ArticleMolecular and cellular biology2009
Adenine nucleotide translocator cooperates with core cell death machinery to promote apoptosis in Caenorhabditis elegans.
Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Analysis ofComputational and structural biotechnology journal · 2024Article
- A Yeast-Based Screening Unravels Potential Therapeutic Molecules for Mitochondrial Diseases Associated with DominantInternational journal of molecular sciences · 2021Article
- Transcriptome changes during the initiation and progression of Duchenne muscular dystrophy in Caenorhabditis elegans.Human molecular genetics · 2020Article
- Article
- Programmed cell death and clearance of cell corpses in Caenorhabditis elegans.Cellular and molecular life sciences : CMLS · 2016Review
- PsANT, the adenine nucleotide translocase of Puccinia striiformis, promotes cell death and fungal growth.Scientific reports · 2015Article
- LAAT-1 is the lysosomal lysine/arginine transporter that maintains amino acid homeostasis.Science (New York, N.Y.) · 2012Article
- Article
- Mitochondrial involvement in cell death of non-mammalian eukaryotes.Biochimica et biophysica acta · 2011Review
- Article
- Adenine nucleotide translocase family: four isoforms for apoptosis modulation in cancer.Oncogene · 2011Review
- The C. elegans B-cell lymphoma 2 (Bcl-2) homolog cell death abnormal 9 (CED-9) associates with and remodels LIPID membranes.Protein science : a publication of the Protein Society · 2011Article
- Targeting mitochondria for cancer therapy.Nature reviews. Drug discovery · 2010Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Caenorhabditis elegans, the central cell-killing process is essentially controlled by the interplay of four apoptotic factors: EGL-1/BH3-only protein, CED-9/Bcl2, CED-4/Apaf1, and CED-3/caspase. In cells destined to die, EGL-1 binds to CED-9 and results in the release of CED-4 from the mitochondrion-tethered CED-9-CED-4 complex to the perinucleus, which facilitates processing of the CED-3 caspase to cause apoptosis. However, whether additional factors exist to regulate the cell-killing process remains largely unknown. We have identified here WAN-1, the C. elegans ortholog of mammalian adenine nucleotide translocator, as an important cell death regulator. Genetic inactivation of wan-1 significantly suppressed both somatic and germ line cell deaths in C. elegans. Consistently, chemical inhibition of WAN-1 activity also caused strong reduction of germ line apoptosis. WAN-1 localizes to mitochondria and can form complex with both CED-4 and CED-9. Importantly, the cell death initiator EGL-1 can disrupt the interaction between CED-9 and WAN-1. In addition, overexpression of WAN-1 induced ectopic cell killing dependently on the core cell death pathway. These findings suggest that WAN-1 is involved in the central cell-killing process and cooperates with the core cell death machinery to promote programmed cell death in C. elegans.
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