References