ArticleDevelopment (Cambridge, England)2015
Phenotypic analysis of mice completely lacking netrin 1.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 71 citations in OpenAlex.
- Coro1A and TRIM67 collaborate in netrin-dependent neuronal morphogenesis.The Journal of cell biology · 2025Article
- Expression of Netrin-1 in the developing mouse heart.Gene expression patterns : GEP · 2025Article
- DCC in the cerebral cortex is required for cognitive functions in mouse.Brain pathology (Zurich, Switzerland) · 2025Article
- A stable NTN1 fluorescent reporter chicken reveals cell specific molecular signatures during optic fissure closure.Scientific reports · 2025Article
- A Novel De Novo Missense Variant in Netrin-1 (NTN1) Associated With Chorioretinal Coloboma, Sensorineural Hearing Loss and Polydactyly.Clinical genetics · 2025Article
- Siah2 antagonism of Pard3/JamC modulates Ntn1-Dcc signaling to regulate cerebellar granule neuron germinal zone exit.Nature communications · 2025Article
- Netrin-1: Dual Roles in Neuroinflammation and Neurodegenerative Disease Dynamics.International journal of inflammation · 2025Review
- Netrin1 patterns the dorsal spinal cord through modulation of Bmp signaling.Cell reports · 2024Article
- Molecular diversity and migration of GABAergic neurons in the developing ventral midbrain.iScience · 2024Article
- Article
- Multiple Guidance Mechanisms Control Axon Growth to Generate Precise T-shaped Bifurcation during Dorsal Funiculus Development in the Spinal Cord.bioRxiv : the preprint server for biology · 2024Article
- Netrin-1 stimulated axon growth requires the polyglutamylase TTLL1.Frontiers in neuroscience · 2024Article
- Insights from the neural guidance factor Netrin-1 into neurodegeneration and other diseases.Frontiers in molecular neuroscience · 2024Review
- Stromal netrin 1 coordinates renal arteriogenesis and mural cell differentiation.Development (Cambridge, England) · 2023Article
- Article
- Glycans and Carbohydrate-Binding/Transforming Proteins in Axon Physiology.Advances in neurobiology · 2023Article
- Parallels between the Developing Vascular and Neural Systems: Signaling Pathways and Future Perspectives for Regenerative Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Review
- Glycosylation in Axonal Guidance.International journal of molecular sciences · 2021Review
- Article
- The TRIM9/TRIM67 neuronal interactome reveals novel activators of morphogenesis.Molecular biology of the cell · 2021Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Netrin 1 (Ntn1) is a multifunctional guidance cue expressed in the ventricular zone and floor plate of the embryonic neural tube. Although Ntn1 is best known for acting as an axon guidance cue through Dcc and neogenin receptors, it is also thought to regulate neuronal survival and blood vessel development through Unc5 family receptors. However, the Ntn1 gene trap mutant mouse does not display all the phenotypes predicted from in vitro assays or analyses of mice lacking predicted receptors. Since the gene trap strain still produces wild-type Ntn1 protein, it is unclear whether the absence of phenotypes reflects the activity of alternative cues or of residual Ntn1. To resolve the full contribution of Ntn1 to development, we generated a null allele of Ntn1 and re-examined tissues exhibiting phenotypic discrepancies between receptor mutants and Ntn1 hypomorphs. We found that in Ntn1 null animals commissural axons rarely cross the midline, resulting in a strongly enhanced phenotype relative to Ntn1 hypomorphs, which retain many axons with normal trajectories. Thus, low levels of Ntn1 can account for persistent attraction to the midline in hypomorphs. By contrast, Ntn1 null mice do not show all of the phenotypes reported for Unc5 receptor mutants, indicating that Ntn1 is not necessarily the dominant ligand for Unc5 family members in vivo and ruling out primary roles in survival or angiogenesis.
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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.