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VGated Ion Channels

QuestionAnswer
Bichet et al 2000 I-II loop of alpha 1 subunit of VGCa channels has ER retention seq, antagonised by beta subunit. Tagged membrane proteins (K+ channel, expression assayed by currents) with the loop, adding beta3 subunit allowed proteins to reach the membrane. IHC used
DeMaria et al 2001 Endogenous CaM is bound to P/Q type Ca channels, prelocalised before activation as Ca insens CaM blocked endogenous CaM. CaM N terminal Ca binding (slow, long term) mediates inactivation of the channel, C terminal binding (rapid, short term) facilitates.
Hoppa et al 2012 a2delta Ca channel subunit expression is rate-limiting for membrane expression (a1 subunit forms pore). Exocytosis measured to gauge Ca entry. ↑ density of channels ↓ chelator sensitivity. ↑ exocyt with ↓ Ca entry (dyes), better coupling.
Huang et al 2012 Edited Cav1.3s have ↓ Ca-dep inactivation (through CaM). Adenosine to inosine in IQ domain (ADAR-mediated). Editing ↑ common in fr cortex and hipcamp. Ca currents may be reqd for SCN rhythm (depends on method used (slice etc.) Bay K 8644 mimics ADAR KO
Cai et al 2004 Plateau potentials are ended by Ca activated K channels, chelator lengthens. TEA blocked the K channel & chelators no longer lengthen (new rate-limiting step). Apamin (SK inh) blocks overshoot repol'n. Kv4.2 keeps plateau pot to dendrites, stops spread
Gu et al 2003 T1 tetramerisation domain is needed for Kv1 targetting to axons, exchanging for a similar domain decr axonal expression. Adding T1 to proteins caused axon targetting. KvBeta interaction site on T1 is needed for Kv1 axonal targetting. Kv1.2 tagged with HA.
McKeown et al 2008 Review: Kvs5-12 make heterotetramers, Kv1-4 can be homo. 5,6,8&9 are silent alone. Kv4.2 uses C terminus to oligomerise (not T1) indicates different for dendritic isoforms. Cuff of cytoskeletal/membrane proteins at axon hillock may block diffusion to axon
Misonou et al 2004 Kainate causes seizures, Kv2.1 moves out of clusters (immhistochem). biotinylation to assay membrane expression. Found decr channel Mr due to dephosphorylation, triggered by Ca entry. Live cell imaging showed large clusters break into smaller ones.
Schulte et al 2006 West blot isolate Lgi1, shown to CoIp with Kv channels. Showed Kv1.1 and Lgi were presynaptic by lesioning the presyn axon. Transfected Kv1.1,1.4&beta1 into XeOocytes with norm and disease Lgi1, showed Lgi1 prevents kvb1 inactivation and speeds kinetics.
Burdakov & Ashcroft 2002 Whole cell patch clamp in mouse ARC nuc slices. pM conc CCK caused rev & dose-dep incr in A current(K+current) amplitude, desensitising over time. Gastrin mimics effects so prob CCK-Brec (both act w/ equal affinity there). 0.5-5 min latency=2nd messenger?
Doyle et al 1998 TEA (tet-eth-amm) blocks all K+ channels. Structure: cavity allows ion to stay hydrated, helices at pore opening w/ -ve charge. Conserved select'y filter. Hydrophob lining decr electrostatic 'friction'. 12 aromatic aa's hold pore open as K+ (not Na) binds
Engbers et al 2012 KCa3.1 channels present in the brain (cerebellar purkinje cells). Causes afterhyperpoln to stop low freq input. Showed association of KCa channels with T-type Ca channels. KCa3.1 CoIP's with Cav3.2 (Ca-T). Used sel blockers to show role in afterhyperpoln.
Morais-Cabral et al 2001 10nanosecs for dehyd, transfer and rehyd. 3 sites. Can pass 2 K+ ions at once with water in the middle site, other ions prefer 1 site over the others, not K+ (optimised). 1 water passes through for every K+
Pietrzykowski et al 2008 BK channel potentiated by alcohol, density in striatum and SON is reduced with repeated use via miRNA-9. Alters BK alt splicing (variants have diff alcohol sensitivity). Transcription block showed alcohol affects existing mRNA. ↓alcorex, ↑STREX exon
Xia et al 1998 No obv binding site on SKca channel. Truncated C terminus prevented Ca opening, CaM bound to beads held up SKca channels, higher affinity when Ca is high. SKCa coIPs with CaM and difficult to break apart, CaM mutations alter SKca Ca opening.
Cuello et al 2010 C-type inactivation of K1 channels is slow via sel filter constriction, S2 is blocked 1st, then S3. N-type is fast via ball&chain. Mutating proton sensor in S1-S2 linker causes consitutive open channel for crystallisation of open-inactive channel form
Jiang et al 2002 Show open & closed pore conformations of 'representative' K+ channels. Inner helices line the pore, with a gating hinge able to bend 30deg & close the channel. Glycine vital for hinge. Voltage barrier concn at sel filter, where binding sites aid passage.
Long et al 2005 Kv channel structure, sel filter and pore are most interesting bits (most conserved). Shows +ve charged N terminus polypep can enter and block the channel. N-type inactivation makes an A current, not delayed rectifier. kvbeta1 has the ball, beta2 doesnt.
Aldritch & Murrell-Lagnado 1993 Showed that N terminal fragments of Kv subunits could block the pore. Strong indication of ball and chain style N-inactivation. Internal TEA competes with the fragment. Incr hydrophobicity incr binding of fragment.
Nowycky et al 1985 Isolation of three calcium channels, T, L and N. Used small step from negative potential (-80) to see T, similar but bigger step up for N (up to +20). Isolated L by starting from -20, stepped to +20, other channels presumably inactivate by voltage.
Chen et al 2007 1st description of pathological mutation in an AKAP (namely yotiao/AKAP9), causes long QT. Normally associates with the Iks channel and allows regulation of this channel by cAMP. Found in 2% of caucasian subjects with long QT
Park et al 2010 STIM1 inhibits Cav1.2 channels, incr internalisation, decr currents. Effects on currents potentiated by Ca depletion but seems to be a basal inhibition whenever the two are co-expressed
Created by: Jonmassie