ArticleBiochemical and biophysical research communications2011
CHFR binds to and regulates MAD2 in the spindle checkpoint through its cysteine-rich domain.
Article in Biochemical and biophysical research communications, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Identification of a Novel Epigenetic Signature CHFR as a Potential Prognostic Gene Involved in Metastatic Clear Cell Renal Cell Carcinoma.Frontiers in genetics · 2021Article
- Review
- The association between MAD2 and prognosis in cancer: a systematic review and meta-analyses.Oncotarget · 2017Article
- Emerging evidence for CHFR as a cancer biomarker: from tumor biology to precision medicine.Cancer metastasis reviews · 2014Review
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
CHFR has been implicated as a tumor suppressor in a multitude of cancers. It was originally identified as a major component of the antephase checkpoint. Recently, CHFR was reported to interact with MAD2, an important component of the spindle assembly checkpoint, where CHFR knockdown resulted in mislocalization of MAD2 and disruption of the MAD2/CDC20 interaction. To further understand how CHFR interacts with MAD2, we deleted key functional domains of CHFR, and investigated the effect on MAD2 binding and function. Here we show that deletion of the cysteine-rich domain of CHFR is required for the CHFR/MAD2 interaction as well as proper localization of MAD2 in the cell. Furthermore, the cysteine-rich domain deletion exhibits impaired ability to promote the MAD2/CDC20 interaction, leading to an increase in mitotic defects relative to wild type CHFR. These data support a critical role for CHFR in the MAD2 spindle checkpoint. Furthermore, these data establish the cysteine-rich domain of CHFR as the essential domain for the CHFR/MAD2 interaction and for promoting interaction between MAD2 and CDC20 to inhibit the anaphase-promoting complex.
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Registered trials
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