Automated Author ProfileSchafer, William R.
MRC Laboratory of Molecular Biology
Schafer, William R.
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets for this author
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the author's datasets
Total Mentions
Total mentions of the author's datasets
S-Index Interpretation
The S-Index (Sharing Index) is a comprehensive metric that represents the cumulative impact of all your datasets. It is calculated as the sum of Dataset Index scores across all your claimed datasets.
What it means:
- A higher S-index indicates greater overall impact of your datasets relative to typical datasets in their fields of research
- The S-Index grows as you add more datasets or as existing datasets gain more citations and mentions
- It provides a single number to track your research data impact over time
Current S-Index: 1.8 (sum of 2 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
AbstractNeurons throughout the mammalian brain possess non-motile cilia, organelles with varied functions in sensory physiology and cellular signaling, yet their roles in these neurons are poorly understood. To shed light into their functions, we studied EFHC1, an evolutionarily conserved protein required for motile cilia function and linked to a common form of inherited epilepsy in humans, juvenile myoclonic epilepsy (JME). We demonstrate that C. elegans EFHC1 functions within specialized non-motile mechanosensory cilia, where it regulates neuronal activation and dopamine signaling. EFHC1 also localizes at the synapse, where it further modulates dopamine signaling in cooperation with the orthologue of an R-type voltage-gated calcium channel. Our findings unveil a previously undescribed dual-regulation of neuronal excitability at sites of neuronal sensory input (cilium) and neuronal output (synapse). Such a distributed regulatory mechanism may be essential for establishing neuronal activation thresholds under physiological conditions, and when impaired, may represent a novel pathomechanism for epilepsy.
Authors
- Loucks, Catrina M. ;
- Park, Kwangjin ;
- Walker, Denise S. ;
- McEwan, Andrea H. ;
- Timbers, Tiffany A. ;
- Ardiel, Evan L. ;
- Grundy, Laura J. ;
- Li, Chunmei ;
- Johnson, Jacque-Lynne ;
- Kennedy, Julie ;
- Blacque, Oliver E. ;
- Schafer, William R. ;
- Rankin, Catharine H. ;
- Leroux, Michel R.
Neurons throughout the mammalian brain possess non-motile cilia, organelles with varied functions in sensory physiology and cellular signaling, yet their roles in these neurons are poorly understood. To shed light into their functions, we studied EFHC1, an evolutionarily conserved protein required for motile cilia function and linked to a common form of inherited epilepsy in humans, juvenile myoclonic epilepsy (JME). We demonstrate that C. elegans EFHC1 functions within specialized non-motile mechanosensory cilia, where it regulates neuronal activation and dopamine signaling. EFHC1 also localizes at the synapse, where it further modulates dopamine signaling in cooperation with the orthologue of an R-type voltage-gated calcium channel. Our findings unveil a previously undescribed dual-regulation of neuronal excitability at sites of neuronal sensory input (cilium) and neuronal output (synapse). Such a distributed regulatory mechanism may be essential for establishing neuronal activation thresholds under physiological conditions, and when impaired, may represent a novel pathomechanism for epilepsy.
Authors
- Loucks, Catrina M. ;
- Park, Kwangjin ;
- Walker, Denise S. ;
- McEwan, Andrea H. ;
- Timbers, Tiffany A. ;
- Ardiel, Evan L. ;
- Grundy, Laura J. ;
- Li, Chunmei ;
- Johnson, Jacque-Lynne ;
- Kennedy, Julie ;
- Blacque, Oliver E. ;
- Schafer, William R. ;
- Rankin, Catharine H. ;
- Leroux, Michel R.