Jan Weiss - Concepedia

Author

Jan Weiss

Saarland University ORCID

Also Known As

J. Weiss, Jan Weiss, Weiss, Jan

Publications

701

Citations

H-Index

Concepts

All Affiliations

Saarland University University College London Physiologie de la Reproduction et des Comportements Université de Tours Max Planck Institute for Brain Research

About

Jan Weiss is an author at Saarland University specializing in medicine, cellular physiology, and cell signaling.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	4	4	391
2	Cellular Physiology	4	4	391
3	Cell Biology	3	3	101
4	Immunology	1	1	35
5	Molecular Genetics	1	1	290

Jan Weiss

Publications

658

Citations

H-Index

Page 1

	Year	Citations
Loss-of-function mutations in sodium channel Nav1.7 cause anosmia Jan Weiss, Martina Pyrski, Eric Jacobi, Nature ChannelopathiesMolecular PhysiologyHyperpolarization (Biology)PhysiologyElectrolyte Disturbance	2011	290
Central role of G protein Gαi2 and Gαi2 <sup>+</sup> vomeronasal neurons in balancing territorial and infant-directed aggression of male mice Anne‐Charlotte Trouillet, Matthieu Keller, Jan Weiss, Proceedings of the National Academy of Sciences	2019	75
A central mechanism of analgesia in mice and humans lacking the sodium channel NaV1.7 Donald Iain MacDonald, Shafaq Sikandar, Jan Weiss, Neuron	2021	73
Ca<sup>2+</sup>–Calmodulin Feedback Mediates Sensory Adaptation and Inhibits Pheromone-Sensitive Ion Channels in the Vomeronasal Organ Jennifer Spehr, Silke Hagendorf, Jan Weiss, Journal of Neuroscience	2009	71
Glycinergic input of small-field amacrine cells in the retinas of wildtype and glycine receptor deficient mice Jan Weiss, Gregory A. O’Sullivan, Larissa Heinze, Molecular and Cellular Neuroscience Ganglion CellPhotoreceptor CellSignal TransductionRetinaOphthalmology	2007	45
Glycinergic input of widefield, displaced amacrine cells of the mouse retina Sriparna Majumdar, Jan Weiss, Heinz Wässle The Journal of Physiology ImmunologyGroup Ii CellsOptogeneticsCellular PhysiologyAmacrine Cells	2009	35
Type 3 inositol 1,4,5-trisphosphate receptor is dispensable for sensory activation of the mammalian vomeronasal organ Pablo Chamero, Jan Weiss, Marı́a Teresa Alonso, Scientific Reports	2017	35
Trpm5 expression in the olfactory epithelium Martina Pyrski, Eugenia Eckstein, Andreas Schmid, Molecular and Cellular Neuroscience Signal TransductionMolecular PhysiologyCell SignalingIntercellular CommunicationTrpm5 Expression	2017	21
Altered synaptic transmission at olfactory and vomeronasal nerve terminals in mice lacking N‐type calcium channel Cav2.2 Jan Weiss, Martina Pyrski, Petra Weißgerber, European Journal of Neuroscience	2014	13

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