J Striessnig

Summary

Affiliation: University of Innsbruck
Country: Austria

Publications

  1. Liss B, Striessnig J. The Potential of L-Type Calcium Channels as a Drug Target for Neuroprotective Therapy in Parkinson's Disease. Annu Rev Pharmacol Toxicol. 2019;59:263-289 pubmed publisher
    ..We discuss different dihydropyridine sensitivities of LTCC isoforms in view of their potential as drug targets for PD neuroprotection, and we conclude by considering how these aspects could guide further drug development. ..
  2. Lieb A, Ortner N, Striessnig J. C-terminal modulatory domain controls coupling of voltage-sensing to pore opening in Cav1.3 L-type Ca(2+) channels. Biophys J. 2014;106:1467-75 pubmed publisher
    ..2 or Cav3.1. Weak coupling of voltage sensing to pore opening is enhanced in the absence of the CTM, allowing short Cav1.342A splice variants to activate at lower voltages without affecting QON-V. ..
  3. Striessnig J, Ortner N, Pinggera A. Pharmacology of L-type Calcium Channels: Novel Drugs for Old Targets?. Curr Mol Pharmacol. 2015;8:110-22 pubmed
    ..In this review we discuss the pathogenetic role of L-type calcium channels, potential new indications for existing or isoform-selective compounds and strategies to minimize potential side effects. ..
  4. Kaur G, Pinggera A, Ortner N, Lieb A, Sinnegger Brauns M, Yarov Yarovoy V, et al. A Polybasic Plasma Membrane Binding Motif in the I-II Linker Stabilizes Voltage-gated CaV1.2 Calcium Channel Function. J Biol Chem. 2015;290:21086-100 pubmed publisher
    ..Our data provide new evidence for a membrane binding motif within the I-II linker of LTCC α1-subunits essential for stabilizing normal Ca(2+) channel function. ..
  5. Pinggera A, Striessnig J. Cav 1.3 (CACNA1D) L-type Ca2+ channel dysfunction in CNS disorders. J Physiol. 2016;594:5839-5849 pubmed publisher
    ..These data strongly suggest that CACNA1D mutations enhancing Cav 1.3 activity confer a strong risk for - or even cause - CNS disorders, such as ASD. ..
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    Striessnig J, Koschak A. Exploring the function and pharmacotherapeutic potential of voltage-gated Ca2+ channels with gene knockout models. Channels (Austin). 2008;2:233-51 pubmed
  7. Ortner N, Bock G, Dougalis A, Kharitonova M, Duda J, Hess S, et al. Lower Affinity of Isradipine for L-Type Ca2+ Channels during Substantia Nigra Dopamine Neuron-Like Activity: Implications for Neuroprotection in Parkinson's Disease. J Neurosci. 2017;37:6761-6777 pubmed publisher
    ..2 LTCCs in resistance blood vessels (mediating dose-limiting vasodilating effects) and even at supratherapeutic concentrations isradipine fails to reduce somatic Ca2+ oscillations of SN DA neurons. ..
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    Striessnig J, Hoda J, Koschak A, Zaghetto F, Mullner C, Sinnegger Brauns M, et al. L-type Ca2+ channels in Ca2+ channelopathies. Biochem Biophys Res Commun. 2004;322:1341-6 pubmed
    ..1 alpha1 in tottering mice. Ca2+ channelopathies provide exciting molecular tools to elucidate the contribution of different LTCC isoforms to human diseases. ..
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    Striessnig J, Koschak A, Sinnegger Brauns M, Hetzenauer A, Nguyen N, Busquet P, et al. Role of voltage-gated L-type Ca2+ channel isoforms for brain function. Biochem Soc Trans. 2006;34:903-9 pubmed
    ..The results described here also allow predictions about the pharmacotherapeutic potential of isoform-selective LTCC modulators. ..

More Information

Publications11

  1. Striessnig J, Bolz H, Koschak A. Channelopathies in Cav1.1, Cav1.3, and Cav1.4 voltage-gated L-type Ca2+ channels. Pflugers Arch. 2010;460:361-74 pubmed publisher
    ..1 alpha1 in tottering mice. Ca2+ channelopathies provide exciting disease-related molecular detail that led to important novel insight not only into disease pathophysiology but also to mechanisms of channel function...
  2. Pinggera A, Lieb A, Benedetti B, Lampert M, Monteleone S, Liedl K, et al. CACNA1D de novo mutations in autism spectrum disorders activate Cav1.3 L-type calcium channels. Biol Psychiatry. 2015;77:816-22 pubmed publisher
    ..Patients should also be explored for other symptoms likely resulting from Cav1.3 hyperactivity, in particular, primary aldosteronism. ..