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Bibliografías temáticas / BKCa channels

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Literatura académica sobre el tema "BKCa channels"

Autor: Grafiati

Publicado: 7 de diciembre de 2024

Última modificación: 31 de julio de 2025

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Artículos de revistas sobre el tema "BKCa channels"

1

Zhu, Shu, Darren D. Browning, Richard E. White, David Fulton та Scott A. Barman. "Mutation of protein kinase C phosphorylation site S1076 on α-subunits affects BKCa channel activity in HEK-293 cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 297, № 4 (2009): L758—L766. http://dx.doi.org/10.1152/ajplung.90518.2008.

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Large conductance, calcium- and voltage-activated potassium (BKCa) channels are important modulators of pulmonary vascular smooth muscle membrane potential, and phosphorylation of BKCa channels by protein kinases regulates pulmonary arterial smooth muscle function. However, little is known about the effect of phosphorylating specific channel subunits on BKCa channel activity. The present study was done to determine the effect of mutating protein kinase C (PKC) phosphorylation site serine 1076 (S1076) on transfected human BKCa channel α-subunits in human embryonic kidney (HEK-293) cells, a hete

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2

Zhao, Guiling, Zachary P. Neeb, M. Dennis Leo, et al. "Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells." Journal of General Physiology 136, no. 3 (2010): 283–91. http://dx.doi.org/10.1085/jgp.201010453.

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Plasma membrane large-conductance Ca2+-activated K+ (BKCa) channels and sarcoplasmic reticulum inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are expressed in a wide variety of cell types, including arterial smooth muscle cells. Here, we studied BKCa channel regulation by IP3 and IP3Rs in rat and mouse cerebral artery smooth muscle cells. IP3 activated BKCa channels both in intact cells and in excised inside-out membrane patches. IP3 caused concentration-dependent BKCa channel activation with an apparent dissociation constant (Kd) of ∼4 µM at physiological voltage (−40 mV) and intracellu

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3

Xie, Man-Jiang, Yu-Guang Ma, Fang Gao, et al. "Activation of BKCa channel is associated with increased apoptosis of cerebrovascular smooth muscle cells in simulated microgravity rats." American Journal of Physiology-Cell Physiology 298, no. 6 (2010): C1489—C1500. http://dx.doi.org/10.1152/ajpcell.00474.2009.

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Cerebral arterial remodeling is one of the critical factors in the occurrence of postspaceflight orthostatic intolerance. We hypothesize that large-conductance calcium-activated K+ (BKCa) channels in vascular smooth muscle cells (VSMCs) may play an important role in regulating cerebrovascular adaptation during microgravity exposure. The aim of this work was to investigate whether activation of BKCa channels is involved in regulation of apoptotic remodeling of cerebral arteries in simulated microgravity rats. In animal studies, Sprague-Dawley rats were subjected to 1-wk hindlimb unweighting to

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4

Ling, Shizhang, Jian-Zhong Sheng, and Andrew P. Braun. "The calcium-dependent activity of large-conductance, calcium-activated K+ channels is enhanced by Pyk2- and Hck-induced tyrosine phosphorylation." American Journal of Physiology-Cell Physiology 287, no. 3 (2004): C698—C706. http://dx.doi.org/10.1152/ajpcell.00030.2004.

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Recent results showing that large-conductance, calcium-activated K+ (BKCa) channels undergo direct tyrosine phosphorylation in the presence of c-Src tyrosine kinase have suggested the involvement of these channels in Src-mediated signaling pathways. Given the important role for c-Src in integrin-mediated signal transduction, we have examined the potential regulation of BKCa channels by proline-rich tyrosine kinase 2 (Pyk2), a calcium-sensitive tyrosine kinase activated upon integrin stimulation. Transient coexpression of murine BKCa channels with either wild-type Pyk2 or hematopoietic cell kin

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5

Kim, Eun Young, Jae Mi Suh, Yu-Hsin Chiu, and Stuart E. Dryer. "Regulation of podocyte BKCa channels by synaptopodin, Rho, and actin microfilaments." American Journal of Physiology-Renal Physiology 299, no. 3 (2010): F594—F604. http://dx.doi.org/10.1152/ajprenal.00206.2010.

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Mechanosensitive large-conductance Ca2+-activated K+ channels encoded by the Slo1 gene (BKCa channels) are expressed in podocytes. Here we show that BKCa channels reciprocally coimmunoprecipitate with synaptopodin (Synpo) in mouse glomeruli, in mouse podocytes, and in a heterologous expression system (HEK293T cells) in which these proteins are transiently expressed. Synpo and Slo1 colocalize along the surface of the glomerular basement membrane in mouse glomeruli. Synpo interacts with BKCa channels at COOH-terminal domains that overlap with an actin-binding domain on the channel molecule that

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Werner, Matthias E., Andrea L. Meredith, Richard W. Aldrich, and Mark T. Nelson. "Hypercontractility and impaired sildenafil relaxations in the BKCa channel deletion model of erectile dysfunction." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 1 (2008): R181—R188. http://dx.doi.org/10.1152/ajpregu.00173.2008.

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Erectile dysfunction (ED) can be elicited by a variety of pathogenic factors, particularly impaired formation of and responsiveness to nitric oxide (NO) and the downstream effectors soluble guanylate cyclase (sGC) and cGMP-dependent protein kinase I (PKGI). One important target of PKGI in smooth muscle is the large-conductance, Ca2+-activated potassium (BKCa) channel. In our previous report ( 42 ), we demonstrated that deletion of the BKCa channel in mice induced force oscillations and led to reduced nerve-evoked relaxations and ED. In the current study, we used this ED model to explore the ro

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Choi, Chang-Rok, Eun-Jin Kim, Tae Hyun Choi, Jaehee Han, and Dawon Kang. "Enhancing Human Cutaneous Wound Healing through Targeted Suppression of Large Conductance Ca2+-Activated K+ Channels." International Journal of Molecular Sciences 25, no. 2 (2024): 803. http://dx.doi.org/10.3390/ijms25020803.

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The modulation of K+ channels plays a crucial role in cell migration and proliferation, but the effect of K+ channels on human cutaneous wound healing (CWH) remains underexplored. This study aimed to determine the necessity of modulating K+ channel activity and expression for human CWH. The use of 25 mM KCl as a K+ channel blocker markedly improved wound healing in vitro (in keratinocytes and fibroblasts) and in vivo (in rat and porcine models). K+ channel blockers, such as quinine and tetraethylammonium, aided in vitro wound healing, while Ba2+ was the exception and did not show similar effec

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8

Barman, Scott A., Shu Zhu, and Richard E. White. "Protein kinase C inhibits BKCa channel activity in pulmonary arterial smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 1 (2004): L149—L155. http://dx.doi.org/10.1152/ajplung.00207.2003.

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Signaling mechanisms that elevate cyclic AMP (cAMP) activate large-conductance, calcium- and voltage-activated potassium (BKCa) channels in pulmonary vascular smooth muscle and cause pulmonary vasodilatation. BKCa channel modulation is important in the regulation of pulmonary arterial pressure, and inhibition (closing) of the BKCa channel has been implicated in the development of pulmonary vasoconstriction. Protein kinase C (PKC) causes pulmonary vasoconstriction, but little is known about the effect of PKC on BKCa channel activity. Accordingly, studies were done to determine the effect of PKC

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9

Khan, Raheela N., Stephen K. Smith, J. J. Morrison, and Michael L. J. Ashford. "Ca2+ dependence and pharmacology of large-conductance K+ channels in nonlabor and labor human uterine myocytes." American Journal of Physiology-Cell Physiology 273, no. 5 (1997): C1721—C1731. http://dx.doi.org/10.1152/ajpcell.1997.273.5.c1721.

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Two populations, Ca2+-dependent (BKCa) and Ca2+-independent K+ (BK) channels of large conductance were identified in inside-out patches of nonlabor and labor freshly dispersed human pregnant myometrial cells, respectively. Cell-attached recordings from nonlabor myometrial cells frequently displayed BKCa channel openings characterized by a relatively low open-state probability, whereas similar recordings from labor tissue displayed either no channel openings or consistently high levels of channel activity that often exhibited clear, oscillatory activity. In inside-out patch recordings, Ba2+ (2–

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Hou, Shangwei, Stefan H. Heinemann, and Toshinori Hoshi. "Modulation of BKCa Channel Gating by Endogenous Signaling Molecules." Physiology 24, no. 1 (2009): 26–35. http://dx.doi.org/10.1152/physiol.00032.2008.

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Large-conductance Ca2+- and voltage-activated K+ (BKCa, MaxiK, or Slo1) channels are expressed in almost every tissue in our body and participate in many critical functions such as neuronal excitability, vascular tone regulation, and neurotransmitter release. The functional versatility of BKCa channels owes in part to the availability of a spectacularly wide array of biological modulators of the channel function. In this review, we focus on modulation of BKCa channels by small endogenous molecules, emphasizing their molecular mechanisms. The mechanistic information available from studies on th

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Tesis sobre el tema "BKCa channels"

1

McCartney, Claire Elizabeth. "Effect of hypoxia on neuronal large conductance calcium-activated potassium (BKca) channels." Thesis, University of Strathclyde, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410156.

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Ferraguto, Celeste. "BKCa channels as therapeutic targets in neurodevelopmental disorders : focus on acoustic dysfunction." Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0134.

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Les troubles du neurodéveloppement (TNDs) se caractérisent par un vaste éventail de phénotypes pathologiques qui englobent diverses anomalies aussi bien physiques, cérébrales que comportementales. Parmi celles-ci, les altérations de la perception auditive sont fréquemment observées dans plusieurs TNDs. L’existence de cette symptomatologie commune suggère que des mécanismes sous-jacents comparables seraient à l’origine des TNDs, et donc que des stratégies thérapeutiques similaires pourraient permettre de palier les déficits observés. Malgré des efforts considérables, des composés pharmacologiqu

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3

Krishnamoorthy, Gayathri. "MECHANISM OF CALCIUM DEPENDENT GATING OF BKCa CHANNELS: RELATING PROTEIN STRUCTURE TO FUNCTION." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1144444855.

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4

Sane, Mukta. "Role of Large Conductance, Calcium-Activated Potassium Channels (BKCa) in Vasorelaxation of Nitrate Tolerant Mesenteric Arteries." Diss., North Dakota State University, 2016. http://hdl.handle.net/10365/25665.

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5

Ayad, Oualid. "Caractérisation fonctionnelle des cellules souches cardiaques humaines dans un but thérapeutique." Thesis, Poitiers, 2017. http://www.theses.fr/2017POIT2303/document.

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L'objectif de cette thèse était de développer et de caractériser un modèle de cellules souches cardiaques humaines dans un contexte de thérapie cellulaire. Après avoir sélectionné et caractérisé une population de cellules souches d'origine mésenchymateuse, isolée à partir d'auricules humaines, exprimant le marqueur W8B2 (CSCs W8B2+), nous nous sommes focalisés (par les techniques de RT-qPCR à haut rendement, d'immuno-marquage, de western-blot et de fluorescence calcique) sur ; 1. la caractérisation génique des canaux ioniques et des acteurs de la signalisation calcique et 2. l'étude de leur di

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6

Gambade, Audrey. "Rôle du peptide LL-37 dans le cancer du sein : son interaction avec la membrane plasmique stimule l'entrée de calcium et la migration cellulaire par l'activation des canaux ioniques TRPV2 et BKCa." Thesis, Tours, 2015. http://www.theses.fr/2015TOUR3312/document.

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Le peptide antimicrobien LL-37 a été retrouvé surexprimé dans différents types de cancer et plus particulièrement dans le cancer du sein dans lequel il est associé au développement des métastases. Nous avons observé, in vitro, que la migration de trois lignées cancéreuses mammaires est augmentée par le peptide LL-37 et son énantiomère (D)-LL-37, excluant la fixation du peptide à un récepteur protéique. Sur les cellules cancéreuses mammaires MDA-MB-435s, le peptide se fixe à la membrane plasmique et diminue sa fluidité. La microscopie électronique localise LL-37 dans les cavéoles et à la surfac

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7

Hdud, Ismail Masaud M. "Expression of TRPV channel isoforms and BKCa channel subunits in equine articular chondrocytes and their potential role in cartilage biology and cellular pathology." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.662204.

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Mechanical injuries play an important role in the pathogenesis of osteoarthritis, especially in horses. Chondrocytes are highly mechanosensitive cells responsible for the production and maintenance of the extracellular matrix (ECM) of articular cartilage. ECM turnover is influenced by mechanical and osmotic factors, and Ca 2+ signalling is a key component of mechanical responsiveness in these cells. Hence, for this thesis, freshly isolated equine articular chondrocytes was used to investigate the influence of mechanical and/or osmotic loading. Immunohistochemistry revealed superficial localisa

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8

Azhikkattuparambil, Bhaskaran Arjun. "Cellular and circuit mechanisms of neocortical dysfunction in Fragile X Syndrome." Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0244/document.

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Cette étude explore les réponses évoquées, l'activité intrinsèque et spontanée de deux populations neuronales différentes dans la région du cerveau correspondant à la patte arrière des souris. Dans cet article, nous nous sommes concentrés sur un modèle murin du syndrome de l'X fragile (SXF), qui est la forme la plus commune de syndrome de retard mental héréditaire et une cause fréquente de troubles du spectre autistique (TSA). SXF est un trouble à gène unique (Fmr1), qui peut être modélisé de manière fiable par un modèle murin transgénique : la souris Fmr1-/y déficiente pour le gène codant Fmr

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9

"TRPV4-TRPC1- BKca tri-complex mediates epoxyeicosatrienoic acid-induced membrane hyperpolarization." Thesis, 2011. http://library.cuhk.edu.hk/record=b6075501.

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Ma, Yan.<br>"Ca" in the title is subscript.<br>Thesis (Ph.D.)--Chinese University of Hong Kong, 2011.<br>Includes bibliographical references (leaves 143-166).<br>Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.<br>Abstract also in Chinese.

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10

Chien-Fu, Chen. "Eugenosedin-A activates BKCa channels in rat basilar artery myocytes." 2005. http://www.cetd.com.tw/ec/thesisdetail.aspx?etdun=U0011-2903200614032202.

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Capítulos de libros sobre el tema "BKCa channels"

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Telezhkin, V., S. P. Brazier, S. Cayzac, C. T. Müller, D. Riccardi, and P. J. Kemp. "Hydrogen Sulfide Inhibits Human BKCa Channels." In Advances in Experimental Medicine and Biology. Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2259-2_7.

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Vaithianathan, Thirumalini, Elizabeth H. Schneider, Anna N. Bukiya, and Alex M. Dopico. "Cholesterol and PIP2 Modulation of BKCa Channels." In Advances in Experimental Medicine and Biology. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-21547-6_8.

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3

de Wet, Heidi, Jonathan D. Lippiat, and Marcus Allen. "Analysing Steroid Modulation of BKCa Channels Reconstituted into Planar Lipid Bilayers." In Methods in Molecular Biology. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-526-8_14.

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4

Neira, Fernanda, Nataly Neira, Javier Torres, and Marcelo González-Ortiz. "Physiological and Pathophysiological Role of Large-Conductance Calcium-Activated Potassium Channels (BKCa) in HUVECs and Placenta." In Advances in Maternal-Fetal Biomedicine. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-32554-0_3.

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Kolář, František. "Mitochondrial BKCa Channel as a Target for Cardioprotection." In NATO Science for Peace and Security Series A: Chemistry and Biology. Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6513-9_13.

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6

Jia, Xiaoling, Jingyun Yang, Liu Yang, Ping Li, Wei Song, and Yubo Fan. "Irrelevance of BKCa Channel Expression to VSMCs Phenotype under Shear Stress." In IFMBE Proceedings. Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-29305-4_56.

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7

Edwards, Gillian, and Arthur H. Weston. "The Pharmacology of Potassium Channel Superfamilies: Modulation of KATP and BKCa." In Molecular and Cellular Mechanisms of Cardiovascular Regulation. Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-65952-5_9.

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Brazier, S. P., V. Telezhkin, R. Mears, C. T. Müller, D. Riccardi, and P. J. Kemp. "Cysteine Residues in the C-terminal Tail of the Human BKCaα Subunit Are Important for Channel Sensitivity to Carbon Monoxide." In Advances in Experimental Medicine and Biology. Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2259-2_5.

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Santiago, Jorge, Cristhian Romero, Santiago Guerrero, Francisco Trejo, and Daniel Robles. "Bio-Informatic Model of Tyrosine Kinases Inhibitors in Trabecular Meshwork Cells." In Frontiers in Artificial Intelligence and Applications. IOS Press, 2021. http://dx.doi.org/10.3233/faia210034.

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The behavior of potassium ion (K+) establishes the repolarization and hyperpolarization states in the cell membrane of trabecular meshwork cells. One of the main proteins that controls this ion is calcium-dependent potassium maxi-channels BKca, their malfunction evoked by tyrosine kinases, destabilize the control of aqueous humor flow and the increase of intraocular pressure, responsible of glaucoma. In the present work, the ionic behavior of ion K+ of trabecular cells is detailed, when genistein and tyrphostin-51 are applied in culture cells. The flow behavior is described by means of mathema

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10

Fajmut, Aleš. "Molecular Mechanisms and Targets of Cyclic Guanosine Monophosphate (cGMP) in Vascular Smooth Muscles." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97708.

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Molecular mechanisms and targets of cyclic guanosine monophosphate (cGMP) accounting for vascular smooth muscles (VSM) contractility are reviewed. Mathematical models of five published mechanisms are presented, and four novel mechanisms are proposed. cGMP, which is primarily produced by the nitric oxide (NO) dependent soluble guanylate cyclase (sGC), activates cGMP-dependent protein kinase (PKG). The NO/cGMP/PKG signaling pathway targets are the mechanisms that regulate cytosolic calcium ([Ca2+]i) signaling and those implicated in the Ca2+-desensitization of the contractile apparatus. In addit

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Actas de conferencias sobre el tema "BKCa channels"

1

Guntur, D., D. Jeremic, V. Foris, H. Olschewski, A. Olschewski, and C. Nagaraj. "Relevance of BKCa Channels in Pulmonary Endothelial Dysfunction." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a4042.

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Zhu, Shu, Richard E. White, Mary L. Meadows, and Scott A. Barman. "Expression Of BKCa Channels In Pulmonary Arterial Smooth Muscle And The Effect Of Protein Kinase C Phosphorylation Site S1076 On The Response To PKCµ On BKCa Channel Activity." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6449.

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