ArticleScientific reports2017
Role of Cytosolic Carboxypeptidase 5 in Neuronal Survival and Spermatogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 44 citations in OpenAlex.
- Post-Translational Modifications of Tubulin in Oocyte Maturation and Female Infertility.Cytoskeleton (Hoboken, N.J.) · 2026Review
- Tubulin hyperglutamylation induces retinal degeneration by disrupting ciliary architecture and protein trafficking.Zoological research · 2026Article
- Tubulin monoglutamylation is sufficient to rescue the ciliary motility defects in aFrontiers in cell and developmental biology · 2026Article
- Specific Glutamylation Patterns of the Cytoskeleton Confer Neuroresistance to Lobe X of the Cerebellum in a Model of Childhood-Onset Neurodegeneration with Cerebellar Atrophy.International journal of molecular sciences · 2025Article
- Rescue of ciliogenesis and hyperglutamylation mutant phenotype in AGBL5BMC molecular and cell biology · 2025Article
- TTBK2 affects sperm quality by regulating the expression of centrosomal proteins and flagellar transporters during spermiogenesis in mice.Molecular human reproduction · 2025Article
- Non-canonical CDK6 activity promotes cilia disassembly by suppressing axoneme polyglutamylation.The Journal of cell biology · 2025Article
- Article
- Structure and Composition of Spermatozoa Fibrous Sheath in Diverse Groups of Metazoa.International journal of molecular sciences · 2024Review
- Article
- Excessive tubulin glutamylation leads to progressive cone-rod dystrophy and loss of outer segment integrity.Human molecular genetics · 2024Article
- Uncovering a multitude of stage-specific splice variants and putative protein isoforms generated along mouse spermatogenesis.BMC genomics · 2024Article
- The distinct initiation sites and processing activities of TTLL4 and TTLL7 in glutamylation of brain tubulin.The Journal of biological chemistry · 2023Article
- Glutamylation is a negative regulator of microtubule growth.Molecular biology of the cell · 2023Article
- CCP5 and CCP6 retain CP110 and negatively regulate ciliogenesis.BMC biology · 2023Article
- CCP1, a Regulator of Tubulin Post-Translational Modifications, Potentially Plays an Essential Role in Cerebellar Development.International journal of molecular sciences · 2023Article
- ThemicroPublication biology · 2023Article
- TTLL1 and TTLL4 polyglutamylases are required for the neurodegenerative phenotypes in pcd mice.PLoS genetics · 2022Article
- Proteolysis in Reproduction: Lessons From Gene-Modified Organism Studies.Frontiers in endocrinology · 2022Review
- Post-translational polymodification of β1-tubulin regulates motor protein localisation in platelet production and function.Haematologica · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Proteins may undergo a type of posttranslational modification - polyglutamylation, where a glutamate residue is enzymatically linked to the γ-carboxyl group of a glutamate in the primary sequence of proteins and additional glutamates are then sequentially added via α-carboxyl-linkages to the growing glutamate side chain. Nna1 (a.k.a. CCP1) defines the 6-member cytosolic carboxypeptidase (CCP) family that metabolizes polyglutamate side chain and its loss results in neurodegeneration and male infertility. Whereas most CCPs catalyze hydrolysis of α-carboxyl-linked glutamates, CCP5 uniquely metabolizes the γ-carboxyl linked, branch point glutamate. Using purified recombinant mouse CCP5, we confirmed that it metabolized γ-carboxyl-linked glutamate of synthetic substrates and tubulin. Despite this unique feature and its indispensible functions in lower species, we found that unlike Nna1, CCP5 is not essential for neuronal survival in mouse. CCP5 deficiency does cause male infertility. However, the mechanism by which this occurs is distinct from that of Nna1 loss. Instead, it is phenotypically reminiscent of the infertility of olt mice. Our findings suggest that Nna1 and CCP5 do not work coordinately in the same pathway in either the nervous system or spermatogenesis. This is the first study addressing the function of CCP5 in mammals.
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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.