ArticleMolecular biology of the cell2014
Nonenzymatic domains of Kalirin7 contribute to spine morphogenesis through interactions with phosphoinositides and Abl.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Manipulation of α4βδ GABABrain research · 2024Article
- Structure of the Sec14 domain of Kalirin reveals a distinct class of lipid-binding module in RhoGEFs.Nature communications · 2023Article
- Functional interdependence of the actin regulators CAP1 and cofilin1 in control of dendritic spine morphology.Cellular and molecular life sciences : CMLS · 2022Article
- A developmental delay linked missense mutation in Kalirin-7 disrupts protein function and neuronal morphology.Frontiers in molecular neuroscience · 2022Article
- Review
- Preventing adolescent synaptic pruning in mouse prelimbic cortex via local knockdown of α4βδ GABAScientific reports · 2021Article
- Trio family proteins as regulators of cell migration and morphogenesis in development and disease - mechanisms and cellular contexts.Journal of cell science · 2021Review
- Review
- DBS is activated by EPHB2/SRC signaling-mediated tyrosine phosphorylation in HEK293 cells.Molecular and cellular biochemistry · 2019Article
- α4βδ GABANeuroscience · 2019Article
- 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
- Using Kalirin conditional knockout mice to distinguish its role in dopamine receptor mediated behaviors.BMC neuroscience · 2017Article
- α4βδ GABANeuroscience · 2017Article
- Alternate promoter usage generates two subpopulations of the neuronal RhoGEF Kalirin-7.Journal of neurochemistry · 2017Article
- Kalirin is required for BDNF-TrkB stimulated neurite outgrowth and branching.Neuropharmacology · 2016Article
- Exome sequencing discloses KALRN homozygous variant as likely cause of intellectual disability and short stature in a consanguineous pedigree.Human genomics · 2016Article
- Article
- O-Glycosylation of a Secretory Granule Membrane Enzyme Is Essential for Its Endocytic Trafficking.The Journal of biological chemistry · 2016Article
- An N-terminal Amphipathic Helix Binds Phosphoinositides and Enhances Kalirin Sec14 Domain-mediated Membrane Interactions.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Like several Rho GDP/GTP exchange factors (GEFs), Kalirin7 (Kal7) contains an N-terminal Sec14 domain and multiple spectrin repeats. A natural splice variant of Kalrn lacking the Sec14 domain and four spectrin repeats is unable to increase spine formation; our goal was to understand the function of the Sec14 and spectrin repeat domains. Kal7 lacking its Sec14 domain still increased spine formation, but the spines were short. Strikingly, Kal7 truncation mutants containing only the Sec14 domain and several spectrin repeats increased spine formation. The Sec14 domain bound phosphoinositides, a minor but crucial component of cellular membranes, and binding was increased by a phosphomimetic mutation. Expression of KalSec14-GFP in nonneuronal cells impaired receptor-mediated endocytosis, linking Kal7 to membrane trafficking. Consistent with genetic studies placing Abl, a non-receptor tyrosine kinase, and the Drosophila orthologue of Kalrn into the same signaling pathway, Abl1 phosphorylated two sites in the fourth spectrin repeat of Kalirin, increasing its sensitivity to calpain-mediated degradation. Treating cortical neurons of the wild-type mouse, but not the Kal7(KO) mouse, with an Abl inhibitor caused an increase in linear spine density. Phosphorylation of multiple sites in the N-terminal Sec14/spectrin region of Kal7 may allow coordination of the many signaling pathways contributing to spine morphogenesis.
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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.