IndraLab

Statements

Pyraclofos activates HCN1. 17 / 17
| 7 10
sparser
"V 1/2 for S791D was shifted to −75.9 mV, indicating a modest but significant hyperpolarizing shift in the voltage-dependent activation of HCN1 channels when S791 is phosphorylated (G/G max at V= −70 mV, WT: 0.480 ± 0.021, n =20; S791D: 0.422 ± 0.017, n =22, p <0.05; xref )."
33571596
reach
"If S4 is static, how do voltage changes trigger the rearrangement of HCN1 to cause the collapse or expansion of the gating canal?"
14676285
reach
"The voltage hysteresis caused the conductance of HCN1 channels to display an unusual hysteresis in response to slow voltage ramps (XREF_FIG C), similar to the hysteresis in spHCN channels (XREF_FIG D)."
15710913
sparser
"As expected, inhibition of p38 MAPK shifted the voltage-dependent activation of WT HCN1 channels in a hyperpolarized direction relative to untreated WT controls (V 1/2 = −77.6 mV; G/G max at V= −70 mV: 0.388 ± 0.023, n =6, p <0.05)."
33571596
reach
"Normally, coexpression of wild-type TRIP8b with wild-type HCN1 in Xenopus oocytes shifts the voltage dependent activation of HCN1 channels to more negative potentials by 10-15 mV."
21411649
sparser
"When expressing a phosphomimetic mutant that is analogous to constitutively phosphorylated S791 (rat HCN1-S791D) in Xenopus oocytes, we observed a hyperpolarizing shift in HCN1 channel voltage-dependent activation, similar to that seen in our rat model of acquired epilepsy ( xref ; xref )."
33571596
reach
"V for S791D was shifted to −75.9 mV, indicating a modest but significant hyperpolarizing shift in the voltage-dependent activation of HCN1 channels when S791 is phosphorylated (G/G at V= −70 mV, WT: 0.480 ± 0.021, n=20; S791D: 0.422 ± 0.017, n=22, p<0.05; Fig. 6A)."
33571596
reach
"As expected, inhibition of p38 MAPK shifted the voltage-dependent activation of WT HCN1 channels in a hyperpolarized direction relative to untreated WT controls (V = −77.6 mV; G/G at V= −70 mV: 0.388 ± 0.023, n=6, p<0.05)."
33571596
sparser
"The combination of two variants, N‐del + P851A (present only in the patient), has the largest negative shift of voltage‐dependent activation of HCN1 channels beyond the early diastolic depolarization of sinus node, which represents the likely cause of profound sinus bradycardia in the patient in the absence of missense variants in other ion channels previously linked to sinus bradycardia."
34621433
sparser
"HCN1 is usually activated by significantly lower hyperpolarized voltages compared to other isoforms (Altomare et al., xref ; Baruscotti et al., xref )."
29867437
sparser
"If, instead, I h passed through separate homomeric HCN1 and HCN4 channels, and if less negative voltages activated HCN1 but not HCN4 ( xref ; xref ), cAMP might be expected to shift the activation range by different amounts at different voltages."
21456027
sparser
"This shift would be smaller at voltages activating only HCN1 and larger at voltages which activate HCN4."
21456027
reach
"Voltage activation of HCN1 occurs at more depolarized potentials than HCN2–4, with HCN4 activated at the most hyperpolarized potentials."
21130878
sparser
"Given that voltage-dependent activation of HCN1 is virtually unaffected by removal of its C terminus ( xref ) (see also), we speculated that the removal of the EAG1 C terminus, rather than addition of the HCN1 equivalent, may account for these observations."
30587580
reach
"Mutations of residues within the putative binding pocket mitigate or eliminate voltage-dependent modulation of HCN1 currents by propofol."
39752505
sparser
"Atomistic simulations of HCN1 voltage sensor activation."
31774399
sparser
"Voltage activation of HCN1 occurs at more depolarized potentials than HCN2–4, with HCN4 activated at the most hyperpolarized potentials."
21130878