IndraLab

Statements


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"MarTX selectively blocks beta4 containing KCa1.1 channels, whereas IbTX blocks KCa1.1 channels that lack beta4."

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"In our experiments, we used the high affinity BK channel blockers IbTX and PAX to investigate on the relationship between their blocking mechanisms and biological effects, such as cell cycle progression and the associated intracellular signaling, morphological changes, and cell proliferation."

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"Overall, IbTX inhibited KCa1.1 channels on FLSs and treated rat models of RA without inducing side effects associated with nonspecific KCa1.1 blockade and could become the basis for the development of a new treatment of RA."

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"We have demonstrated that TEA and IBTX inhibit the BK channel currents by the same extent of 53% in uterine arterial myocytes XREF_BIBR."

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"Interestingly, IBTX inhibition of urothelial MaxiK activity results in changes in metabolism in both the mucosa and detrusor."

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"Notwithstanding these results originating from whole carotid body preparations, or from the isolated type I cell in culture, it was observed, by other laboratories, that IbTX inhibition of maxiK channels of type I cells in vitro could, just like hypoxia, induce neurosecretion from type I cells maintained in clusters or in thin slice preparations of the carotid body, where even drug induced secretion from quiescent cells was often noted."

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"The capacity of the IbTX and PAX used in the killing and phospholipase degradation assays to inhibit BK channel currents was confirmed in cells expressing native BK channels and in COS-7 cells transfected with BK channels."

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"IbTx inhibits the Ca 2+ -dependent large-conductance potassium channel KCNMA1, while Clt inhibits the Ca 2+ -dependent intermediate-conductance potassium channel KCNN4."

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"Either the selective BK channel blockers IbTX and PAX induced early an accumulation in the G2 phase and AKT1p ser473 dephosphorylation after 6 h of incubation time with a reduction of cell proliferation."

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"IbTX inhibited KCa1.1 channels expressed by FLSs from patients with RA and by FLSs from rat models of RA and reduced FLS invasiveness."

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"These observations suggest that IBTX inhibition of urothelial MaxiK may activate signaling pathways which specifically affects peroxisomal mediated lipid metabolism in the detrusor."

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"An alternative explanation is that IBTX disrupts the interaction of MaxiK with proteins, such as those involved in signal transduction (several potential candidates were recently identified as part of the MaxiK interactome) or translocation of MaxiK into the mitochondria (for example, through disrupting its interaction with Tom22) [XREF_BIBR, XREF_BIBR]."

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"Both these values are rather close to the reported EC 50 values for Pax- and Ibtx induced BK channel blockade."

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"Because maxi-K + channels are blocked by TEA or IbTX, we tested to see whether, like hypoxia, addition of these agents to the external solution induces Ca 2+ entry and secretion from glomus cells.In m[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"