The cardiac transient outward potassium current (referred to as Ito1 or Ito ) is one of the ion currents across the cell membrane of heart muscle cells. It is the main contributing current during the repolarizing phase 1 of the cardiac action potential. It is a result of the movement of positively charged potassium (K+) ions from the intracellular to the extracellular space. Ito1 is complemented with Ito2 resulting from Cl− ions to form the transient outward current Ito. Ito1 is rapidly activated and deactivated. It is activated after the fast increase of the membrane potential following the phase 0 of the cardiac action potential. Once activated, (K+) ions from inside the cells flow to the extracellular space. This outward flow of positively charged ions constitutes the Ito1 and causes the transmembrane voltage to decrease.This decrease of the transmembrane potential is known as repolarization. Ito1 is then quickly deactivated, stopping the repolarization and ending the phase 1 of the action ...
Aims: The human cardiac transient outward K + current Ito (encoded by Kv4.3 or KCND3) plays an important role in phase 1 rapid repolarization of cardiac action potentials in the heart. However, modulation of I to by intracellular signal transduction is not fully understood. The present study was therefore designed to determine whether/how human atrial I to and hKv4.3 channels stably expressed in HEK 293 cells are regulated by protein tyrosine kinases (PTKs). Methods and results: Whole-cell patch voltage-clamp, immunoprecipitation, western blotting, and site-directed mutagenesis approaches were employed in the present study. We found that human atrial I to was inhibited by the broad-spectrum PTK inhibitor genistein, the selective epidermal growth factor receptor (EGFR) kinase inhibitor AG556, and the Src-family kinases inhibitor PP2. The inhibitory effect was countered by the protein tyrosine phosphatase inhibitor orthovanadate. In HEK 293 cells stably expressing human KCND3, genistein, AG556, ...
Potassium voltage-gated channel subfamily D member 2 is a protein that in humans is encoded by the KCND2 gene. It contributes to the cardiac transient outward potassium current (Ito1), the main contributing current to the repolarizing phase 1 of the cardiac action potential. Voltage-gated potassium (Kv) channels represent the most complex class of voltage-gated ion channels from both functional and structural standpoints. Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume. Four sequence-related potassium channel genes - shaker, shaw, shab, and shal - have been identified in Drosophila, and each has been shown to have human homolog(s). This gene encodes a member of the potassium channel, voltage-gated, shal-related subfamily, members of which form voltage-activated A-type potassium ion channels and are prominent in the repolarization phase of the ...
TY - JOUR. T1 - Up-regulation of A-type potassium currents protects neurons against cerebral ischemia. AU - Deng, Ping. AU - Pang, Zhi Ping. AU - Lei, Zhigang. AU - Shikano, Sojin. AU - Xiong, Qiaojie. AU - Harvey, Brandon K.. AU - London, Barry. AU - Wang, Yun. AU - Li, Min. AU - Xu, Zao C.. PY - 2011/9/1. Y1 - 2011/9/1. N2 - Excitotoxicity is the major cause of many neurologic disorders including stroke. Potassium currents modulate neuronal excitability and therefore influence the pathological process. A-type potassium current (IA) is one of the major voltage-dependent potassium currents, yet its roles in excitotoxic cell death are not well understood. We report that, following ischemic insults, the IA increases significantly in large aspiny (LA) neurons but not medium spiny (MS) neurons in the striatum, which correlates with the higher resistance of LA neurons to ischemia. Activation of protein kinase Cα increases IA in LA neurons after ischemia. Cultured neurons from transgenic mice lacking ...
Neurons could alter the properties and the amount ofI A by differentially regulating A-channel gene expression. Like their Drosophila homologs, thePanulirus shaker and shal genes both encode α-subunits for rapidly inactivating A-type channels, although with somewhat different properties than for the Drosophilachannels (Fig. 2, Table 1; M. Kim et al., 1995, 1996; Baro et al., 1996a). We compared the I As obtained from overexpressing shaker and shal cRNA inXenopus oocytes (lobsterI shaker and lobsterI shal) with the six pyloricI As (Fig. 2, Table 1). We discovered that the variations in pyloric I As were not consistent with the idea that distinct pyloric I As result from different mixtures of shaker and shal A-channels. Instead, we found that the pyloric cell I As qualitatively resemble lobster I shal more than lobster I shaker; however, no pyloricI A was identical in all parameters to lobsterI shal.. The voltage dependence of the six pyloric I As was quite variable but generally resembled ...
White blood cells called lymphocytes are found in lymph tissues. They help prevent infections. Most lymphomas start in a type of white blood cells called B lymphocytes, or B cells. For most patients, the cause of this cancer is unknown. However, lymphomas may develop in people with weakened immune systems. For example, the risk of lymphoma increases after an organ transplant or in people with HIV infection. There are many different types of non-Hodgkins lymphoma (NHL). It is grouped according to how fast the cancer spreads. ...
Mouse=100% identity (216/216 amino acids). Target Description: Kv channel-interacting protein 1, Potassium Voltage-Gated Channel Interacting Protein 1 or Kchip1 is a member of the family of voltage-gated potassium (Kv) channel-interacting proteins (KCNIPs), which belongs to the recoverin or neuronal calcium sensor (NCS) family branch of the EF-hand superfamily. Kchip1 associates with Kv4 alpha subunits to form native Kv4 channel complexes. Kchip1 is expressed in the brain and detected in the hippocampus and the dentate gyrus . Diseases associated with KCNIP1 include diastolic hypertension, attention deficit-hyperactivity disorder.. Gene ID: Kcnip1 Kchip1. Antibody Registry ID (RRID): AB_10673162. Physical State: Liquid. ...
FUNCTION: [Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the family of voltage-gated potassium (Kv) channel-interacting proteins, which belong to the recoverin branch of the EF-hand superfamily. Members of this family are small calcium binding proteins containing EF-hand-like domains. They are integral subunit components of native Kv4 channel complexes that may regulate A-type currents, and hence neuronal excitability, in response to changes in intracellular calcium. The encoded protein also functions as a calcium-regulated transcriptional repressor, and interacts with presenilins. Alternatively spliced transcript variants encoding different isoforms have been described. [provided by RefSeq, Jul 2008 ...
Kv4 channels underlie somatodendritic A-type currents in neurons (Birnbaum et al., 2004; Jerng et al., 2004b). These channels are formed by four Kv4 α subunits in association with cytoplasmic KChIP (An et al., 2000; Rhodes et al., 2004) and/or transmembrane DPPX (Nadal et al., 2003) or dipeptidylpeptidase 10 (Jerng et al., 2004a; Zagha et al., 2005) auxiliary subunits. Coexpression of KChIP1-KChIP3, but not KChIP4, with Kv4 α subunits in heterologous cells dramatically increases surface expression and slows the turnover rate of Kv4 protein, and slows the inactivation kinetics and speeds the rate of recovery from inactivation of Kv4 channels (An et al., 2000; Shibata et al., 2003; Jerng et al., 2004b). The pattern of association and colocalization of Kv4.2, Kv4.3, and KChIP1-KChIP4 varies across brain regions and cell types (Rhodes et al., 2004; Strassle et al., 2005), suggesting specific yet undefined requirements for precise compositions of Kv4 α subunits and KChIPs in channel ...
CaM; DREAM; Frq1; GCAP; KChIP; NCS-1 Calmodulin, Downstream response element antagonist modulator, Yeast frequenin, Guanylate cyclase activator protein, Potassium channel-interacting protein,...
Global Markets Directs, Potassium Voltage Gated Channel Subfamily C Member 1 (Voltage Gated Potassium Channel Subunit Kv3.1 or Voltage Gated Potassium Channel Subunit Kv4 or KCNC1) - Pipeline
During cognitive tasks, synchronicity of neural activity varies and is correlated with performance. However, there may be an upper limit to normal synchronised activity - specifically, epileptogenic activity is characterized byexcess spiking at high synchronicity. An epileptic seizure has a complicated course of events and I therefore focused on the synchronised activity preceding a seizure (fast ripples). These high frequency oscillations (200-1000 Hz) have been identified as possible signature markers of epileptogenic activity and may be involved in generating seizures. Moreover, a range of ionic currents have been suggested to be involved in distinct aspects of epileptogenesis. Based on pharmacological and genetic studies, potassium currents have been implicated, in particular the transient A-type potassium channel (KA). Our first objective was to investigate if KA could suppress synchronized input while minimally affecting desynchronised input. The second objective was to investigate if ...
Kv4 subunits are the main pore-forming proteins responsible for the fast transient outward currents observed in the CNS (rat brain), where they have been described as A
Potassium voltage-gated channel subfamily C member 1 (KCNC1) antibody | P48547 | NGK2, Voltage-gated potassium channel subunit Kv3.1, Voltage-gated potassium channel subunit Kv4
K+ selective channels are some of the most widespread ion trafficking molecules in living organisms, with more than 70 genes encoding different K+ channels in humans. KV channels fall into one of the two classical categories of delayed rectifier (DR) and A-type. Delayed rectifier was the original name attributed to voltage-dependent K+ channels due to their delayed activation in squid giant axons. A-type channels are low voltage-activated, fast inactivating (therefore, transient) K+ channels. Specific KV toxins are often used to dissect the particular contribution of different subunits to native currents.. Alomone Labs is excited to offer a line of Overexpressed Membrane Fractions. These membrane fractions are Xenopus oocyte membrane lysates overexpressing a specific ion channel. Fractions are sold as a set of injected and non-injected oocytes and can be used as controls for Alomone Labs antibodies. Overexpressed Membrane Fractions can also be purchased as a kit with their respective antibody. ...
Im just going to link you to another post here, which I believe answers the same question. Its because the facilitation of the transient outward current if much more prominent in epicardial regions than in endocardial regions.. And the following citation, "Transient outward potassium current, Ito, phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms," provides some mechanistic insight.. To answer the rest of the question:. So in an ECG you have leads that record whether a charge is moving toward, or away from the lead. These net charges are reflected on the ECG as either positive or negative deflections. You have a signal from the sinoatrial node that causes a depolarization in the right atrium, then the left atrium (biphasic p wave). In each case, however, we see the positive p wave because in this depolarization the net charge is moving toward the electrodes. Studies on atrial repolarization note that yes, the atrial repolarization is ...
BRISBANE, Calif., June 18, 2014 (GLOBE NEWSWIRE) -- Hyperion Therapeutics (Nasdaq:HPTX) today announced that the company is scheduled to present at the JMP Healthcare Conference on Tuesday, June 24, 2014, at 2:00 p.m. ET.
BmP02, a short-chain peptide with 28 residues from the venom of Chinese scorpion Buthus martensi Karsch, has been reported to inhibit the transient outward potassium currents (Ito) in rat ventricular muscle cells. However, it remains unclear whether BmP02 modulates the Kv4.2 channel, one of the main contributors to Ito. The present study investigated the effects of BmP02 on Kv4.2 kinetics and its underlying molecular mechanism. The electrophysiological recordings showed that the inactivation of Kv4.2 expressed in HEK293T cells was significantly delayed by BmP02 in a dose-response manner with EC50 of ~850 nM while the peak current, activation and voltage-dependent inactivation of Kv4.2 were not affected. Meanwhile, the recovery from inactivation of Kv4.2 was accelerated and the deactivation was slowed after the application of BmP02. The site-directed mutagenesis combined with computational modelling identified that K347 and K353, located in the turret motif of the Kv4.2, and E4/E5, D20/D21 in BmP02 are
Total myocytes RNA was isolated using TRIzol Reagent (Invitrogen) after transfection and treatment with vehicle or Ang II. DNA was removed by DNase I treatment before cDNA synthesis. Relative quantitation by real-time PCR was performed using SYBR-green detection of PCR products in real time using the ABI PRISM 7700 Sequence Detection System (Applied Biosystems). In each experiment, the human 18S RNA was amplified as a reference standard. PCR primers were 18S-F, 5′-CCCTGTAATTGGAATGAGTCCAC; 18S-R, 5′-GCTGGAATTACCGCGGCT; Luc-F, 5′-GCCTGAAGTCTCTGATTAAGT; and Luc-R, 5′-ACACCTGCGTCGAAGATGT. RT without Superscript II reverse transcriptase and genomic DNA samples were included as negative controls in all real-time PCR experiments. Each real-time PCR (25 μL) contained 2.5 μL of cDNA (for 18S RNA detection, cDNAs were diluted 1000-fold), 12.5 μL of 2× SYBR Green Master Mix (Applied Biosystems), and primers at a final concentration of 350 nmol/L and 900 nmol/L. Reactions were prepared in ...
Expression of KCND3 (KSHIVB, Kv4.3, SCA19, SCA22) in epididymis tissue. Antibody staining with HPA029452 in immunohistochemistry.
Page contains details about ITO/ZnO-In/CdS . It has composition images, properties, Characterization methods, synthesis, applications and reference articles : nano.nature.com
Background: Cardiac fibrosis is associated with a variety of heart diseases including atrial fibrillation (AF). Cardiac fibroblast is the major cell type in cardiac fibrogenesis cascade. However, the biological as well as electrophysiological properties of cardiac fibroblasts are not fully understood. In this study, we investigated the functional expression of voltage-gated and non-voltage-gated ion channels in artial fibroblasts from AF patients and SR patients, and their contribution to atrial fibrogenesis.. Methods: With informed consent, right atrial biopsies were obtained from AF patients or sinus rhythm (SR) patients undergoing cardiac surgery. Fibroblasts were dissociated from the biopsy samples from SR patients or AF patients. The freshly isolated cells were used for patch-clamp and ratio Ca2+-imaging experiments.. Results: We found that there are two types of voltage-gated outward potassium channels in the fibroblasts from SR patients: one is transient outward potassium current (Ito), ...
Potassium channels are key determinants of neuronal excitability. We recently identified KChIPs as a family of calcium binding proteins that coassociate and colocalize with Kv4 family potassium channels in mammalian brain (An et al. [2000] Nature 403:553). Here, we used light microscopic immunohistochemistry and multilabel immunofluorescence labeling, together with transmission electron microscopic immunohistochemistry, to examine the subcellular distribution of KChIPs and Kv4 channels in adult rat cerebellum. Light microscopic immunohistochemistry was performed on 40-μm free-floating sections using a diaminobenzidine labeling procedure. Multilabel immunofluorescence staining was performed on free-floating sections and on 1-μm ultrathin cryosections. Electron microscopic immunohistochemistry was performed using an immunoperoxidase pre-embedding labeling procedure. By light microscopy, immunoperoxidase labeling showed that Kv4.2, Kv4.3, and KChIPs 1, 3, and 4 (but not KChIP2) were expressed at ...
It is quite possible that inactivation recovery takes a different route. This can be accounted for by the addition to Model 2 of a parallel pathway for inactivation recovery, similar to what has been proposed for the sodium channel inactivation (Armstrong and Bezanilla, 1977; Vandenberg and Bezanilla, 1991) or for Shaker fast inactivation (Bezanilla et al., 1991; Bezanilla and Stefani, 1996). The existence of deeper N-inactivated states is supported by the influence of the L382I mutation on the activation and inactivation kinetics of Shaker channels, interpreted as enhanced closed-state inactivation (Ayek and Sigworth, 1997), as well as the influence of hyperpolarization on the proportions of fast and slow components of ionic current recovery (Kuo, 1997). To decrease the number of free parameters in Model 3 (see Fig. 13), the voltage dependencies were conserved between parallel transitions. In addition, slow inactivated states were simplified into a single state (Ic). The ON and OFF rates of a ...
CYP2J2 is abundant in cardiac tissue and active in the biosynthesis of eicosanoids such as epoxyeicosatrienoic acids (EETs). To determine the effects of CYP2J2 and its eicosanoid products in the heart, we characterized the electrophysiology of single cardiomyocytes isolated from adult transgenic (Tr) mice with cardiac-specific overexpression of CYP2J2. CYP2J2 Tr cardiomyocytes had a shortened action potential. At 90% repolarization, the action potential duration (APD) was 30.6 ± 3.0 ms (n = 22) in wild-type (Wt) cells and 20.2 ± 2.3 ms (n = 19) in CYP2J2 Tr cells (p , 0.005). This shortening was probably due to enhanced maximal peak transient outward K+ currents (Ito,peak), which were 38.6 ± 2.8 and 54.4 ± 4.9 pA/pF in Wt and CYP2J2 Tr cells, respectively (p , 0.05). In contrast, the late portion of the transient outward K+ current (Ito,280ms), the slowly inactivating outward K+ current (IK,slow), and the voltage-gated Na+ current (INa) were not significantly altered in CYP2J2 Tr cells. ...
HARADA Masahito , ABUMI Kuniyoshi , ITO Manabu , KANEDA Kiyoshi Spine 25(15), 1932-1937, 2000-08-01 参考文献31件 被引用文献4件 ...
Results Compared with baseline value, AngII (0.1μmol/l), Telmisartan (0.01 μmol/l) and AngII plus Telmisartan group significantly decreased the peak density of Ito in SD rat atrial myocytes (22.48±2.75 vs 15.71±2.06 pA/pF, p,0.01), (24.16±2.36 vs 16.15±1.82 pA/pF, p,0.01) and (24.41±2.27 vs 21.35±1.46 pA/pF, p,0.05), respectively. AngII (0.1 μmol/l) significantly increased the peak density of ICa-L in SD rat atrial myocytes (−4.51±0.38 vs −5.16±0.29 pA/pF, p,0.01). Telmisartan (0.01 μmol/l) had no significant effect on ICa-L in the rat atrial myocytes (−4.35±0.27 vs −4.29±0.34 pA/pF, p,0.05), but it could antagonise the effects of AngII. In the Ang IIcombined telmisartan group, the peak density of ICa-L was (−4.08±0.28 vs −4.20±0.31 pA/pF, p,0.05), which was significantly different from that of AngII group (p,0.05).. ...
BACKGROUND: Growing evidence suggests that autoimmune mechanisms may participate in the pathogenesis of dilated cardiomyopathy (DCM). Previously, we identified auto-antibodies against the brain Kv channel interacting protein 1 (KChIP1) in sera from DCM patients by protein array screening. In hearts and endothelial cells, KChIP2 is the predominantly expressed form and exists in 8 different isoforms reflecting splice variants. We analysed the distribution of auto-antibodies against the isoform 6 (KChIP2.6), and two known targets of auto-antibodies, cardiac troponin I (cTnI), and the beta1-adrenergic receptor in sera from patients with DCM or ischemic cardiomyopathy (ICM), and control subjects.. METHODS: The coding sequence of cardiac KChIP2.6 was cloned by RT-PCR and fused in frame to the strep-tag coding sequence of pASK-IBA7. KChIP2.6 was expressed in E .coli ER256 and purified by affinity chromatography. IgG fractions were purified from plasma of patients with DCM (n = 104) or ICM (n = 60; ...
The density and activity of delayed rectifier potassium channels is known to correlate with the differentiation and proliferation of cell types as diverse as T lymphocytes (DeCoursey et al., 1984) and Schwann cells (Sobko et al., 1998). These fast-activating and slowly inactivating channels have an integrative role in the physiology of T lymphocytes that includes the regulation of membrane potential (Cahalan et al., 2001), calcium signaling (Lin et al., 1993), lymphokine secretion (Chandy et al., 1984), integrin function (Levite et al., 2000), and mitogen-stimulated proliferation (DeCoursey et al., 1984). Therefore, any modulation of the electrical properties of these channels is expected to have a direct effect on T-lymphocyte physiology. The present report provides direct evidence that the endogenous ligand Glu differentially modulates native Kv1.3 channels of human T lymphocytes, in a concentration-dependent manner, and postulates on the mechanism through which Glu exerts its action on ...
ABCC9, AKAP9, ANK2, CACNA1C, CACNA2D1, CACNB2, CALM1, CALM2, CALM3, CASQ2, CAV3, FGF12, GPD1L, HCN4, KCND2, KCND3, KCNE1, KCNE2, KCNE3, KCNE5, KCNH2, KCNJ2, KCNJ5, KCNJ8, KCNQ1, NOS1AP, PKP2, RANGRF, RYR2, SCN10A, SCN1B, SCN2B, SCN3B, SCN4B, SCN5A, SEMA3A, SLMAP, SNTA1, TECRL, TRDN, ...
ABCC9, AKAP9, ANK2, CACNA1C, CACNA2D1, CACNB2, CALM1, CALM2, CALM3, CASQ2, CAV3, FGF12, GPD1L, HCN4, KCND2, KCND3, KCNE1, KCNE2, KCNE3, KCNE5, KCNH2, KCNJ2, KCNJ5, KCNJ8, KCNQ1, NOS1AP, PKP2, RANGRF, RYR2, SCN10A, SCN1B, SCN2B, SCN3B, SCN4B, SCN5A, SEMA3A, SLMAP, SNTA1, TECRL, TRDN, ...
Article: Early exposure to alcohol leads to permanent impairment of dendritic excitability in neocortical pyramidal neurons. ...
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This Histri was built automatically but not manually verified. As a consequence, the Histri can be incomplete or can contain errors ...
Compare N(alpha)-acetyltransferase 38, NatC auxiliary subunit ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
Results RVOT cardiacmyocytes had a wider APD dispersion: the marked-prolonged APDs and the marked-shortened APDs both existed. 4-AP, an inhibitor of the transient outward potassium current (Ito), abolished the marked-shortened APDs. Some cardiomyoctes in rabbit RVOT showed significant prolongation in APD compared with RV (RVOT 727.25±44.52 ms; RV 481.0±97.12 ms; p.05). Some of their AP with long plateau could not even repolarise back to resting potential. In addition, EAD, AD and the second plateau response could emerge spontaneously in these cells. However, these phenomena were not observed in RV. These cells showed a higher current density of ICa-L compared with that of RV (RVOT 13.16±0.87 pA/pF; RV 8.59±1.97 pA/Pf; p0.05). Applying CdCl2, a blocker of ICa-L, could decrease the current density of ICa-L and diminish EAD, DAD and the second plateau response.. ...
ID KCNH2_CANLF Reviewed; 1158 AA. AC Q9TSZ3; O02719; O18820; DT 28-NOV-2002, integrated into UniProtKB/Swiss-Prot. DT 01-MAY-2000, sequence version 1. DT 27-SEP-2017, entry version 129. DE RecName: Full=Potassium voltage-gated channel subfamily H member 2; DE AltName: Full=Ether-a-go-go-related gene potassium channel 1; DE Short=DERG; DE Short=ERG-1; DE Short=Eag-related protein 1; DE Short=Ether-a-go-go-related protein 1; DE Short=c-ERG; DE AltName: Full=Voltage-gated potassium channel subunit Kv11.1; GN Name=KCNH2; Synonyms=CERG, ERG; OS Canis lupus familiaris (Dog) (Canis familiaris). OC Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; OC Mammalia; Eutheria; Laurasiatheria; Carnivora; Caniformia; Canidae; OC Canis. OX NCBI_TaxID=9615; RN [1] RP NUCLEOTIDE SEQUENCE [MRNA]. RC TISSUE=Heart; RX PubMed=11417212; DOI=10.1007/s004240100524; RA Zehelein J., Zhang W., Koenen M., Graf M., Heinemann S.H., Katus H.A.; RT "Molecular cloning and expression of cERG, the ether a ...
The Kvβ subunit of voltage-dependent potassium (Kv) channels has structural similarity to aldo-keto reductases (AKRs), enzymes that catalyze reduction of aldehyde groups to alcohols that are coupled to oxidation of an NADPH cofactor. However, it was unclear whether the Kvβ protein functioned in a catalytic capacity in its interaction with Kv channels, which allow voltage-sensitive conductance of potassium ions that is critical for action potentials in excitable cells. Weng et al. used spectrophotometric assays to show that purified rat Kvβ2 had associated NADPH and could reduce small-molecule aldehydes known to serve as substrates for other AKRs. Under other conditions, Kvβ2 could promote the reverse reaction--transfer of a hydride from an alcohol to reduce NADP+. Mutation of residues in the active site of the enzyme diminished the enzymatic activity. Application of a Kvβ substrate to Kv channels in inside-out patches from oocytes expressing the channel subunits decreased channel ...
anti-Potassium Voltage-Gated Channel, Shal-Related Subfamily, Member 1 (Kcnd1) antibody (Alexa Fluor 350) ABIN903487 from antibodies-online
Diabetes significantly modifies action potential, Ca2+ transient and Ca2+ sensitivity of contractile elements in cardiomyocytes [62, 63, 64, 65, 66]. Prolongation of action potential duration (APD) and slower decay of Ca2+ transient are consistently observed in diabetic cardiomyocytes. It is notable that such changes in the Ca2+ transient were observed before development of systolic ventricular dysfunction. Peak amplitude of Ca2+ transient was reduced in some [64, 65, 67, 68, 69], but not all [70, 71, 72], models of diabetes.. As for prolongation of APD, reduction in transient outward K+ (Ito) current has been shown in most animal models of diabetes [62, 63, 65, 66, 73], though reduced expression of L-type Ca2+ channel was an additional abnormality in some models [64, 74]. The prolongation of APD is potentially a compensatory mechanism for preserving Ca2+ influx in cardiomyocytes with down-regulated L-type Ca2+ channel. However, it could lead to untoward outcomes. A study by Sah et al. [75] ...
lambda(F26DP, G6P, kv4_1, kv4_2, kv4_3, kv4_4, kv4_5, (kv4_2*(1-F26DP^kv4_5/(F26DP+kv4_3)^kv4_5)+kv4_1*F26DP^kv4_5/(F26DP+kv4_3)^kv4_5)*(G6P/kv4_4)^2/(1+(G6P/kv4_4)^2 ...
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Emerin and A-type lamin-deficient cells have impaired mechanotransduction. (a) Expression of the mechanosensitive genes iex-1 and egr-1 in response to mechanica