Affinage

UNC5C

Netrin receptor UNC5C · UniProt O95185

Length
931 aa
Mass
103.1 kDa
Annotated
2026-06-10
42 papers in source corpus 21 papers cited in narrative 21 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

UNC5C is a transmembrane netrin-1 dependence receptor that transduces repulsive guidance cues in the developing nervous system and acts as a pro-apoptotic effector when deprived of its ligand (PMID:16723533, PMID:33863723). In axon guidance, UNC5C is required cell-autonomously for netrin-1-dependent repulsion of multiple axon and motor-neuron populations in vivo, defining a signaling pathway distinct from DCC, Neogenin1, and netrin1 (PMID:16723533, PMID:21307253, PMID:17543537). At the growth cone, netrin-1 stimulates a DSCAM-UNC5C complex that recruits FAK, Fyn, and PAK1 and increases UNC5C tyrosine phosphorylation through Src-family kinases to drive growth cone collapse (PMID:22685302), while UNC5C transduces repulsion by uncoupling from polymerized TUBB3 in microtubules, an event that locally remodels microtubule dynamics during turning (PMID:28483977). Surface levels and mobility of UNC5C at the growth cone are controlled by the brain-enriched E3 ubiquitin ligase TRIM9, which also restrains FAK activity in the absence of netrin-1 (PMID:39871643). In the absence of netrin-1, UNC5C induces caspase-3-dependent apoptosis, a function amplified by δ-secretase/AEP cleavage at N467 and N547 that generates pro-apoptotic intracellular fragments contributing to Alzheimer's-type and Parkinson's-type neurodegeneration (PMID:33863723, PMID:35023303). This death-promoting activity underlies UNC5C's role as a tumor suppressor, where loss of UNC5C reduces tumor-cell apoptosis and accelerates intestinal tumor progression, and where UNC5C is silenced by promoter methylation in human colorectal cancer (PMID:17967459). The Alzheimer-associated T835M variant heightens neuronal vulnerability: it increases susceptibility to Aβ, glutamate, and staurosporine in vitro (PMID:25419706) and drives hippocampal atrophy, oxidative-stress and JNK pathway activation, and neuronal apoptosis in knock-in mice, exacerbating amyloid pathology (PMID:40468412). UNC5C expression is held in check by transcriptional repressors including RHOX5 in Sertoli cells and Ctip2 in cortical neurons (PMID:18077458, PMID:24739528).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 2006 High

    Established that UNC5C is genetically required for netrin-1-mediated repulsive axon guidance in vivo and operates in a pathway separable from DCC, Neogenin1, and netrin1.

    Evidence Unc5c null mouse axonal tracing with epistatic comparison to DCC/Neogenin/netrin1 nulls and modifier-locus mapping

    PMID:16723533

    Open questions at the time
    • Did not resolve the molecular signaling output downstream of the receptor
    • Genetic background modifier on Chr17 not molecularly identified
  2. 2007 High

    Showed UNC5C is a tumor suppressor whose loss reduces apoptosis and accelerates tumor progression, linking its guidance receptor identity to programmed cell death.

    Evidence UNC5C/APC1638N double-mutant mouse with intestinal tumor apoptosis quantification and human CRC promoter methylation analysis

    PMID:17967459

    Open questions at the time
    • Molecular apoptotic effector pathway not defined here
    • Whether loss acts purely through reduced apoptosis vs other tumor-suppressive functions unresolved
  3. 2007 Medium

    Identified RHOX5 as a transcriptional repressor of Unc5c in Sertoli cells, connecting receptor dosage to germ cell apoptosis.

    Evidence 5'-UTR deletion analysis, transfection reporter assays, and Unc5c mutant testis apoptosis analysis

    PMID:18077458

    Open questions at the time
    • Sertoli-specific cofactor not identified
    • Direct apoptotic mechanism in germ cells not dissected
  4. 2011 High

    Demonstrated cell-autonomous UNC5C function in long-range dorsal axon guidance through transgenic rescue, extending its role beyond a single neuronal population.

    Evidence Unc5c null mouse axon tracing with Atoh1-promoter transgenic rescue

    PMID:21307253

    Open questions at the time
    • Ligand-receptor signaling steps not resolved
    • Cause of downstream neuronal degeneration unexplained
  5. 2011 Medium

    Linked a human UNC5C coding variant (A628K) to reduced apoptosis and familial colorectal cancer, providing genetic support for apoptosis-driven tumor suppression.

    Evidence HEK293T active caspase-3 assay of A628K mutant plus family segregation analysis

    PMID:21893118

    Open questions at the time
    • Single functional assay for the variant
    • Structural basis of reduced apoptotic activity unknown
  6. 2012 High

    Defined the growth-cone signaling complex: netrin-1 drives a DSCAM-UNC5C interaction and recruitment of FAK, Fyn, and PAK1 via Src-family-kinase-dependent phosphorylation to collapse growth cones.

    Evidence Reciprocal Co-IP, shRNA knockdown, dominant-negative mutants, SFK inhibition, and growth cone collapse assays in cortical and cerebellar granule neurons

    PMID:22685302

    Open questions at the time
    • Order of recruitment events not fully resolved
    • How phosphorylation links to cytoskeletal collapse not mechanistically traced
  7. 2014 Medium

    Identified the T835M variant as a hinge-region mutation that sensitizes neurons to multiple death stimuli, implicating UNC5C in Alzheimer's disease risk.

    Evidence Cell death assays in HEK293T and primary rodent neurons with WT and T835M overexpression and Aβ/glutamate/staurosporine challenge

    PMID:25419706

    Open questions at the time
    • No structural validation of the hinge alteration
    • In vivo relevance not yet demonstrated at this stage
  8. 2014 Medium

    Placed Unc5c under direct negative transcriptional control by Ctip2 in the context of corticofugal and callosal projections.

    Evidence Transcription factor binding analysis and mouse genetic epistasis with Ctip2/Satb2 mutants

    PMID:24739528

    Open questions at the time
    • Direct binding site not finely mapped
    • Quantitative contribution of Unc5c repression to projection phenotype unclear
  9. 2017 High

    Revealed the cytoskeletal mechanism of repulsion: UNC5C binds polymerized TUBB3 in microtubules and netrin-1 uncouples this interaction to remodel growth-cone microtubule dynamics.

    Evidence Co-IP, in vitro microtubule co-sedimentation, EB3-GFP live imaging, and in vivo knockdown axon analysis

    PMID:28483977

    Open questions at the time
    • How ligand binding triggers receptor-microtubule uncoupling not mechanistically defined
    • Link between TUBB3 release and DSCAM/FAK signaling not integrated
  10. 2021 High

    Showed δ-secretase/AEP cleaves UNC5C at N467 and N547 to amplify its pro-apoptotic activity, mechanistically connecting netrin-1 loss to Alzheimer's pathology.

    Evidence Site-directed mutagenesis, in vitro cleavage and caspase-3 assays, viral fragment delivery in APP/PS1 mice, and UNC5C deletion rescue

    PMID:33863723

    Open questions at the time
    • Structure of the active cleaved fragment not solved
    • Downstream apoptotic effectors of the fragment not enumerated
  11. 2022 Medium

    Extended AEP-mediated UNC5C cleavage to Parkinson's disease, where truncated fragments promote α-synuclein aggregation and dopaminergic loss.

    Evidence In vitro cleavage assays, viral expression of AEP-truncated fragments, and behavioral testing in α-SNCA transgenic and netrin-1 flox mice

    PMID:35023303

    Open questions at the time
    • Specific cleavage sites not explicitly defined in this context
    • Mechanism by which fragments promote α-synuclein aggregation unresolved
  12. 2024 Medium

    Provided in vivo evidence that a transient Netrin-1 gradient guides UNC5C-expressing dopamine axons to the prefrontal cortex with developmentally phase-locked timing.

    Evidence Rodent axon tracing, Netrin-1 gradient disruption with axon rerouting, and a seasonal daylength model

    PMID:39056276

    Open questions at the time
    • Receptor-level signaling during this guidance not dissected
    • Mechanism of sexually dimorphic regulation unknown
  13. 2025 High

    Demonstrated TRIM9 as an E3 ligase that controls UNC5C surface levels and mobility at the growth cone and restrains FAK activity basally, identifying a regulatory node for repulsive turning.

    Evidence Reciprocal Co-IP, co-localization, Trim9 knockout neurons, pH-mScarlet-UNC5C surface imaging, and microfluidic netrin-1 gradient turning assays

    PMID:38765979 PMID:39871643

    Open questions at the time
    • Whether UNC5C is a direct ubiquitination substrate of TRIM9 not established
    • Acute netrin-1-induced surface drop is TRIM9-independent, so that effector is unknown
  14. 2025 High

    Established in vivo causality for the T835M variant by showing a knock-in mouse develops hippocampal atrophy, oxidative/JNK stress signaling, and apoptosis that worsens amyloid pathology.

    Evidence T835M knock-in mouse with TUNEL, caspase 3/7, proteomics, MRI volumetry, and crosses to AppNL-G-F mice

    PMID:40468412

    Open questions at the time
    • Mechanistic link between T835M and oxidative-stress/JNK activation not resolved
    • Whether δ-secretase cleavage drives the in vivo phenotype not directly tested here
  15. 2026 Medium

    Provided the first biophysical characterization of a UNC5C domain by mapping a small-molecule binding site on the ZU5 domain.

    Evidence Phage display, fluorescence spectroscopy, ITC, and molecular dynamics of ZU5-Schisandrin A binding

    PMID:41724002

    Open questions at the time
    • Functional consequence of ZU5 binding on receptor signaling not demonstrated
    • Computational component prominent; structural change not validated experimentally

Open questions

Synthesis pass · forward-looking unresolved questions
  • How netrin-1 binding mechanically switches UNC5C between its repulsive cytoskeletal/kinase signaling mode and its ligand-deprivation-triggered apoptotic mode at the molecular and structural level remains unresolved.
  • No full-length structural model of the receptor in either state
  • Integration of TUBB3 uncoupling, DSCAM/FAK signaling, TRIM9 regulation, and AEP cleavage into one switch is incomplete

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 3 GO:0098772 molecular function regulator activity 2 GO:0008092 cytoskeletal protein binding 1
Localization
GO:0005886 plasma membrane 3 GO:0005856 cytoskeleton 1
Pathway
R-HSA-1266738 Developmental Biology 4 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-5357801 Programmed Cell Death 3
Partners
DSCAMFAKFYNITGA6PAK1TRIM9TUBB3

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2012 DSCAM physically interacts with UNC5C, and this interaction is stimulated by netrin-1 in primary cortical neurons and cerebellar granule cells. Knockdown of DSCAM or UNC5C, or dominant-negative mutants of either, suppresses netrin-1-induced growth cone collapse. Netrin-1 increases tyrosine phosphorylation of UNC5C and promotes complex formation of DSCAM with FAK, Fyn, and PAK1. Src family kinase inhibition reduces the DSCAM-UNC5C interaction and blocks growth cone collapse. Co-immunoprecipitation, shRNA knockdown, dominant-negative overexpression, tyrosine phosphorylation assays, growth cone collapse assay in primary neurons The Journal of biological chemistry High 22685302
2017 TUBB3 (polymerized β-tubulin) directly interacts with UNC5C and partially co-localizes with it in the peripheral growth cone. Netrin-1 reduces this interaction and the co-localization. UNC5C interacts with polymerized TUBB3 in microtubules as shown by in vitro co-sedimentation, and netrin-1 decreases this interaction. Knockdown of TUBB3 or UNC5C blocks netrin-1-promoted axon repulsion in vitro and causes axon projection defects in vivo. Netrin-1 differentially increases MT dynamics in the distal versus proximal growth cone during repulsion, and this effect is abolished by knockdown of UNC5C or TUBB3. Co-immunoprecipitation, in vitro co-sedimentation assay, shRNA knockdown, live-cell imaging (EB3-GFP), in vivo axon projection analysis The Journal of neuroscience High 28483977
2021 δ-secretase (AEP/legumain) cleaves UNC5C at N467 and N547 residues, enhancing its pro-apoptotic activity and caspase-3 activation. Netrin-1 deficiency activates δ-secretase, which truncates UNC5C. Blockade of δ-secretase cleavage of UNC5C diminishes the T835M mutant's pro-apoptotic activity. Viral expression of δ-secretase-truncated UNC5C fragments in APP/PS1 mice accelerates AD pathologies and impairs learning and memory. Deletion of UNC5C from netrin-1-depleted mice attenuates AD pathologies and rescues cognitive disorders. Site-directed mutagenesis (N467, N547), in vitro cleavage assay, caspase-3 activation assay, viral gene delivery in mouse models, behavioral testing Science advances High 33863723
2022 AEP (asparagine endopeptidase) cleaves UNC5C in a Parkinson's disease context, producing intracellular fragments that facilitate dopaminergic neuronal loss. AEP-truncated UNC5C fragments promote α-synuclein aggregation and dopaminergic loss in α-SNCA transgenic mice. Netrin-1 deprivation induces AEP and caspase-3 activation, triggering UNC5C proteolytic fragmentation. Blocking UNC5C cleavage by AEP attenuates netrin-1 deprivation-elicited neuronal death and motor disorders. In vitro cleavage assay, viral overexpression of AEP-truncated UNC5C fragments, mouse behavioral assays, netrin-1 flox/flox mouse model Advanced science Medium 35023303
2014 The T835M mutation in UNC5C increases neuronal cell death in HEK293T cells and rodent neurons, and increases susceptibility to Aβ, glutamate, and staurosporine-induced cell death. The mutation alters a conserved residue in the hinge region of UNC5C. In vitro cell death assay in HEK293T cells and primary rodent neurons, overexpression of wild-type and T835M UNC5C Nature medicine Medium 25419706
2025 T835M knock-in (Unc5cKI/KI) mice develop hippocampal volume reduction, increased ventricular volume, dendritic disorganization, neuronal apoptosis (TUNEL+ and caspase 3/7 activation) by 12 months. Proteomic analysis revealed upregulation of oxidative stress pathways, increased JNK phosphorylation, and elevated NADPH oxidase. Crossing with AppNL-G-F/NL-G-F mice exacerbated these changes and increased Aβ42 levels, demonstrating that T835M increases neuronal susceptibility to amyloid pathology. Knock-in mouse model, TUNEL assay, caspase 3/7 assay, quantitative proteomics, immunohistochemistry, MRI volumetry, genetic crosses Molecular neurodegeneration High 40468412
2007 Loss of UNC5C in mice with APC1638N mutations increases intestinal tumor progression and decreases tumor cell apoptosis, establishing UNC5C as a tumor suppressor in colorectal cancer. UNC5C expression is down-regulated in human colorectal cancers primarily through promoter methylation. Double-mutant mouse model (UNC5C/APC1638N), apoptosis measurement in intestinal tumors, promoter methylation analysis Gastroenterology High 17967459
2011 The UNC5C A628K variant significantly reduces apoptosis compared with wild-type UNC5C as measured by active caspase-3 assay in transfected HEK293T cells, and segregates with colorectal cancer in families, supporting a role for UNC5C-mediated apoptosis in tumor suppression. Transfection of HEK293T cells with A628K mutant, active caspase-3 assay, family segregation analysis Gastroenterology Medium 21893118
2006 Unc5c null mice on C57BL/6J background exhibit ventral/ipsilateral trochlear nerve misprojections and incomplete phrenic nerve innervation of the diaphragm, demonstrating that UNC5C is required for repulsive netrin-1 signaling in motor axon guidance in vivo. These phenotypes were not observed in mice lacking DCC, Neogenin1, or netrin1, placing UNC5C in a distinct signaling pathway. A major SJL-derived suppressor locus on Chromosome 17 modifies these phenotypes. Unc5c null mouse analysis, axonal tracing, genetic background experiments, genome-wide scan for modifier loci The Journal of neuroscience High 16723533
2011 Unc5c deletion in mice disrupts long-range dorsal guidance of inferior olivary and pontine axons after crossing the midline, affects dorsal guidance of medial deep cerebellar and external cuneate axons, and causes degeneration of neurons in the external cuneate nucleus and inferior olivary nucleus. Transgenic expression of Unc5c in deep neurons and pontine neurons by the Atoh1 promoter rescues the medial deep cerebellar and pontine axon guidance defects, demonstrating cell-autonomous action. Unc5c null mouse, axonal tracing, transgenic rescue with Atoh1 promoter The Journal of neuroscience High 21307253
2014 Unc5C expression is under direct negative transcriptional regulation by the transcription factor Ctip2, and Unc5C acts downstream of Ctip2 in controlling corticofugal axon projections. Netrin1-Unc5C interaction is involved in controlling interhemispheric projection in deep-layer callosal neurons. ChIP or transcription factor binding analysis, mouse genetic studies with Ctip2/Satb2 mutants, axon guidance assays Nature communications Medium 24739528
2007 RHOX5 homeodomain protein transcriptionally represses Unc5c expression in Sertoli cells in vivo, requiring a Sertoli-cell-specific cofactor. The repression is mediated through a RHOX5-responsive element in the Unc5c 5'-UTR at the transcriptional level. RHOX2, RHOX3, and human RHOXF2/PEPP2 also repress Unc5c expression, indicating conserved regulation. Unc5c mutant mice have decreased germ cell apoptosis in the testis. Transfection analysis in cell lines, deletion analysis of 5'-UTR, in vivo testis expression analysis, Unc5c mutant mouse apoptosis analysis The Journal of biological chemistry Medium 18077458
2007 UNC5C is required for the dorsal migration of spinal accessory motor neuron (SACMN) cell bodies away from the ventral midline. In Unc5C null mice, many SACMN cell bodies fail to migrate away from the ventral midline and cluster inappropriately in the ventrolateral spinal cord. UNC5A null mice show no such phenotype. Unc5C and Unc5A null mouse analysis, SACMN cell body position analysis in embryos Molecular and cellular neurosciences Medium 17543537
2025 TRIM9, a brain-enriched E3 ubiquitin ligase, physically interacts with and co-localizes with UNC5C at the growth cone. TRIM9 is required for netrin-1-dependent changes in surface levels of UNC5C in the growth cone. Deletion of Trim9 impairs repulsive axon turning in a netrin gradient (which is UNC5C-dependent), and TRIM9 negatively regulates FAK activity in the absence of netrin-1. Co-immunoprecipitation, co-localization imaging, Trim9 knockout mouse neurons, microfluidic netrin-1 gradient, pH-mScarlet-UNC5C surface level imaging, shRNA knockdown of UNC5C Journal of neurochemistry High 39871643
2024 TRIM9 interacts with UNC5C and regulates its mobility in the plasma membrane in the absence of netrin-1. Minutes after netrin-1 addition, UNC5C surface levels drop in a TRIM9-independent fashion. Repulsive turning in a netrin gradient is blocked by UNC5C knockdown. pH-mScarlet-UNC5C surface imaging, TRIM9 knockout, shRNA knockdown, microfluidic netrin-1 gradient bioRxivpreprint Medium 38765979
2019 UNC5C directly interacts with integrin α6 in breast cancer cells. UNC5C knockdown enhances phosphorylation of FAK and SRC and increases MMP3, MMP7, MMP9, MMP10 expression via PI3K/AKT, ERK and p38 MAPK pathways. UNC5C knockdown potentiates netrin-1/integrin α6/β4 signaling and inhibits integrin-linked kinase phosphorylation at Thr-173. Co-immunoprecipitation (UNC5C-integrin α6), shRNA knockdown, overexpression in breast cancer cells, Western blot for signaling pathway components International journal of oncology Medium 31789389
2019 Unc5c is necessary and sufficient to guide retinal ganglion cell axons to the opposite retina (retino-retinal projection). Netrin1, an Unc5c ligand, is expressed in the ventral diencephalon in a pattern consistent with impeding the growth of Unc5c-positive retinal axons into the brain. Unc5c null mouse analysis, axonal tracing, in situ hybridization for Netrin1, comparative species analysis Current biology Medium 30905607
2013 Unc5c is selectively expressed by dopamine neurons of the VTA from adolescence onwards. Unc5c haploinsufficiency leads to increased tyrosine hydroxylase expression in medial prefrontal cortex (but not nucleus accumbens) and diminished amphetamine-induced locomotion, a phenotype identical to dcc haploinsufficiency and observed only after adolescence. In situ hybridization, immunofluorescence, Western blot in unc5c heterozygous mice, behavioral testing (amphetamine-induced locomotion) The European journal of neuroscience Medium 23738838
2024 Dopamine axons reach the prefrontal cortex guided by a transient gradient of Netrin-1-expressing cells, and UNC5C is expressed on dopamine axons during adolescence. Disrupting the Netrin-1 gradient reroutes dopamine axons away from their target. The timings of dopamine axon growth and UNC5C expression are phase-locked, including in a seasonal model where mesocortical dopamine development is regulated by daylength in a sexually dimorphic manner. Rodent in vivo axon tracing, Netrin-1 gradient disruption experiments, immunofluorescence, seasonal model (Siberian hamsters) eLife Medium 39056276
2022 UNC5C is expressed by a fraction of undifferentiated spermatogonia, and loss of Unc5c leads to accumulation of transit-amplifying progenitors, increased quiescent undifferentiated progenitors, and decline in spermatocyte I, without altering cell death rates. Netrin-1 repulses both undifferentiated and differentiating spermatogonia in vitro, suggesting UNC5C mediates adhesion/migration control in spermatogonial differentiation. Unc5crcm mutant mouse analysis, immunofluorescence, in vitro repulsion assay with Netrin-1 Stem cell research Medium 35247845
2026 The ZU5 domain of UNC5C binds Schisandrin A with equimolar stoichiometry driven by enthalpy change, with van der Waals forces and hydrogen bonds as main forces. Leu61 and Leu96 of ZU5 are key binding residues. Binding induces loop fluctuations and a random coil-to-α-helix transformation in ZU5. Phage display peptide library screening, fluorescence spectroscopy, isothermal titration calorimetry, molecular dynamics simulation Bioorganic chemistry Medium 41724002

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2014 A rare mutation in UNC5C predisposes to late-onset Alzheimer's disease and increases neuronal cell death. Nature medicine 129 25419706
2007 Inactivation of the UNC5C Netrin-1 receptor is associated with tumor progression in colorectal malignancies. Gastroenterology 107 17967459
2007 Epigenetic and genetic alterations in Netrin-1 receptors UNC5C and DCC in human colon cancer. Gastroenterology 89 18054557
2012 Down syndrome cell adhesion molecule (DSCAM) associates with uncoordinated-5C (UNC5C) in netrin-1-mediated growth cone collapse. The Journal of biological chemistry 65 22685302
2014 Unc5C and DCC act downstream of Ctip2 and Satb2 and contribute to corpus callosum formation. Nature communications 59 24739528
2006 Motor axon guidance of the mammalian trochlear and phrenic nerves: dependence on the netrin receptor Unc5c and modifier loci. The Journal of neuroscience : the official journal of the Society for Neuroscience 52 16723533
2011 The UNC5C netrin receptor regulates dorsal guidance of mouse hindbrain axons. The Journal of neuroscience : the official journal of the Society for Neuroscience 50 21307253
2021 Netrin-1 receptor UNC5C cleavage by active δ-secretase enhances neurodegeneration, promoting Alzheimer's disease pathologies. Science advances 42 33863723
2017 Uncoupling of UNC5C with Polymerized TUBB3 in Microtubules Mediates Netrin-1 Repulsion. The Journal of neuroscience : the official journal of the Society for Neuroscience 39 28483977
2007 UNC5C is required for spinal accessory motor neuron development. Molecular and cellular neurosciences 34 17543537
2011 Variants in the netrin-1 receptor UNC5C prevent apoptosis and increase risk of familial colorectal cancer. Gastroenterology 31 21893118
2019 A Retino-retinal Projection Guided by Unc5c Emerged in Species with Retinal Waves. Current biology : CB 28 30905607
2009 Aberrant methylation of the netrin-1 receptor genes UNC5C and DCC detected in advanced colorectal cancer. World journal of surgery 28 19242752
2007 The RHOX5 homeodomain protein mediates transcriptional repression of the netrin-1 receptor gene Unc5c. The Journal of biological chemistry 28 18077458
1998 Cloning and mapping of the UNC5C gene to human chromosome 4q21-q23. Genomics 27 9782087
2022 UNC5C Receptor Proteolytic Cleavage by Active AEP Promotes Dopaminergic Neuronal Degeneration in Parkinson's Disease. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 25 35023303
2011 Genetic and epigenetic control of UNC5C expression in human renal cell carcinoma. European journal of cancer (Oxford, England : 1990) 24 21600761
2018 The role of UNC5C in Alzheimer's disease. Annals of translational medicine 23 29951500
2015 The Impact of UNC5C Genetic Variations on Neuroimaging in Alzheimer's Disease. Molecular neurobiology 23 26660111
2019 UNC5C‑knockdown enhances the growth and metastasis of breast cancer cells by potentiating the integrin α6/β4 signaling pathway. International journal of oncology 16 31789389
2009 Aberrant methylation of the UNC5C gene is frequently detected in advanced colorectal cancer. Anticancer research 15 19331160
2017 UNC5C variants are associated with cerebral amyloid angiopathy. Neurology. Genetics 12 28761931
2014 Evaluation of the colorectal cancer risk conferred by rare UNC5C alleles. World journal of gastroenterology 12 24415873
2013 unc5c haploinsufficient phenotype: striking similarities with the dcc haploinsufficiency model. The European journal of neuroscience 12 23738838
2009 Changes in UNC5C gene methylation during human gastric carcinogenesis. Anticancer research 12 20032384
2016 Scarce evidence of the causal role of germline mutations in UNC5C in hereditary colorectal cancer and polyposis. Scientific reports 10 26852919
2024 UNC5C: Novel Gene Associated with Psychiatric Disorders Impacts Dysregulation of Axon Guidance Pathways. Genes 9 38540364
2018 Significant Pattern of Promoter Hypermethylation of UNC5C Gene in Colorectal Cancer and Its Implication in Late Stage Disease. Asian Pacific journal of cancer prevention : APJCP 9 29801399
2024 The scheduling of adolescence with Netrin-1 and UNC5C. eLife 8 39056276
2021 A global integrated analysis of UNC5C down-regulation in cancers: insights from mechanism and combined treatment strategy. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 7 33706130
2013 Target-dependent expression of the netrin-1 receptor, UNC5C, in projection neurons of the ventral tegmental area. Neuroscience 6 24333968
2012 Methylation of the UNC5C gene is frequently detected in hepatocellular carcinoma. Hepato-gastroenterology 5 23178624
2025 The impact of blood MCP-1 levels on Alzheimer's disease with genetic variation at the NAV3 and UNC5C loci. Translational psychiatry 4 40830334
2023 The impact of blood MCP-1 levels on Alzheimer's disease with genetic variation of UNC5C and NAV3 loci. Research square 4 37841863
2025 TRIM9 Controls Growth Cone Responses to Netrin Through DCC and UNC5C. Journal of neurochemistry 3 39871643
2015 Expression and significance of netrin-1 and its receptor UNC5C in precocious puberty female rat hypothalamus. Asian Pacific journal of tropical medicine 3 25902168
2024 TRIM9 controls growth cone responses to netrin through DCC and UNC5C. bioRxiv : the preprint server for biology 2 38765979
2022 The netrin-1 receptor UNC5C contributes to the homeostasis of undifferentiated spermatogonia in adult mice. Stem cell research 2 35247845
2025 The UNC5C T835M mutation associated with Alzheimer's disease leads to neurodegeneration involving oxidative stress and hippocampal atrophy in aged mice. Molecular neurodegeneration 1 40468412
2024 The scheduling of adolescence with Netrin-1 and UNC5C. bioRxiv : the preprint server for biology 1 36711625
2026 LncRNA UNC5C-AS1 inhibits angiogenesis and induces endothelial apoptosis via the miR-148a-3p/EMP1 axis in preeclampsia. Cell adhesion & migration 0 41649849
2026 Identification of the ZU5 domain in UNC5C as a potential receptor for Schisandrin A: experimental and computational insights. Bioorganic chemistry 0 41724002

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