ArticleMolecular and cellular biology2002
The septin CDCrel-1 is dispensable for normal development and neurotransmitter release.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of septin 7 in physiology and pathological disease: A systematic review of current status.Journal of cellular and molecular medicine · 2018Pooled it
- Septin5 deficiency impairs both recent and remote contextual fear memory.Molecular brain · 2025Article
- Septin complexes: Ahead of the curve.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Septin5 deletion enhances β-cell exocytosis by releasing microtubule-tethered insulin granules onto plasma membrane.Nature communications · 2025Article
- The Rho1 GTPase controls anillo-septin assembly to facilitate contractile ring closure during cytokinesis.iScience · 2023Article
- Downregulation of SEPTIN5 inhibits prostate cancer progression by increasing CD8International journal of biological sciences · 2022Article
- Septins, a cytoskeletal protein family, with emerging role in striated muscle.Journal of muscle research and cell motility · 2021Review
- Biochemical and morphological characterization of SEPT1 in mouse brain.Medical molecular morphology · 2020Article
- Article
- The septin cytoskeleton regulates natural killer cell lytic granule release.The Journal of cell biology · 2020Article
- Production and analysis of a mammalian septin hetero-octamer complex.Cytoskeleton (Hoboken, N.J.) · 2020Article
- Synergistic Neuroprotective Effect of Endogenously-Produced Hydroxytyrosol and Synaptic Vesicle Proteins on Pheochromocytoma Cell Line Against Salsolinol.Molecules (Basel, Switzerland) · 2020Article
- Septin2 mediates podosome maturation and endothelial cell invasion associated with angiogenesis.The Journal of cell biology · 2020Article
- In the line-up: deleted genes associated with DiGeorge/22q11.2 deletion syndrome: are they all suspects?Journal of neurodevelopmental disorders · 2019Review
- Repression of Septin9 and Septin2 suppresses tumor growth of human glioblastoma cells.Cell death & disease · 2018Article
- Interaction of Recombinant Gallus gallus SEPT5 and Brain Proteins of H5N1-Avian Influenza Virus-Infected Chickens.Proteomes · 2017Article
- Functional Redundancy of Septin Homologs in Dendritic Branching.Frontiers in cell and developmental biology · 2017Article
- A CDC42EP4/septin-based perisynaptic glial scaffold facilitates glutamate clearance.Nature communications · 2015Article
- A Synaptic Function Approach to Investigating Complex Psychiatric Diseases.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014Review
- Chronic overload of SEPT4, a parkin substrate that aggregates in Parkinson's disease, causes behavioral alterations but not neurodegeneration in mice.Molecular brain · 2013Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Septins are GTPases required for the completion of cytokinesis in a variety of organisms, yet their role in this process is not known. Septins may have additional functions since the mammalian septin CDCrel-1 is predominantly expressed in the nervous system, a largely postmitotic tissue. While relatively little is known about the function of this protein, we have previously shown that it is involved in regulated secretion. In addition, the gene encoding this protein maps to a locus often deleted in velo-cardiofacial and DiGeorge syndromes, and CDCrel-1 has recently been shown to be a direct target of the E3 ubiquitin ligase activity of Parkin, a causative agent in autosomal recessive forms of Parkinson's disease. Here we show that CDCrel-1 expression rises at the time of synaptic maturation and that CDCrel-1 is present in a complex that includes the septins Nedd5 and CDC10. To investigate its function in the nervous system, we generated homozygotic CDCrel-1 null mice and showed that these mice appear normal with respect to synaptic properties and hippocampal neuron growth in vitro. Moreover, we found that while the expression of a number of synaptic proteins is not affected in the CDCrel-1 mutant mice, the expression of other septins is altered. Together, these data suggest that CDCrel-1 is not essential for neuronal development or function, and that changes in expression of other septins may account for its functional redundancy.
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