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Potassium channel, subfamily T, member 2

Slick, Slo2.1
a K+ channel activated by intracellular Na+ and Cl- and inhibited by intracellular ATP [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: Slack, CAN, CLN8, HAD, SET
Papers on Slick
The Impact of Failing to Identify Suspect Effort in Patients Undergoing Adult Attention-Deficit/Hyperactivity Disorder (ADHD) Assessment.
Nelson et al., In Psychol Assess, Feb 2016
A total of 102 were diagnosed with ADHD based on cognitive testing, behavior rating scales, effort testing, and clinical interview; 115 were identified as putting forth suspect effort in accordance with the Slick, Sherman, and Iverson (1999) criteria.
Hydrophobic interactions between the S5 segment and the pore helix stabilizes the closed state of Slo2.1 potassium channels.
Sanguinetti et al., Salt Lake City, United States. In Biochim Biophys Acta, Jan 2016
Fenamates such as niflumic acid also activate Slo2.1.
Differential distribution of the sodium-activated potassium channels Slick and Slack in mouse brain.
Schwarzer et al., Innsbruck, Austria. In J Comp Neurol, Dec 2015
UNASSIGNED: The sodium-activated potassium channels Slick (Slo2.1,
Official Position of the American Academy of Clinical Neuropsychology Social Security Administration Policy on Validity Testing: Guidance and Recommendations for Change.
Ord et al., New Orleans, United States. In Clin Neuropsychol, Aug 2015
UNLABELLED: The milestone publication by Slick, Sherman, and Iverson (1999) of criteria for determining malingered neurocognitive dysfunction led to extensive research on validity testing.
Transcriptional Regulation of the Sodium-activated Potassium Channel SLICK (KCNT2) Promoter by Nuclear Factor-κB.
Bhattacharjee et al., Buffalo, United States. In J Biol Chem, Aug 2015
Although recent studies have shown the sodium-activated potassium channel SLACK (KCNT1) can contribute to neuronal excitability, there remains little information on the physiological role of the closely related SLICK (KCNT2) channel.
Identification of the Intracellular Na+ Sensor in Slo2.1 Potassium Channels.
Sanguinetti et al., Salt Lake City, United States. In J Biol Chem, Jul 2015
Based loosely on this sequence, we identified five potential Na(+) coordination motifs in the C terminus of the Slo2.1 subunit.
"Comparative evaluation of surface modified elastomeric ligatures for microbial colonization": An in vivo study.
Vaz et al., Bāgalkot, India. In Indian J Dent Res, Mar 2015
This in vivo study compared the Super Slick and Safe-T-Ties with their unmodified counterparts for bacterial adhesion.
Knockout of Slo2.2 enhances itch, abolishes KNa current, and increases action potential firing frequency in DRG neurons.
Lingle et al., Saint Louis, United States. In Elife, 2014
Here, we report the genetic disruption of both Kcnt1 and Kcnt2, confirm the loss of Slo2.2 and Slo2.1 protein, respectively, in KO animals, and define tissues enriched in Slo2 expression.
A comparative evaluation of static frictional resistance using various methods of ligation at different time intervals: an in vitro study.
Sarin et al., Farīdkot, India. In Int J Dent, 2014
Alastik Easy to Tie modules, Super Slick Mini Stix elastomeric modules, Power "O" modules, and 0.009(″) Stainless Steel ligatures were used to compare the static friction using maxillary canine and premolar Preadjusted Edgewise brackets with 0.022(″) × 0.028(″) slot and 0.019(″) × 0.025(″) stainless steel wires.
Evaluation of the MMPI-2-RF for Detecting Over-reported Symptoms in a Civil Forensic and Disability Setting.
Barr et al., Teaneck, United States. In Clin Neuropsychol, 2014
METHOD: A criterion-groups design was used, classifying examinees as "Failed Slick Criteria" through low performance on at least two performance validity indices (stand-alone or embedded) and "Passed Slick Criteria."
Efficacy of Super Slick elastomeric modules in reducing friction during sliding: a comparative in vitro study.
Pathan et al., Guntūr, India. In J Contemp Dent Pract, 2014
AIM: To evaluate and compare the frictional resistance produced by Super Slick modules during sliding with four different types of brackets and four ligature types both in conventional and figure-of-8 ligation method with saliva as lubricant.
Emerging role of the KCNT1 Slack channel in intellectual disability.
Kaczmarek et al., New Haven, United States. In Front Cell Neurosci, 2013
The sodium-activated potassium KNa channels Slack and Slick are encoded by KCNT1 and KCNT2, respectively.
Slick science: will new BP funds keep Gulf genomics afloat?
Alvania, Cambridge, United States. In Cell, 2011
Funding injections by British Petroleum this summer are fueling studies in the Gulf Coast, raising hopes that the Deepwater Horizon oil spill might provide answers to long-standing questions on the nature of cellular toxicity.
The N-terminal domain of Slack determines the formation and trafficking of Slick/Slack heteromeric sodium-activated potassium channels.
Kaczmarek et al., Albany, United States. In J Neurosci, 2009
Heteromer formation between Slick and Slack-B requires a specific epitope that is found in the N-terminal domain of Slack-B and that is absent in the Slack-A isoform.
Slack and Slick KNa channels are required for the depolarizing afterpotential of acutely isolated, medium diameter rat dorsal root ganglion neurons.
Ding et al., Wuhan, China. In Acta Pharmacol Sin, 2008
We conclude that Slack and Slick K(Na) channels are required for depolarizing afterpotential of medium diameter rat dorsal root ganglion neurons
Slack and Slick K(Na) channels regulate the accuracy of timing of auditory neurons.
Kaczmarek et al., New Haven, United States. In J Neurosci, 2007
Slick and Slack are expressed at high levels auditory brainstem. Activation of these KNa channels allows temporal accuracy of firing to be increased at high frequencies of stimulation.
Regulation of the timing of MNTB neurons by short-term and long-term modulation of potassium channels.
Yang et al., New Haven, United States. In Hear Res, 2005
To preserve the fidelity of timing of action potentials that is required for sound localization, these neurons express several types of potassium channels, including the Kv3 and Kv1 families of voltage-dependent channels and the Slick and Slack sodium-dependent channels.
For K+ channels, Na+ is the new Ca2+.
Kaczmarek et al., Buffalo, United States. In Trends Neurosci, 2005
Two genes encoding these channels, Slick and Slack, are expressed throughout the brain.
Localization of the Na+-activated K+ channel Slick in the rat central nervous system.
Kaczmarek et al., New Haven, United States. In J Comp Neurol, 2005
we report the localization of Slick in the rat central nervous system using in situ and immunohistochemical techniques
Slick (Slo2.1), a rapidly-gating sodium-activated potassium channel inhibited by ATP.
Kaczmarek et al., New Haven, United States. In J Neurosci, 2004
Cloning and regulation of slick channel activity.
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