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1 affinity Kv1 channel antagonist, 125I-alpha-dendrotoxin.
2 s identical to a previously identified delta-dendrotoxin.
3 bolished by blocking Kv1 channels with alpha-dendrotoxin.
4 endent of firing, and is eliminated by alpha-dendrotoxin (0.1 microM), implicating slow inactivation
6 (10 muM) and margatoxin (10 muM) but not by dendrotoxin (100 nM), indicating that it arose from augm
7 ol/L, respectively, and insensitive to alpha-dendrotoxin (100 to 500 nmol/L), charybdotoxin (100 to 5
8 oimmunoprecipitation of radioiodinated alpha-dendrotoxin ((125)I-alphaDTX)-labelled VGKC complexes fr
9 haracteristic firing patterns, we used alpha-dendrotoxin (alpha-DTX) to eliminate the contribution of
11 presence of 2 nM externally superfused alpha-dendrotoxin (alpha-DTX), or 50 nM superfused beta-BuTX,
13 -aminopyridine (4-AP) and 0.5-1 microM alpha-dendrotoxin (alpha-DTX)] played a prominent role in sett
14 the functional interaction surfaces of delta-dendrotoxin and its voltage-gated potassium channel rece
17 nt due to structural differences between the dendrotoxins and BPTI at the anti-protease loop; this ex
18 rative model building studies, involving the dendrotoxins and the proteinases, reveal that the key in
21 Major secondary structural regions of the dendrotoxins are stable without much fluctuation during
22 onformation and protein folding of the three dendrotoxins are very similar to the published crystal s
24 pyridine (4-AP, at micromolar levels), alpha-dendrotoxin at nanomolar levels, or blood-depressing sub
26 ory effects of these analogs on 125I-labeled dendrotoxin binding to rat brain membranes showed that r
27 annels and their ability to displace [(125)I]dendrotoxin binding to rat brain synaptosomal membranes.
28 nits and increase the number of cell surface dendrotoxin-binding sites when coexpressed with Kv1.2.
30 d substitutions in ROMK1 indicate that delta-dendrotoxin binds to the pore region of ROMK1 even thoug
33 ent by low doses of 4-aminopyridine or alpha-dendrotoxin dramatically slows the falling phase of acti
36 shold dynamics in layer 2-3 PNs, using alpha-dendrotoxin (DTX) or 4-aminopyridine (4-AP) to block the
39 apezoid body (MNTB) revealed a low-threshold dendrotoxin (DTX)-sensitive current (ILT) and a high-thr
43 hannel current was blocked by 1 microM alpha-dendrotoxin (DTX); we also observed two other DTX-sensit
45 cal recordings reveal that recombinant delta-dendrotoxin has a half-maximal inhibition constant (Kd)
50 generation threshold by the activation of a dendrotoxin-I-sensitive, voltage-gated K(+) conductance.
51 ntibodies were detected using a (125)I-alpha-dendrotoxin immunoprecipitation assay in 38% of group A
56 ing Kv1.1 and Kv1.2 containing channels with dendrotoxin-K (DTX-K) and tityustoxin-Kalpha (TsTX-Kalph
57 v1.1 demonstrated that the mamba snake toxin dendrotoxin-K (DTX-K) blocked the Kv1.1 outward current
61 roteins that are complexed with (125)I-alpha-dendrotoxin-labelled potassium channels in brain extract
63 tibodies that immunoprecipitate (125)I-alpha-dendrotoxin-labelled voltage-gated potassium channels ex
64 cy were occluded by the K+ channel blockers, dendrotoxin, margatoxin, and agitoxin, but not dendrotox
65 contrast, inhibiting Kv1 channels with alpha-dendrotoxin or maurotoxin strongly increased firing rate
66 subthreshold current was resistant to alpha-dendrotoxin, paxilline, apamin, and tetraethylammonium b
67 lockers, including tetraethylammonium, alpha-dendrotoxin, phrixotoxin-2, and BDS-I, did not mimic or
71 ownregulation of a low-threshold, sustained, dendrotoxin-sensitive (DTX) potassium current, I(DS).
74 eature of auditory neurons, is regulated via dendrotoxin-sensitive low-threshold voltage-activated (L
75 ogical demonstration of the involvement of a dendrotoxin-sensitive potassium current in presynaptic i
80 osing the proposed active site region of the dendrotoxins to the anionic sites of the K+ channel rece
81 ndritic recordings, and focal application of dendrotoxin together indicate that the channels mediatin
84 rom the CHO/K(V)1.3 cells, except that alpha-dendrotoxin was more potent at blocking binding to rat b
85 esults constrain the possible orientation of dendrotoxin with respect to the K(+) channel structure.
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