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M T Keating

Showing results (61-70 of 76) with videos related to

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Human Molecular Genetics|July 1, 1997
Elastin point mutations cause an obstructive vascular disease, supravalvular aortic stenosisD Y Li, A E Toland, B B Boak, et al.
Nature Genetics|September 1, 1993
Hemizygosity at the elastin locus in a developmental disorder, Williams syndromeA K Ewart, C A Morris, D Atkinson, et al.
Journal of Medical Genetics|May 4, 2004
The common SCN5A mutation R1193Q causes LQTS-type electrophysiological alterations of the cardiac sodium channelQ Wang, S Chen, Q Chen, et al.
Cell|April 29, 1999
MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmiaG W Abbott, F Sesti, I Splawski, et al.
Nature|June 2, 1998
Elastin is an essential determinant of arterial morphogenesisD Y Li, B Brooke, E C Davis, et al.
Cell|March 10, 1995
SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndromeQ Wang, J Shen, I Splawski, et al.
The Journal of Clinical Investigation|November 20, 1998
Novel arterial pathology in mice and humans hemizygous for elastinD Y Li, G Faury, D G Taylor, et al.
Circulation|September 1, 1996
Genetically defined therapy of inherited long-QT syndrome. Correction of abnormal repolarization by potassiumS J Compton, R L Lux, M R Ramsey, et al.
Circulation|December 15, 1995
Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapyP J Schwartz, S G Priori, E H Locati, et al.
Circulation|September 7, 2000
Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2I Splawski, J Shen, K W Timothy, et al.
Pageof 8

Showing results (61-70 of 76) with videos related to

Sort By:
Pageof 8
Human Molecular Genetics|July 1, 1997
Elastin point mutations cause an obstructive vascular disease, supravalvular aortic stenosisD Y Li, A E Toland, B B Boak, et al.
Nature Genetics|September 1, 1993
Hemizygosity at the elastin locus in a developmental disorder, Williams syndromeA K Ewart, C A Morris, D Atkinson, et al.
Journal of Medical Genetics|May 4, 2004
The common SCN5A mutation R1193Q causes LQTS-type electrophysiological alterations of the cardiac sodium channelQ Wang, S Chen, Q Chen, et al.
Cell|April 29, 1999
MiRP1 forms IKr potassium channels with HERG and is associated with cardiac arrhythmiaG W Abbott, F Sesti, I Splawski, et al.
Nature|June 2, 1998
Elastin is an essential determinant of arterial morphogenesisD Y Li, B Brooke, E C Davis, et al.
Cell|March 10, 1995
SCN5A mutations associated with an inherited cardiac arrhythmia, long QT syndromeQ Wang, J Shen, I Splawski, et al.
The Journal of Clinical Investigation|November 20, 1998
Novel arterial pathology in mice and humans hemizygous for elastinD Y Li, G Faury, D G Taylor, et al.
Circulation|September 1, 1996
Genetically defined therapy of inherited long-QT syndrome. Correction of abnormal repolarization by potassiumS J Compton, R L Lux, M R Ramsey, et al.
Circulation|December 15, 1995
Long QT syndrome patients with mutations of the SCN5A and HERG genes have differential responses to Na+ channel blockade and to increases in heart rate. Implications for gene-specific therapyP J Schwartz, S G Priori, E H Locati, et al.
Circulation|September 7, 2000
Spectrum of mutations in long-QT syndrome genes. KVLQT1, HERG, SCN5A, KCNE1, and KCNE2I Splawski, J Shen, K W Timothy, et al.
Pageof 8