ArticleThe Journal of cell biology2007
Very-KIND, a KIND domain containing RasGEF, controls dendrite growth by linking Ras small GTPases and MAP2.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- MTCL2 Is Essential for the Bipolar-to-Multipolar Transition in the Dendrite Extension of Cerebellar Granule Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Early Life Injury Alters Spinal Astrocyte Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Sexually dimorphic transcriptional programs of early-phase response in regenerating peripheral nerves.Frontiers in molecular neuroscience · 2022Article
- 40 Years of RAS-A Historic Overview.Genes · 2021Review
- Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Effect of KNDC1 overexpression on the senescence of human umbilical vein endothelial cells.Molecular medicine reports · 2018Article
- Article
- Recent advances in avian egg science: A review.Poultry science · 2017Review
- The brain-specific RasGEF very-KIND is required for normal dendritic growth in cerebellar granule cells and proper motor coordination.PloS one · 2017Article
- Genetic architecture dissection by genome-wide association analysis reveals avian eggshell ultrastructure traits.Scientific reports · 2016Article
- Membrane targeting of the Spir·formin actin nucleator complex requires a sequential handshake of polar interactions.The Journal of biological chemistry · 2015Article
- KNDC1 knockdown protects human umbilical vein endothelial cells from senescence.Molecular medicine reports · 2014Article
- Spliceosome integrity is defective in the motor neuron diseases ALS and SMA.EMBO molecular medicine · 2013Article
- Design principles underpinning the regulatory diversity of protein kinases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2012Review
- An autism-associated variant of Epac2 reveals a role for Ras/Epac2 signaling in controlling basal dendrite maintenance in mice.PLoS biology · 2012Article
- Molecular basis of actin nucleation factor cooperativity: crystal structure of the Spir-1 kinase non-catalytic C-lobe domain (KIND)•formin-2 formin SPIR interaction motif (FSI) complex.The Journal of biological chemistry · 2011Article
- Structure and function of the interacting domains of Spire and Fmn-family formins.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Systematizing and cloning of genes involved in the cerebellar cortex circuit development.Neurochemical research · 2011Review
- Evolutionary expansion of the Ras switch regulatory module in eukaryotes.Nucleic acids research · 2011Article
- Trio is a key guanine nucleotide exchange factor coordinating regulation of the migration and morphogenesis of granule cells in the developing cerebellum.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of cytoskeletal components in the dendritic shaft core is critical for dendrite elongation and branching. Here, we report that a brain-specific Ras guanine nucleotide exchange factor (RasGEF) carrying two kinase non-catalytic C-lobe domains (KINDs), very-KIND (v-KIND), regulates microtubule-associated protein 2 (MAP2). v-KIND is expressed in developing mouse brain, predominantly in the cerebellar granule cells. v-KIND not only activates Ras small GTPases via the C-terminal RasGEF domain, but also specifically binds to MAP2 via the second KIND domain (KIND2), leading to threonine phosphorylation of MAP2. v-KIND overexpression suppresses dendritic extension and branching of hippocampal neurons and cerebellar granule cells, whereas knockdown of endogenous v-KIND expression promotes dendrite growth. These findings suggest that v-KIND mediates a signaling pathway that links Ras and MAP2 to control dendrite growth.
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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.