ArticleJournal of proteome research2011
Identification of kalirin-7 as a potential post-synaptic density signaling hub.
Article in Journal of proteome research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Amyloid beta pathology induces astrocytic pTDP-43 mislocalization and disrupts TDP-43-regulated cryptic exon transcripts.Frontiers in aging neuroscience · 2026Article
- Review
- Trio family proteins as regulators of cell migration and morphogenesis in development and disease - mechanisms and cellular contexts.Journal of cell science · 2021Review
- Kalirin and Trio: RhoGEFs in Synaptic Transmission, Plasticity, and Complex Brain Disorders.Trends in neurosciences · 2020Review
- Granulocyte-Colony-Stimulating Factor Alters the Proteomic Landscape of the Ventral Tegmental Area.Proteomes · 2018Article
- Neurodevelopmental disease-associated de novo mutations and rare sequence variants affect TRIO GDP/GTP exchange factor activity.Human molecular genetics · 2017Article
- Brain Region and Isoform-Specific Phosphorylation Alters Kalirin SH2 Domain Interaction Sites and Calpain Sensitivity.ACS chemical neuroscience · 2017Article
- Kalirin and Trio proteins serve critical roles in excitatory synaptic transmission and LTP.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Kalirin-9 and Kalirin-12 Play Essential Roles in Dendritic Outgrowth and Branching.Cerebral cortex (New York, N.Y. : 1991) · 2015Article
- A role for Kalirin-7 in nociceptive sensitization via activity-dependent modulation of spinal synapses.Nature communications · 2015Article
- Regulating Rac in the nervous system: molecular function and disease implication of Rac GEFs and GAPs.BioMed research international · 2015Review
- Nonenzymatic domains of Kalirin7 contribute to spine morphogenesis through interactions with phosphoinositides and Abl.Molecular biology of the cell · 2014Article
- Kalirin-7 mediates cocaine-induced AMPA receptor and spine plasticity, enabling incentive sensitization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Neuronal Rho GEFs in synaptic physiology and behavior.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2013Review
- Spinal serum-inducible and glucocorticoid-inducible kinase 1 mediates neuropathic pain via kalirin and downstream PSD-95-dependent NR2B phosphorylation in rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Kalrn plays key roles within and outside of the nervous system.BMC neuroscience · 2012Article
- The extracellular signal-regulated kinase 3 (mitogen-activated protein kinase 6 [MAPK6])-MAPK-activated protein kinase 5 signaling complex regulates septin function and dendrite morphology.Molecular and cellular biology · 2012Article
- Kalirin, a key player in synapse formation, is implicated in human diseases.Neural plasticity · 2012Review
- Kalirin binds the NR2B subunit of the NMDA receptor, altering its synaptic localization and function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Kalirin-7 (Kal7), a multifunctional Rho GDP/GTP exchange factor (GEF) for Rac1 and RhoG, is embedded in the postsynaptic density at excitatory synapses, where it participates in the formation and maintenance of dendritic spines. Kal7 has been implicated in long-term potentiation, fear memories, and addiction-like behaviors. Using liquid chromatography and tandem mass spectroscopy, we identified sites phosphorylated by six PSD-localized kinases implicated in synaptic plasticity and behavior, sites phosphorylated when myc-Kal7 was expressed in non-neuronal cells and sites phosphorylated in mouse brain Kal7. A site in the Sec14p domain phosphorylated by calcium/calmodulin dependent protein kinase II, protein kinase A and protein kinase C, was phosphorylated in mouse brain but not in non-neuronal cells. Phosphorylation in the spectrin-like repeat region was more extensive in mouse brain than in non-neuronal cells, with a total of 20 sites identified. Sites in the pleckstrin homology domain and in the linker region connecting the GEF domain to the PDZ binding motif were heavily phosphorylated in both non-neuronal cells and in mouse brain and affected GEF activity. We postulate that the kinase convergence and divergence observed in Kal7 identify it as a key player in integration of the multiple inputs that regulate synaptic structure and function.
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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.