ArticleCell death & disease2014
Apolipoprotein L2 contains a BH3-like domain but it does not behave as a BH3-only protein.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular Underpinning of Treatment-Resistant Schizophrenia: A Putative Different Neurobiology from Treatment-Responsive Schizophrenia.International journal of molecular sciences · 2025Review
- Review
- Apolipoprotein L2's Role in Liver Fibrosis.Gastro hep advances · 2025Article
- Apolipoprotein L genes are novel mediators of inflammation in beta cells.Diabetologia · 2024Article
- Panoramic analysis of cell death patterns reveals prognostic and immune profiles of head and neck squamous cell carcinoma.American journal of cancer research · 2024Article
- Review
- Identification of novel functional brain proteins for treatment-resistant schizophrenia: Based on a proteome-wide association study.European psychiatry : the journal of the Association of European Psychiatrists · 2023Article
- Intravesical BCG in patients with non-muscle invasive bladder cancer induces trained immunity and decreases respiratory infections.Journal for immunotherapy of cancer · 2023Observational
- Structural Details of BH3 Motifs and BH3-Mediated Interactions: an Updated Perspective.Frontiers in molecular biosciences · 2022Review
- Structures of the ApoL1 and ApoL2 N-terminal domains reveal a non-classical four-helix bundle motif.Communications biology · 2021Article
- The function of apolipoproteins L (APOLs): relevance for kidney disease, neurotransmission disorders, cancer and viral infection.The FEBS journal · 2021Review
- Nascent Transcriptomics Reveal Cellular Prolytic Factors Upregulated Upstream of the Latent-to-Lytic Switch Protein of Epstein-Barr Virus.Journal of virology · 2020Article
- Epigenetic aging is accelerated in alcohol use disorder and regulated by genetic variation in APOL2.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020Article
- Deciphering the Relationship between Obesity and Various Diseases from a Network Perspective.Genes · 2017Article
- Gene expression profiles in peripheral blood mononuclear cells correlate with salience network activity in chronic visceral pain: A pilot study.Neurogastroenterology and motility · 2017Article
- Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice.Nature medicine · 2017Article
- The trans-membrane domain of Bcl-2α, but not its hydrophobic cleft, is a critical determinant for efficient IP3 receptor inhibition.Oncotarget · 2016Article
- Low miR-187 expression promotes resistance to chemoradiation therapy in vitro and correlates with treatment failure in patients with esophageal adenocarcinoma.Molecular medicine (Cambridge, Mass.) · 2016Article
- BH3 domain-independent apolipoprotein L1 toxicity rescued by BCL2 prosurvival proteins.American journal of physiology. Cell physiology · 2015Article
- APOL1 toxin, innate immunity, and kidney injury.Kidney international · 2015Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoproteins of the L family are lipid-binding proteins whose function is largely unknown. Apolipoprotein L1 and apolipoprotein L6 have been recently described as novel pro-death BH3-only proteins that are also capable of regulating autophagy. In an in-silico screening to discover novel putative BH3-only proteins, we identified yet another member of the apolipoprotein L family, apolipoprotein L2 (ApoL2), as a BH3 motif-containing protein. ApoL2 has been suggested to behave as a BH3-only protein and mediate cell death induced by interferon-gamma or viral infection. As previously described, we observed that ApoL2 protein was induced by interferon-gamma. However, knocking down its expression in HeLa cells did not regulate cell death induced by interferon-gamma. Overexpression of ApoL2 did not induce cell death on its own. ApoL2 did not sensitize or protect cells from overexpression of the BH3-only proteins Bmf or Noxa. Furthermore, siRNA against ApoL2 did not alter sensitivity to a variety of death stimuli. We could, however, detect a weak interaction between ApoL2 and Bcl-2 by immunoprecipitation of the former, suggesting a role of ApoL2 in a Bcl-2-regulated process like autophagy. However, in contrast to what has been described about its homologs ApoL1 and ApoL6, ApoL2 did not regulate autophagy. Thus, the role, if any, of ApoL2 in cell death remains to be clarified.
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