ArticleProceedings of the National Academy of Sciences of the United States of America2003
BIR-1, a Caenorhabditis elegans homologue of Survivin, regulates transcription and development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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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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
6 citing papers in PubMed, 15 citations in OpenAlex.
- Survivin promotes a glycolytic switch in CD4iScience · 2022Article
- Survivin contributes to DNA repair by homologous recombination in breast cancer cells.Breast cancer research and treatment · 2016Article
- Survivin modulates genes with divergent molecular functions and regulates proliferation of hematopoietic stem cells through Evi-1.Leukemia · 2015Article
- Survivin selectively modulates genes deregulated in human leukemia stem cells.Journal of oncology · 2011Article
- Transcriptional and post-transcriptional controls of survivin in cancer cells: novel approaches for cancer treatment.Journal of experimental & clinical cancer research : CR · 2006Review
- Survivin regulates the p53 tumor suppressor gene family.Oncogene · 2004Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
bir-1, a Caenorhabditis elegans inhibitor-of-apoptosis gene homologous to Survivin is organized in an operon with the transcription cofactor C. elegans SKIP (skp-1). Because genes arranged in operons are frequently linked functionally, we have asked whether BIR-1 also functions in transcription. bir-1 inhibition resulted in multiple developmental defects that overlapped with C. elegans SKIP loss-of-function phenotypes: retention of eggs, dumpy, movement defects, and lethality. bir-1 RNA-mediated interference decreased expression of several gfp transgenes and the endogenous genes dpy-7 and hlh-1. Immunoblot analysis revealed decreased phosphoacetylated histones in bir-1 RNA-mediated interference-treated worms. In a heterologous transfection system, BIR-1 augments thyroid hormone-regulated transcription and has an additive effect with SKIP. These results show that BIR-1 functions in the regulation of transcription and development.
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Registered trials
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