Luis F. Santana

Modulation of the molecular composition of large conductance, Ca(2+) activated K(+) channels in vascular smooth muscle during hypertension.

NFATc3 regulates Kv2.1 expression in arterial smooth muscle.

Alterations in early action potential repolarization causes localized failure of sarcoplasmic reticulum Ca2+ release.

Constitutively active L-type Ca2+ channels.

Mechanisms underlying variations in excitation-contraction coupling across the mouse left ventricular free wall.

On the loose: uncaging Ca2+ -induced Ca2+ release in smooth muscle.

Kv2 channels oppose myogenic constriction of rat cerebral arteries.

Differential calcineurin/NFATc3 activity contributes to the Ito transmural gradient in the mouse heart.

Mechanisms underlying heterogeneous Ca2+ sparklet activity in arterial smooth muscle.

Phosphoinositide 3-kinase binds to TRPV1 and mediates NGF-stimulated TRPV1 trafficking to the plasma membrane.

Activation of NFATc3 down-regulates the beta1 subunit of large conductance, calcium-activated K+ channels in arterial smooth muscle and contributes to hypertension.

Calcium sparklets regulate local and global calcium in murine arterial smooth muscle.

Sodium current and arrhythmogenesis in heart failure.

Ca(v)1.3 channels produce persistent calcium sparklets, but Ca(v)1.2 channels are responsible for sparklets in mouse arterial smooth muscle.

SMAKing Ca2+ sparks in arterial myocytes.

AKAP150 is required for stuttering persistent Ca2+ sparklets and angiotensin II-induced hypertension.

Calcium sparklets in arterial smooth muscle.

NFAT-dependent excitation-transcription coupling in heart.

The control of Ca2+ influx and NFATc3 signaling in arterial smooth muscle during hypertension.

NFATc3-dependent loss of I(to) gradient across the left ventricular wall during chronic beta adrenergic stimulation.

Local control of excitation-contraction coupling in human embryonic stem cell-derived cardiomyocytes.

Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging.

Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscle.

Myostatin represses physiological hypertrophy of the heart and excitation-contraction coupling.

Elevated Ca2+ sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells.

Increased coupled gating of L-type Ca2+ channels during hypertension and Timothy syndrome.

Knockout of Na+/Ca2+ exchanger in smooth muscle attenuates vasoconstriction and L-type Ca2+ channel current and lowers blood pressure.

A-kinase anchoring proteins: getting to the heart of the matter.

Phosphodiesterase 8A (PDE8A) regulates excitation-contraction coupling in ventricular myocytes.

Natural inequalities: why some L-type Ca2+ channels work harder than others.

Sympathetic stimulation of adult cardiomyocytes requires association of AKAP5 with a subpopulation of L-type calcium channels.

How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?

Eosinophil cysteinyl leukotriene synthesis mediated by exogenous secreted phospholipase A2 group X.

Mitochondrial oxidative stress mediates angiotensin II-induced cardiac hypertrophy and Galphaq overexpression-induced heart failure.

Mitochondrial targeted antioxidant Peptide ameliorates hypertensive cardiomyopathy.

Restoration of normal L-type Ca2+ channel function during Timothy syndrome by ablation of an anchoring protein.

Relationship between Ca2+ sparklets and sarcoplasmic reticulum Ca2+ load and release in rat cerebral arterial smooth muscle.

An entirely specific type I A-kinase anchoring protein that can sequester two molecules of protein kinase A at mitochondria.

Dynamic changes in sarcoplasmic reticulum structure in ventricular myocytes.

Ca2+ signaling amplification by oligomerization of L-type Cav1.2 channels.