ArticleMolecules and cells2015
NELL2 function in the protection of cells against endoplasmic reticulum stress.
Article in Molecules and cells, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Sex-Specific Transcriptomic Profiles in Psoriatic Lesions: A Large-Scale Integrative Study.International journal of molecular sciences · 2026Article
- NELL2 suppresses epithelial-mesenchymal transition and induces ferroptosis via notch signaling pathway in HCC.Scientific reports · 2025Article
- A selective ER-phagy exerts neuroprotective effects via modulation of α-synuclein clearance in parkinsonian models.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A united model for diagnosing pulmonary tuberculosis with random forest and artificial neural network.Frontiers in genetics · 2023Article
- Transcriptional Regulatory Role of NELL2 in Preproenkephalin Gene Expression.Molecules and cells · 2022Article
- Comparison of the transcriptome in circulating leukocytes in early lactation between primiparous and multiparous cows provides evidence for age-related changes.BMC genomics · 2021Article
- Unfolded Protein Response as a Therapeutic Target in Cardiovascular Disease.Current topics in medicinal chemistry · 2019Review
- Unfolded protein response is activated in Krabbe disease in a manner dependent on the mutation type.Journal of human genetics · 2018Article
- Salubrinal Alleviates Pressure Overload-Induced Cardiac Hypertrophy by Inhibiting Endoplasmic Reticulum Stress Pathway.Molecules and cells · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Continuous intra- and extracellular stresses induce disorder of Ca(2+) homeostasis and accumulation of unfolded protein in the endoplasmic reticulum (ER), which results in ER stress. Severe long-term ER stress triggers apoptosis signaling pathways, resulting in cell death. Neural epidermal growth factor-like like protein 2 (NELL2) has been reported to be important in protection of cells from cell death-inducing environments. In this study, we investigated the cytoprotective effect of NELL2 in the context of ER stress induced by thapsigargin, a strong ER stress inducer, in Cos7 cells. Overexpression of NELL2 prevented ER stress-mediated apoptosis by decreasing expression of ER stress-induced C/EBP homologous protein (CHOP) and increasing ER chaperones. In this context, expression of anti-apoptotic Bcl-xL was increased by NELL2, whereas NELL2 decreased expression of pro-apoptotic proteins, such as cleaved caspases 3 and 7. This anti-apoptotic effect of NELL2 is likely mediated by extracellular signal-regulated kinase (ERK) signaling, because its inhibitor, U0126, inhibited effects of NELL2 on the expression of anti- and pro-apoptotic proteins and on the protection from ER stress-induced cell death.
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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.