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APB

FIG. 2. Mechanism of phenylephrine (PE)-mediated wave-like [Ca2+] oscillations in the rabbit inferior vena cava. (A) PE-mediated [Ca2+]j oscillations are completely inhibited by 10 fiM cyclopiazonic acid (CPA), but the average [Ca2+ ]j remains elevated. (B) PE-mediated [Ca2+]j oscillations are abolished by 75 /iM 2-aminoethoxydiphenyl borate (2-APB). (C) Application of 10 piM nifedipine (Nif) reduced the frequency of PE-mediated [Ca2+]j oscillations while additional application of SKF96365 (SKF) completely abolished the remaining [Ca2+] oscillations. (D) Application of 100 /iM 2,4-dichlorobenzamil (2,4-DCB) completely inhibited nifedipine-resistant PE-induced [Ca2+]j oscillations and lowered the [Ca2+]j to a level that is slightly higher than baseline. Additional application of SKF96365 returned the [Ca2+]j level to baseline. (Experimental traces reproduced with permission from Lee et al 2001.)... [Pg.32]

Sanders I thought there was a report of TRP channels being blocked by 2-APB. [Pg.42]

Blaustein 2-aminoethoxydiphenyl borate (2-APB) is used as a selective blocker of InsP3 receptors. However, I think I have seen recent papers showing that 2-APB also blocks Ca2+ entry in some way. Do you think it blocks Ca2+ entry and reduces the tonic component in this way ... [Pg.66]

FIG. 2. Simultaneous recording of membrane currents and Ca2+ fluorescence. (A) Upper and lower traces indicate the time courses of membrane current and [Ca2+] respectively. Cells were voltage-clamped at — 60 mV. Pipette contained Cs aspartate internal solution supplemented with 50 M fura-2. (B) Expanded time-courses of membrane current and [Ca2+] form the dotted box in A. TG, thapsigargin 2-APB, 2-aminoethoxydiphenyl borate. [Pg.87]

Fig. 5. Effect of WH on [Ca +], in Ang II-, CaCU or Bay K8644-stimulated VSMC. Ang II (10 UM)-induced [Ca " ]/ elevation (a) in Fura-2/AM-loaded VSMC was measured in the absence (Control) or presence of WH (300 juM). One pM PD 123177 as an AT2-receptor antagonist was added 10 min before Ang II addition. CaCf (2.5 mM) was added to VSMC treated with 2-APB (200 /xM IP3-R blocker)-containing Ca free PSS buffer (b). Effect of WH on [Ca ]/ in Bay K8644-stimulated VSMC was measured using a con-focal microscope and a fluorescent spectrometer (c). Bay K8644 (50 /xM)-induced [Ca ]/ elevation in VSMC was measured in the absence (Control) or presence of WH (300 /xM). Fig. 5. Effect of WH on [Ca +], in Ang II-, CaCU or Bay K8644-stimulated VSMC. Ang II (10 UM)-induced [Ca " ]/ elevation (a) in Fura-2/AM-loaded VSMC was measured in the absence (Control) or presence of WH (300 juM). One pM PD 123177 as an AT2-receptor antagonist was added 10 min before Ang II addition. CaCf (2.5 mM) was added to VSMC treated with 2-APB (200 /xM IP3-R blocker)-containing Ca free PSS buffer (b). Effect of WH on [Ca ]/ in Bay K8644-stimulated VSMC was measured using a con-focal microscope and a fluorescent spectrometer (c). Bay K8644 (50 /xM)-induced [Ca ]/ elevation in VSMC was measured in the absence (Control) or presence of WH (300 /xM).
Enfissi, A., Prigent, S., Colosetti, P. and Capiod, T., 2004, The blocking of capacitative calcium entry by 2-aminoethyl diphenylborate (2-APB) and carboxyamidotriazole (CAI) inhibits proliferation in Hep G2 and Huh-7 human hepatoma cells. Cell Calcium 36, 459-467. [Pg.422]

Influx of Ca2+ through a-LTX pores might explain Ca2+-dependent secretion, but not the bursts of miniatures. These may be due to Ca2+ waves caused by activation of phospholipase C (PLC) (Vicentini and Meldolesi 1984 Davletov et al. 1998) and release of intracellular Ca2+ (Ca2+,). In fact, U73122 (blocks PLC activation by G proteins), thapsigargin (depletes Ca2+ stores), and 2-APB (inhibits activation of Ca2+ stores) block a-LTX action (Davletov et al. 1998 Ashton et al. 2001 Capogna et al. 2003), impheating a G protein cascade in Ca2+-dependent toxin-induced release. [Pg.175]

As shown in Table 7.1, B3LYP/6-31G calculations reproduce adequately the activation energies of Cope reactions. These calculations confirm (Table 7.2, APB in kcal... [Pg.232]

This paper describes the reduction of hypoxic but not hypercapnic chemosensory discharge of not carotid body key cell permanent IP, inhibitors, 2-aminocthoxydiphenylgorene (2-APB, 50-200 pM) in a dose-dependent way. [Pg.236]

Rat carotid sinus nerve activity is diminished by 2-APB during hypoxia (From Roy et al., 2006)... [Pg.237]

Glomus cell responses (a) Oligomycin abolished the calcium response to hypoxia (Hx), but exaggerated the same to hypercapnia, (b) 2-APB (IP3 antagonist) drastically reduced (From Lahiri, 2004)... [Pg.237]

Roy A, Mokashi A, Baby SM, DiGiulio C, Lahiri S. 2006. 2-APB and curcumin inhibit the hypoxic but not the hypercapnic carotid chemosensory discharge, (communicated). [Pg.240]

D. (2007) IP3 receptor antagonist, 2-APB, attenuates cisplatin induced Ca +-influx in HeLa-S3 cells and prevents activation of cal-pain and induction of apoptosis. Brit J Pharmacol, 151, 1176-1186. [Pg.129]


See other pages where APB is mentioned: [Pg.43]    [Pg.44]    [Pg.44]    [Pg.47]    [Pg.29]    [Pg.31]    [Pg.32]    [Pg.32]    [Pg.42]    [Pg.43]    [Pg.43]    [Pg.66]    [Pg.75]    [Pg.95]    [Pg.229]    [Pg.85]    [Pg.330]    [Pg.331]    [Pg.444]    [Pg.585]    [Pg.62]    [Pg.317]    [Pg.237]    [Pg.114]    [Pg.241]    [Pg.136]    [Pg.74]    [Pg.81]    [Pg.87]   
See also in sourсe #XX -- [ Pg.43 , Pg.47 ]

See also in sourсe #XX -- [ Pg.32 , Pg.43 , Pg.66 , Pg.95 ]

See also in sourсe #XX -- [ Pg.85 ]




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