J. Striessnig

发表

Generation of a neuro-specific microarray reveals novel differentially expressed noncoding RNAs in mouse models for neurodegenerative diseases

A. Hüttenhofer, R. Gstir, S. Schafferer, 2014, RNA.

Loss of Cav1.3 Channels Reveals the Critical Role of L-Type and BK Channel Coupling in Pacemaking Mouse Adrenal Chromaffin Cells

J. Striessnig, D. Vandael, E. Carbone, 2010, The Journal of Neuroscience.

International Union of Pharmacology. XLVIII. Nomenclature and Structure-Function Relationships of Voltage-Gated Calcium Channels

W. Catterall, J. Striessnig, T. Snutch, 2005, Pharmacological Reviews.

Down-regulation of L-type calcium channels in inflamed circular smooth muscle cells of the canine colon.

J. Striessnig, S. Sarna, N. Rusch, 2001, Gastroenterology.

CaV1.3-Driven SK Channel Activation Regulates Pacemaking and Spike Frequency Adaptation in Mouse Chromaffin Cells

A. Zuccotti, J. Striessnig, D. Vandael, 2012, The Journal of Neuroscience.

Separation of the CaV1.2‐CaV1.3 calcium channel duo prevents type 2 allergic airway inflammation

J. Striessnig, M. Savignac, J. E. Mejía, 2021, Allergy.

L-type Cav1.3 channels regulate ryanodine receptor-dependent Ca2+ release during sino-atrial node pacemaker activity.

J. Striessnig, A. Torrente, M. Mangoni, 2016, Cardiovascular research.

Cav1.3 L-Type Calcium Channels-Mediated Ryanodine Receptor Dependent Calcium Release Controls Heart Rate

J. Striessnig, A. Torrente, M. Mangoni, 2011 .

CaV1.3 L-type Ca2+ channel contributes to the heartbeat by generating a dihydropyridine-sensitive persistent Na+ current

F. Toyoda, J. Striessnig, W. Ding, 2017, Scientific Reports.

Distinct localization and modulation of Cav1.2 and Cav1.3 L‐type Ca2+ channels in mouse sinoatrial node

F. Hofmann, J. Striessnig, A. Ludwig, 2012, The Journal of physiology.

International Union of Pharmacology. XL. Compendium of Voltage-Gated Ion Channels: Calcium Channels

William A. Catterall, W. Catterall, J. Striessnig, 2003, Pharmacological Reviews.

The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential

A. Dolphin, J. Striessnig, A. Koschak, 2015, Pharmacological Reviews.

Neurological phenotype and synaptic function in mice lacking the CaV1.3 α subunit of neuronal L-type voltage-dependent Ca2+ channels

F. Kuenzi, D. Kullmann, S. Boyce, 2003, Neuroscience.

Stimulation of 5-HT(2) receptors in prefrontal pyramidal neurons inhibits Ca(v)1.2 L type Ca(2+) currents via a PLCbeta/IP3/calcineurin signaling cascade.

D. Surmeier, P. A. Olson, J. Striessnig, 2002, Journal of neurophysiology.

Iron Overload Decreases CaV1.3-Dependent L-Type Ca2+ Currents Leading to Bradycardia, Altered Electrical Conduction, and Atrial Fibrillation

S. Heximer, J. Striessnig, R. Rose, 2011, Circulation. Arrhythmia and electrophysiology.

Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson’s disease

O. Pongs, B. Liss, P. Kloppenburg, 2019, Nature Communications.

Somatic mutations in ATP1A1 and CACNA1D underlie a common subtype of adrenal hypertension

James Hadfield, Poul Nissen, Sumedha Garg, 2013, Nature Genetics.

Familial hemiplegic migraine mutations increase Ca2+ influx through single human CaV2.1 channels and decrease maximal CaV2.1 current density in neurons

C. Fletcher, T. Fellin, J. Striessnig, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Molecular Switch from L-Type Cav1.3 to Cav1.2 Ca2+ Channel Signaling Underlies Long-Term Psychostimulant-Induced Behavioral and Molecular Plasticity

B. Kosofsky, T. Giordano, J. Striessnig, 2010, The Journal of Neuroscience.

CaV1.3 Channels Are Essential for Development and Presynaptic Activity of Cochlear Inner Hair Cells

J. Striessnig, T. Moser, A. Brandt, 2003, The Journal of Neuroscience.

G protein-gated IKACh channels as therapeutic targets for treatment of sick sinus syndrome and heart block

Khai Le Quang, F. Charpentier, J. Striessnig, 2016, Proceedings of the National Academy of Sciences.

Enhancing dopaminergic signaling and histone acetylation promotes long-term rescue of deficient fear extinction

J. Rainer, J. Striessnig, N. Singewald, 2016, Translational psychiatry.

Cav1.3 channels control D2-autoreceptor responses via NCS-1 in substantia nigra dopamine neurons

Masahiko Watanabe, S. Lammel, R. Malenka, 2014, Brain : a journal of neurology.

Compensatory T-type Ca2+ channel activity alters D2-autoreceptor responses of Substantia nigra dopamine neurons from Cav1.3 L-type Ca2+ channel KO mice

B. Liss, J. Striessnig, J. Benkert, 2015, Scientific Reports.

Cav1.3 L-type Ca2+ channels mediate long-term adaptation in dopamine D2L-mediated GluA1 trafficking in the dorsal striatum following cocaine exposure

T. Giordano, F. Hofmann, J. Striessnig, 2012, Channels.

Cav1.2 L-Type Ca2+ Channels Mediate Cocaine-Induced GluA1 Trafficking in the Nucleus Accumbens, a Long-Term Adaptation Dependent on Ventral Tegmental Area Cav1.3 Channels

T. Giordano, F. Hofmann, J. Striessnig, 2011, The Journal of Neuroscience.

Enhancing VTA Cav1.3 L-type Ca2+ channel activity promotes cocaine and mood - related behaviors via overlapping AMPA receptor mechanisms in the nucleus accumbens

Richard C. Rice, R. Huganir, Shizhong Han, 2016, Molecular Psychiatry.

CaV1.3 L-type Ca2+ channel contributes to the heartbeat by generating a dihydropyridine-sensitive persistent Na+ current

F. Toyoda, J. Striessnig, W. Ding, 2017, Scientific Reports.

Aldosterone-Producing Adenomas: Histopathology–Genotype Correlation and Identification of a Novel CACNA1D Mutation

Morris J. Brown, I. Mohamed Rose, J. Striessnig, 2017, Hypertension.

CACNA1A gene mutations in familial hemiplegic migraine

M. Ferrari, J. Striessnig, R. Frants, 2000, The Journal of Headache and Pain.

Up‐regulation of dopamine D2L mRNA levels in the ventral tegmental area and dorsal striatum of amphetamine‐sensitized C57BL/6 mice: role of Cav1.3 L‐type Ca2+ channels

B. Kosofsky, T. Giordano, J. Striessnig, 2006, Journal of neurochemistry.