ArticleThe Biochemical journal2005
Pro-apoptotic Bid induces membrane perturbation by inserting selected lysolipids into the bilayer.
Article in The Biochemical journal, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- Higher levels of plasma phosphatidylcholine (17:0_18:1) raise the risk of developing Parkinson's disease.Scientific reports · 2025Article
- Mitochondrial Lipids: From Membrane Organization to Apoptotic Facilitation.International journal of molecular sciences · 2022Review
- Exploratory Data Analysis of Cell and Mitochondrial High-Fat, High-Sugar Toxicity on Human HepG2 Cells.Nutrients · 2021Article
- Differential role of FL-BID and t-BID during verotoxin-1-induced apoptosis in Burkitt's lymphoma cells.Oncogene · 2018Article
- Phospholipids in mitochondrial dysfunction during hemorrhagic shock.Journal of bioenergetics and biomembranes · 2017Review
- Article
- Major Alterations of Phosphatidylcholine and Lysophosphotidylcholine Lipids in the Substantia Nigra Using an Early Stage Model of Parkinson's Disease.International journal of molecular sciences · 2015Article
- JNK1/2 regulate Bid by direct phosphorylation at Thr59 in response to ALDH1L1.Cell death & disease · 2014Article
- miR-499 protects cardiomyocytes from H 2O 2-induced apoptosis via its effects on Pdcd4 and Pacs2.RNA biology · 2014Article
- Bioactive oxidatively truncated phospholipids in inflammation and apoptosis: formation, targets, and inactivation.Biochimica et biophysica acta · 2012Review
- The ubiquitin/proteasome system-dependent control of mitochondrial steps in apoptosis.Seminars in cell & developmental biology · 2012Review
- Exogenous ether lipids predominantly target mitochondria.PloS one · 2012Article
- BCL2 and CASP8 regulation by NF-kappaB differentially affect mitochondrial function and cell fate in antiestrogen-sensitive and -resistant breast cancer cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Bid binding to negatively charged phospholipids may not be required for its pro-apoptotic activity in vivo.Biochimica et biophysica acta · 2009Article
- Suppression of mitochondrial function by oxidatively truncated phospholipids is reversible, aided by bid, and suppressed by Bcl-XL.The Journal of biological chemistry · 2009Article
- Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induced mitochondrial pathway to apoptosis and caspase activation is potentiated by phospholipid scramblase-3.Apoptosis : an international journal on programmed cell death · 2008Article
- Review
- Following the TRAIL to apoptosis.Immunologic research · 2006Review
- Tumor necrosis factor-related apoptosis-inducing ligand alters mitochondrial membrane lipids.Cancer research · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bid is a BH3-only member of the Bcl-2 family that regulates cell death at the level of mitochondrial membranes. Bid appears to link the mitochondrial pathway with the death receptor-mediated pathway of cell death. It is generally assumed that the f.l. (full-length) protein becomes activated after proteolytic cleavage, especially by apical caspases like caspase 8. The cleaved protein then relocates to mitochondria and promotes membrane permeabilization, presumably by interaction with mitochondrial lipids and other Bcl-2 proteins that facilitate the release of apoptogenic proteins like cytochrome c. Although the major action may reside in the C-terminus part, tBid (cleaved Bid), un-cleaved Bid also has pro-apoptotic potential when ectopically expressed in cells or in vitro. This pro-apoptotic action of f.l. Bid has remained unexplained, especially at the biochemical level. In the present study, we show that f.l. (full-length) Bid can insert specific lysolipids into the membrane surface, thereby priming mitochondria for the release of apoptogenic factors. This is most effective for lysophosphatidylcholine species that we report to accumulate in mitochondria during apoptosis induction. A Bid mutant that is not pro-apoptotic in vivo is defective in lysophosphatidylcholine-mediated membrane perturbation in vitro. Our results thus provide a biochemical explanation for the pro-apoptotic action of f.l. Bid.
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Registered trials
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.