ArticleOncotarget2016
A potential molecular model for studying apoptosis enhanced by the interaction of BCL-G with JAB1 in swine.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- BCL-G: 20 years of research on a non-typical protein from the BCL-2 family.Cell death and differentiation · 2023Review
- TRIM44 promotes cell proliferation and migration by inhibiting FRK in renal cell carcinoma.Cancer science · 2020Article
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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
BCL-G, an apoptotic factor in Bcl-2 family, is involved in several kinds of diseases by interacting with several proteins. Although many studies on mouse and human BCL-G have been reported, porcine BCL-G (pBCL-G) has been little investigated. In this study, our results showed that pBCL-G was universally expressed in porcine tissues. The BH2 domain affected the subcellular distribution of pBCL-G protein. pBCL-G could interact with porcine JAB1 (pJAB1), by which its subcellular distribution was affected. pBCL-G promoted staurosporine-induced apoptosis that was significantly enhanced by interaction of pBCL-G with pJAB1. The apoptosis at least partially depended on the activated caspase-8, -9 and -3. Owing to the close phylogenetic distance between pigs and humans and their many physiological similarities, our findings may provide a potential molecular model to study human BCL-G and also may have implications in the treatment of diseases relevant with BCL-G.
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Registered trials
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