ArticleNeuro-Signals2011
The type I inositol 1,4,5-trisphosphate receptor interacts with protein 4.1N to mediate neurite formation through intracellular Ca waves.
Article in Neuro-Signals, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- 4.1N-Mediated Interactions and Functions in Nerve System and Cancer.Frontiers in molecular biosciences · 2021Review
- Selective effects of protein 4.1N deficiency on neuroendocrine and reproductive systems.Scientific reports · 2020Article
- Dysregulation of Neuronal Calcium Signaling via Store-Operated Channels in Huntington's Disease.Frontiers in cell and developmental biology · 2020Review
- Inositol 1,4,5-trisphosphate receptor in the liver: Expression and function.World journal of gastroenterology · 2019Review
- Differential regulation of ion channels function by proteolysis.Biochimica et biophysica acta. Molecular cell research · 2018Review
- Inositol Hexakisphosphate Kinase-2 in Cerebellar Granule Cells Regulates Purkinje Cells and Motor Coordination via Protein 4.1N.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Proteolytic fragmentation of inositol 1,4,5-trisphosphate receptors: a novel mechanism regulating channel activity?The Journal of physiology · 2016Review
- Nuclear Factor, Erythroid 2-Like 2 Regulates Expression of Type 3 Inositol 1,4,5-Trisphosphate Receptor and Calcium Signaling in Cholangiocytes.Gastroenterology · 2015Article
- Comprehensive characterization of protein 4.1 expression in epithelium of large intestine.Histochemistry and cell biology · 2014Article
- Exome sequencing followed by large-scale genotyping suggests a limited role for moderately rare risk factors of strong effect in schizophrenia.American journal of human genetics · 2012Article
- Long-term dantrolene treatment reduced intraneuronal amyloid in aged Alzheimer triple transgenic mice.Alzheimer disease and associated disordersArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+) waves are an important mechanism for encoding Ca(2+) signaling information, but the molecular basis for wave formation and how this regulates neuronal function is not entirely understood. Using nerve growth factor-differentiated PC12 cells as a model system, we investigated the interaction between the type I inositol 1,4,5-trisphosphate receptor (IP3R1) and the cytoskeletal linker, protein 4.1N, to examine the relationship between Ca(2+) wave formation and neurite development. This was examined using RNAi and overexpressed dominant negative binding regions of each protein. Confocal microscopy was used to monitor neurite formation and Ca(2+) waves. Knockdown of IP3R1 or 4.1N attenuated neurite formation, as did binding regions of IP3R1 and 4.1N, which colocalized with endogenous 4.1N and IP3R1, respectively. Upon stimulation with the IP3-producing agonist carbachol, both RNAi and dominant negative molecules shifted signaling events from waves to homogeneous patterns of Ca(2+) release. These findings provide evidence that IP3R1 localization, via protein 4.1N, is necessary for Ca(2+) wave formation, which in turn mediates neurite formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.