ArticleJournal of cell science2008
Regulation of Kalirin by Cdk5.
Article in Journal of cell science, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The trial behind it
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- 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
- Role of Cdk5 in Kalirin7-Mediated Formation of Dendritic Spines.Neurochemical research · 2019Article
- Cdk5 Contributes to Huntington's Disease Learning and Memory Deficits via Modulation of Brain Region-Specific Substrates.Molecular neurobiology · 2018Article
- Tale of the Good and the Bad Cdk5: Remodeling of the Actin Cytoskeleton in the Brain.Molecular neurobiology · 2018Review
- The transcription factor XBP1s restores hippocampal synaptic plasticity and memory by control of the Kalirin-7 pathway in Alzheimer model.Molecular psychiatry · 2017Article
- Brain Region and Isoform-Specific Phosphorylation Alters Kalirin SH2 Domain Interaction Sites and Calpain Sensitivity.ACS chemical neuroscience · 2017Article
- Synaptic roles of cyclin-dependent kinase 5 & its implications in epilepsy.The Indian journal of medical research · 2017Review
- Stimuli associated with the presence or absence of amphetamine regulate cytoskeletal signaling and behavior.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2016Article
- Inhibiting cyclin-dependent kinase 5 in the nucleus accumbens enhances the expression of amphetamine-induced locomotor conditioning.Behavioural brain research · 2014Article
- Locomotor conditioning by amphetamine requires cyclin-dependent kinase 5 signaling in the nucleus accumbens.Neuropharmacology · 2014Article
- Analysis of Cdk5-related phosphoproteomics in growth cones.Journal of molecular neuroscience : MN · 2014Article
- Structural organization of the nine spectrin repeats of Kalirin.Biochemistry · 2012Article
- At the Fulcrum in Health and Disease: Cdk5 and the Balancing Acts of Neuronal Structure and Physiology.Brain disorders & therapy · 2012Article
- Deconstructing signal transduction pathways that regulate the actin cytoskeleton in dendritic spines.Cytoskeleton (Hoboken, N.J.) · 2012Review
- Kalirin, a key player in synapse formation, is implicated in human diseases.Neural plasticity · 2012Review
- Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity.BMC neuroscience · 2011Article
- 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
- Identification of kalirin-7 as a potential post-synaptic density signaling hub.Journal of proteome research · 2011Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Kalirin, one of the few Rho guanine nucleotide exchange factors (GEFs) that contains spectrin-like repeats, plays a critical role in axon extension and maintenance of dendritic spines. PC12 cells were used to determine whether Cdk5, a critical participant in both processes, regulates the action of Kalirin. Expression of Kalirin-7 in nondifferentiated PC12 cells caused GEF-activity-dependent extension of broad cytoplasmic protrusions; coexpression of dominant-negative Cdk5 largely eliminated this response. The spectrin-like repeat region of Kalirin plays an essential role in this response, which is not mimicked by the GEF domain alone. Thr1590, which follows the first GEF domain of Kalirin, is the only Cdk5 phosphorylation site in Kalirin-7. Although mutant Kalirin-7 with Ala1590 retains GEF activity, it is unable to cause extension of protrusions. Kalirin-7 with an Asp1590 mutation has slightly increased GEF activity and dominant-negative Cdk5 fails to block its ability to cause extension of protrusions. Phosphorylation of Thr1590 causes a slight increase in GEF activity and Kalirin-7 solubility. Dendritic spines formed by cortical neurons in response to the expression of Kalirin-7 with Ala1590 differ in shape from those formed in response to wild-type Kalirin-7 or Kalirin-7 containing Asp1590. The presence of Thr1590 in each major Kalirin isoform would allow Cdk5 to regulate Kalirin function throughout development.
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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.