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Stac Proteins Suppress Ca2+-Dependent Inactivation of Neuronal l-type Ca2+ Channels.

Polster A, Dittmer PJ, Perni S, Bichraoui H, Sather WA, Beam KG.

J Neurosci. 2018 Oct 24;38(43):9215-9227. doi: 10.1523/JNEUROSCI.0695-18.2018. Epub 2018 Sep 10.


Stac proteins associate with the critical domain for excitation-contraction coupling in the II-III loop of CaV1.1.

Polster A, Nelson BR, Papadopoulos S, Olson EN, Beam KG.

J Gen Physiol. 2018 Apr 2;150(4):613-624. doi: 10.1085/jgp.201711917. Epub 2018 Feb 21.


Junctional trafficking and restoration of retrograde signaling by the cytoplasmic RyR1 domain.

Polster A, Perni S, Filipova D, Moua O, Ohrtman JD, Bichraoui H, Beam KG, Papadopoulos S.

J Gen Physiol. 2018 Feb 5;150(2):293-306. doi: 10.1085/jgp.201711879. Epub 2017 Dec 28.


De novo reconstitution reveals the proteins required for skeletal muscle voltage-induced Ca2+ release.

Perni S, Lavorato M, Beam KG.

Proc Natl Acad Sci U S A. 2017 Dec 26;114(52):13822-13827. doi: 10.1073/pnas.1716461115. Epub 2017 Dec 11.


Stac3 has a direct role in skeletal muscle-type excitation-contraction coupling that is disrupted by a myopathy-causing mutation.

Polster A, Nelson BR, Olson EN, Beam KG.

Proc Natl Acad Sci U S A. 2016 Sep 27;113(39):10986-91. doi: 10.1073/pnas.1612441113. Epub 2016 Sep 12.


Distinct Components of Retrograde Ca(V)1.1-RyR1 Coupling Revealed by a Lethal Mutation in RyR1.

Bannister RA, Sheridan DC, Beam KG.

Biophys J. 2016 Feb 23;110(4):912-21. doi: 10.1016/j.bpj.2015.12.031.


Apparent lack of physical or functional interaction between CaV1.1 and its distal C terminus.

Ohrtman JD, Romberg CF, Moua O, Bannister RA, Levinson SR, Beam KG.

J Gen Physiol. 2015 Apr;145(4):303-14. doi: 10.1085/jgp.201411292. Epub 2015 Mar 16.


Stac adaptor proteins regulate trafficking and function of muscle and neuronal L-type Ca2+ channels.

Polster A, Perni S, Bichraoui H, Beam KG.

Proc Natl Acad Sci U S A. 2015 Jan 13;112(2):602-6. doi: 10.1073/pnas.1423113112. Epub 2014 Dec 29.


Impaired gating of an L-Type Ca(2+) channel carrying a mutation linked to malignant hyperthermia.

Bannister RA, Beam KG.

Biophys J. 2013 May 7;104(9):1917-22. doi: 10.1016/j.bpj.2013.03.035. Erratum in: Biophys J. 2015 May 5;108(9):2420.


Three-dimensional localization of the α and β subunits and of the II-III loop in the skeletal muscle L-type Ca2+ channel.

Szpyt J, Lorenzon N, Perez CF, Norris E, Allen PD, Beam KG, Samsó M.

J Biol Chem. 2012 Dec 21;287(52):43853-61. doi: 10.1074/jbc.M112.419283. Epub 2012 Nov 1.


Ca(V)1.1: The atypical prototypical voltage-gated Ca²⁺ channel.

Bannister RA, Beam KG.

Biochim Biophys Acta. 2013 Jul;1828(7):1587-97. doi: 10.1016/j.bbamem.2012.09.007. Epub 2012 Sep 13. Review.


Triclosan impairs excitation-contraction coupling and Ca2+ dynamics in striated muscle.

Cherednichenko G, Zhang R, Bannister RA, Timofeyev V, Li N, Fritsch EB, Feng W, Barrientos GC, Schebb NH, Hammock BD, Beam KG, Chiamvimonvat N, Pessah IN.

Proc Natl Acad Sci U S A. 2012 Aug 28;109(35):14158-63. doi: 10.1073/pnas.1211314109. Epub 2012 Aug 13. Erratum in: Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16393.


Malignant hyperthermia susceptibility arising from altered resting coupling between the skeletal muscle L-type Ca2+ channel and the type 1 ryanodine receptor.

Eltit JM, Bannister RA, Moua O, Altamirano F, Hopkins PM, Pessah IN, Molinski TF, López JR, Beam KG, Allen PD.

Proc Natl Acad Sci U S A. 2012 May 15;109(20):7923-8. doi: 10.1073/pnas.1119207109. Epub 2012 Apr 30.


Bimolecular fluorescence complementation and targeted biotinylation provide insight into the topology of the skeletal muscle Ca ( 2+) channel β1a subunit.

Sheridan DC, Moua O, Lorenzon NM, Beam KG.

Channels (Austin). 2012 Jan-Feb;6(1):26-40. doi: 10.4161/chan.18916. Epub 2012 Jan 1.


Properties of Na+ currents conducted by a skeletal muscle L-type Ca2+ channel pore mutant (SkEIIIK).

Bannister RA, Beam KG.

Channels (Austin). 2011 May-Jun;5(3):262-8. Epub 2011 May 1.


Looking for answers to EC coupling's persistent questions.

Beam KG, Bannister RA.

J Gen Physiol. 2010 Jul;136(1):7-12. doi: 10.1085/jgp.201010461. No abstract available.


A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.

Estève E, Eltit JM, Bannister RA, Liu K, Pessah IN, Beam KG, Allen PD, López JR.

J Gen Physiol. 2010 Jun;135(6):619-28. doi: 10.1085/jgp.200910328. Epub 2010 May 17.


A malignant hyperthermia-inducing mutation in RYR1 (R163C): consequent alterations in the functional properties of DHPR channels.

Bannister RA, Estève E, Eltit JM, Pessah IN, Allen PD, López JR, Beam KG.

J Gen Physiol. 2010 Jun;135(6):629-40. doi: 10.1085/jgp.200910329. Epub 2010 May 17.


Ryanodine modification of RyR1 retrogradely affects L-type Ca(2+) channel gating in skeletal muscle.

Bannister RA, Beam KG.

J Muscle Res Cell Motil. 2009;30(5-6):217-23. doi: 10.1007/s10974-009-9190-0. Epub 2009 Oct 3.


The cardiac alpha(1C) subunit can support excitation-triggered Ca2+ entry in dysgenic and dyspedic myotubes.

Bannister RA, Beam KG.

Channels (Austin). 2009 Jul-Aug;3(4):268-73. Epub 2009 Jul 24.


Effects of inserting fluorescent proteins into the alpha1S II-III loop: insights into excitation-contraction coupling.

Bannister RA, Papadopoulos S, Haarmann CS, Beam KG.

J Gen Physiol. 2009 Jul;134(1):35-51. doi: 10.1085/jgp.200910241.


The skeletal L-type Ca(2+) current is a major contributor to excitation-coupled Ca(2+) entry.

Bannister RA, Pessah IN, Beam KG.

J Gen Physiol. 2009 Jan;133(1):79-91. doi: 10.1085/jgp.200810105.


Disease causing mutations of calcium channels.

Lorenzon NM, Beam KG.

Channels (Austin). 2008 May-Jun;2(3):163-79. Epub 2008 May 29. Review.


Sequence differences in the IQ motifs of CaV1.1 and CaV1.2 strongly impact calmodulin binding and calcium-dependent inactivation.

Ohrtman J, Ritter B, Polster A, Beam KG, Papadopoulos S.

J Biol Chem. 2008 Oct 24;283(43):29301-11. doi: 10.1074/jbc.M805152200. Epub 2008 Aug 21.


Rem inhibits skeletal muscle EC coupling by reducing the number of functional L-type Ca2+ channels.

Bannister RA, Colecraft HM, Beam KG.

Biophys J. 2008 Apr 1;94(7):2631-8. doi: 10.1529/biophysj.107.116467. Epub 2008 Jan 11.


Alpha2delta1 dihydropyridine receptor subunit is a critical element for excitation-coupled calcium entry but not for formation of tetrads in skeletal myotubes.

Gach MP, Cherednichenko G, Haarmann C, Lopez JR, Beam KG, Pessah IN, Franzini-Armstrong C, Allen PD.

Biophys J. 2008 Apr 15;94(8):3023-34. doi: 10.1529/biophysj.107.118893. Epub 2008 Jan 11.


Bidirectional signaling between calcium channels of skeletal muscle requires multiple direct and indirect interactions.

Sheridan DC, Takekura H, Franzini-Armstrong C, Beam KG, Allen PD, Perez CF.

Proc Natl Acad Sci U S A. 2006 Dec 26;103(52):19760-5. Epub 2006 Dec 15.


Organization of calcium channel beta1a subunits in triad junctions in skeletal muscle.

Leuranguer V, Papadopoulos S, Beam KG.

J Biol Chem. 2006 Feb 10;281(6):3521-7. Epub 2005 Nov 28.


The alpha1S N-terminus is not essential for bi-directional coupling with RyR1.

Bannister RA, Beam KG.

Biochem Biophys Res Commun. 2005 Oct 14;336(1):134-41.


Ryanodine receptor type 1 (RyR1) mutations C4958S and C4961S reveal excitation-coupled calcium entry (ECCE) is independent of sarcoplasmic reticulum store depletion.

Hurne AM, O'Brien JJ, Wingrove D, Cherednichenko G, Allen PD, Beam KG, Pessah IN.

J Biol Chem. 2005 Nov 4;280(44):36994-7004. Epub 2005 Aug 24.


Conformational activation of Ca2+ entry by depolarization of skeletal myotubes.

Cherednichenko G, Hurne AM, Fessenden JD, Lee EH, Allen PD, Beam KG, Pessah IN.

Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15793-8. Epub 2004 Oct 25.


Metabolic biotinylation as a probe of supramolecular structure of the triad junction in skeletal muscle.

Lorenzon NM, Haarmann CS, Norris EE, Papadopoulos S, Beam KG.

J Biol Chem. 2004 Oct 15;279(42):44057-64. Epub 2004 Jul 27.


Potentiated L-type Ca2+ channels rectify.

Leuranguer V, Dirksen RT, Beam KG.

J Gen Physiol. 2003 Jun;121(6):541-50. Epub 2003 May 12.


Multiple regions of RyR1 mediate functional and structural interactions with alpha(1S)-dihydropyridine receptors in skeletal muscle.

Protasi F, Paolini C, Nakai J, Beam KG, Franzini-Armstrong C, Allen PD.

Biophys J. 2002 Dec;83(6):3230-44.


Ca2+ activation of RyR1 is not necessary for the initiation of skeletal-type excitation-contraction coupling.

O'Brien JJ, Feng W, Allen PD, Chen SR, Pessah IN, Beam KG.

Biophys J. 2002 May;82(5):2428-35.


Identification of a region of RyR1 that participates in allosteric coupling with the alpha(1S) (Ca(V)1.1) II-III loop.

Proenza C, O'Brien J, Nakai J, Mukherjee S, Allen PD, Beam KG.

J Biol Chem. 2002 Feb 22;277(8):6530-5. Epub 2001 Nov 28.


Structure and targeting of RyR1: implications from fusion of green fluorescent protein at the amino-terminal.

Lorenzon NM, Grabner M, Suda N, Beam KG.

Arch Biochem Biophys. 2001 Apr 1;388(1):13-7.


Excitation-contraction coupling is unaffected by drastic alteration of the sequence surrounding residues L720-L764 of the alpha 1S II-III loop.

Wilkens CM, Kasielke N, Flucher BE, Beam KG, Grabner M.

Proc Natl Acad Sci U S A. 2001 May 8;98(10):5892-7. Epub 2001 Apr 24.


A carboxyl-terminal region important for the expression and targeting of the skeletal muscle dihydropyridine receptor.

Proenza C, Wilkens C, Lorenzon NM, Beam KG.

J Biol Chem. 2000 Jul 28;275(30):23169-74.


Low serum promotes maturation of excitation-contraction coupling in myotubes.

Suda N, Dirksen RT, Gonzalez A, Beam KG.

Pflugers Arch. 2000 Mar;439(5):555-8.


Calcium channelopathies.

Lorenzon NM, Beam KG.

Kidney Int. 2000 Mar;57(3):794-802. Review.


The absence of resurgent sodium current in mouse spinal neurons.

Pan F, Beam KG.

Brain Res. 1999 Dec 4;849(1-2):162-8.


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