Ask about this productRelated genes to: NDEL1 antibody
- Gene:
- NDEL1 NIH gene
- Name:
- nudE neurodevelopment protein 1 like 1
- Previous symbol:
- -
- Synonyms:
- NUDEL, MITAP1, NDE1L1, NDE2
- Chromosome:
- 17p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-10
- Date modifiied:
- 2016-01-06
Related products to: NDEL1 antibody
Related articles to: NDEL1 antibody
- Structural remodeling of the dentate gyrus is a hallmark of temporal lobe epilepsy (TLE), yet the underlying molecular mechanisms remain incompletely understood. Nuclear distribution element-like 1 (Ndel1), a cytoskeleton-associated protein involved in neuronal migration and dendritic development, has not been characterized in dentate gyrus remodeling during epileptogenesis. Here, we investigated region- and cell-type-specific alterations in Ndel1 expression in a pilocarpine-induced mouse model of TLE and examined the effects of adeno-associated virus (AAV)-mediated Ndel1 expression on structural remodeling. Immunofluorescence was used to define Ndel1 localization across neural stem cells, granule lineage cells, mature neurons, and astrocytes, and dendritic architecture was assessed using Golgi staining and Sholl analysis. Total hippocampal Ndel1 expression increased after status epilepticus, whereas Ndel1-positive cells decreased selectively in the subgranular zone but increased among granule lineage cells in the hilus. Ndel1 was preferentially expressed in BLBP-positive neural stem cells and mature neurons, but not in neuroblasts. Activated astrocytic processes exhibited increased spatial association with Ndel1-positive cells during early remodeling. Ndel1 overexpression was associated with partial normalization of neuronal marker distribution, increased dendritic spine density, and reduced dendritic branching complexity. These findings suggest that Ndel1 is associated with region- and lineage-specific structural remodeling in the dentate gyrus during epileptogenesis. - Source: PubMed
Publication date: 2026/08/13
Xu JingZhu LinChen LuDu XiaoyuXu YueWu Qian - Depression is a leading cause of global disability, yet its biological mechanisms remain elusive, limiting therapeutic efficacy. We investigated Ndel1 oligopeptidase (NudE Neurodevelopment Protein 1 Like 1), a neurodevelopmental enzyme involved in neuronal migration and brain morphology with neuropeptidase activity, as a potential biomarker in major depressive disorder/unipolar depression (MDD/UD) or bipolar depression (BD). Serum Ndel1 activity was significantly elevated in both MDD/UD and BD compared to age- and sex-matched healthy control (HC). In vitro assays revealed that while psychotropics and patient serum both reduced neurite density - indicating circulating neurotoxic factors - intracellular responses differed. Indeed, only MDD/UD serum upregulated neuronal intracellular Ndel1 (iNdel1) activity, suggesting a disorder-specific mechanism against serum-induced neuronal stress evidenced by decreased neuronal cell viability. Additionally, we identified distinct immune signatures since sera from both disorders activated human Toll-like receptor 3 (TLR3), while TLR4 activation was exclusive to MDD/UD serum. These findings support the potential of Ndel1 as a peripheral biomarker candidate of neuronal injury, and propose TLR profiles as tools for differential diagnosis, strengthening the rationale for mechanism-based neuroimmune therapeutics for depression. Furthermore, a possible link between specific immune activation and Ndel1 activity modulation in neurons underscores a broader connection between the immune system and the cytoskeletal dynamics, while integrating the pharmacological response and neuronal structural morphology. - Source: PubMed
Publication date: 2026/03/19
de Farias Ingrid SOyadomari William YParra Larissa RibinoXimenes Ana PCordeiro Júnior QuirinoFidalgo Thiago MarquesHayashi Mirian A F - Recent studies have identified recurrent features of metastatic cancer cells such as their increased chromosomal instability (CIN) and frequent loss of the short arm of chromosome 17 (Chr17p). However, it remains unclear whether these features induce synthetic lethal vulnerabilities that can be used to specifically target metastatic disease. Using whole-genome CRISPR/Cas9 loss-of-function screens performed in matched primary and CIN-high brain-metastatic tumor models, we discovered that brain-metastatic cells exhibit increased sensitivity to the loss of diverse regulators of chromosome segregation. Knockout of one such regulator, selectively inhibited the growth of brain-metastatic models and , an effect driven by the loss of STAG2 and consequent induction of CIN. Surprisingly, dependence on was also highly correlated with loss of Chr17p across hundreds of cancer cell lines in DepMap, the result of losing the paralog , which resides at this locus. CIN and Chr17p loss are thus independently sufficient to drive dependence in brain-metastatic cells, and the presence of both features increases dependence additively. These findings demonstrate that metastasis evolution endows cancer cells with specific vulnerabilities, including one that is driven by two recurrently altered molecular features of metastatic disease. - Source: PubMed
Publication date: 2026/02/12
Teddy Caroline MHoj Jacob PCaci JuliaLu MinKillarney Shane TBen-Yishay TalBen-David UriWood Kris C - The oligopeptidase Ndel1 (NudE neurodevelopment protein 1 like 1) is a multifunctional protein implicated in neurodevelopmental processes, intensively investigated as a potential biomarker in psychiatric disorders. While its roles in regulating the cytoskeleton are well-studied, the global consequences of its loss on the brain's peptide landscape are unknown. This study presents a comprehensive, region-resolved peptidomic resource detailing the consequences of postnatal Ndel1 loss in the mouse cortex, hippocampus, striatum, and cerebellum. We also validated this method of microwave protease inactivation followed by acidic and organic extractions by means of this peptidome analysis across several brain regions. More specifically, using a conditional knockout mouse model with Ndel1 deletion in forebrain excitatory neurons, we employed complementary acidic and alcoholic extraction workflows coupled to liquid chromatography-tandem mass spectrometry (LC-MS/MS). We generated a comparative atlas of differentially abundant peptides (DAPs), identifying hundreds of peptide changes across the different brain regions and extraction methods. Gene Ontology analysis of the inferred source proteins revealed alterations in pathways related to cytoskeletal organization, synaptic function, and cellular metabolism. This dataset provides a foundational resource for generating new hypotheses about Ndel1's region-specific functions and serves as a valuable reference for the neurodevelopmental and neuropeptidomics communities. Understanding these Ndel1-driven changes is crucial, providing valuable insights into the pathophysiology of neurodevelopmental and mental disorders linked to reduced Ndel1 activity, such as schizophrenia, autism, and bipolar disorder. This holistic view may reveal novel therapeutic targets for these complex conditions. - Source: PubMed
Nani João VHayashi Jackelinne YukaCampeiro Joana DCâmara Guilherme AraújoSaito AtsushiOyadomari William YSawa AkiraKamiya AtsushiTashima Alexandre KHayashi Mirian A F - In early pregnancy, approximately 70% of women experience nausea and vomiting, with hyperemesis gravidarum (HG) can potentially lead to severe fluid and nutritional imbalances that require hospitalization. Although HG often resolves on its own in the early stages of pregnancy, its severity is linked to ketosis and elevated serum urea levels, as well as an increased risk of neurodevelopmental disorders in children. To further investigate the immune status of HG patients, we plan to conduct single-cell transcriptomic sequencing and plasma proteomic analysis of peripheral blood samples. This approach aims to elucidate the interactions and mechanisms of PBMCs and provide new insights into potential therapeutic interventions. Our findings indicate an increased proportion of neutrophils in HG patients, along with the upregulation of interferon genes and associated pathways. Notably, the activity of interferon-related TFs, such as STAT1, IRF7, and IRF9, was significantly elevated. Additionally, we observed a decrease in T cell activity in HG patients, while the functionality of NK cells and CD14 monocytes was enhanced. The elevated plasma levels of NDEL1 may also have implications for fetal development. We have constructed a single-cell atlas of PBMCs from pregnant women with HG, which is expected to enhance our understanding of the immune response in HG and identify potential therapeutic targets for this condition. - Source: PubMed
Wu KeYao XueqiangWen JieHu Haixi