ArticlePloS one2018
ALG-2 participates in recovery of cells after plasma membrane damage by electroporation and digitonin treatment.
Article in PloS one, 2018. 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, 13 citations in OpenAlex.
- The penta-EF-hand protein Pef1 of Candida albicans functions at sites of membrane perturbation to support polarized growth and membrane integrity.G3 (Bethesda, Md.) · 2026Article
- Artificial intelligence-enabled "inherited noninvasive intracellular recording" for prolonged monitoring of cardiac action potentials.Science advances · 2026Article
- CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Role of calcium-sensor proteins in cell membrane repair.Bioscience reports · 2023Review
- The Novel ALG-2 Target Protein CDIP1 Promotes Cell Death by Interacting with ESCRT-I and VAPA/B.International journal of molecular sciences · 2021Article
- How Reversible Are the Effects of Fumed Silica on Macrophages? A Proteomics-Informed View.Nanomaterials (Basel, Switzerland) · 2020Article
- ESCRT puts its thumb on the nanoscale: Fixing tiny holes in endolysosomes.Current opinion in cell biology · 2020Review
- ALG-2 couples T cell activation and apoptosis by regulating proteasome activity and influencing MCL1 stability.Cell death & disease · 2020Article
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The calcium binding protein ALG-2 is upregulated in several types of cancerous tissues and cancer cell death may be a consequence of ALG-2 downregulation. Novel research suggests that ALG-2 is involved in membrane repair mechanisms, in line with several published studies linking ALG-2 to processes of membrane remodeling and transport, which may contribute to the fitness of cells or protect them from damage. To investigate the involvement of ALG-2 in cell recovery after membrane damage we disrupted the PDCD6 gene encoding the ALG-2 protein in DT-40 cells and exposed them to electroporation. ALG-2 knock-out cells were more sensitive to electroporation as compared to wild type cells. This phenotype could be reversed by reestablishing ALG-2 expression confirming that ALG-2 plays an important role in cell recovery after plasma membrane damage. We found that overexpression of wild type ALG-2 but not a mutated form unable to bind Ca2+ partially protected HeLa cells from digitonin-induced cell death. Further, we were able to inhibit the cell protective function of ALG-2 after digitonin treatment by adding a peptide with the ALG-2 binding sequence of ALIX, which has been proposed to serve as the ALG-2 downstream target in a number of processes including cell membrane repair. Our results suggest that ALG-2 may serve as a novel therapeutic target in combination with membrane damaging interventions.
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