Parafibromin inhibits cancer cell growth and causes G1 phase arrest
Biochemical and Biophysical Research Communications, ISSN: 0006-291X, Vol: 350, Issue: 1, Page: 17-24
2006
- 71Citations
- 32Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations71
- Citation Indexes71
- 71
- CrossRef57
- Captures32
- Readers32
- 32
Article Description
The HRPT2 (hereditary hyperparathyroidism type 2) tumor suppressor gene encodes a ubiquitously expressed 531 amino acid protein termed parafibromin. Inactivation of parafibromin predisposes one to the development of HPT-JT syndrome. To date, the role of parafibromin in tumorigenesis is largely unknown. Here, we report that parafibromin is a nuclear protein that possesses anti-proliferative properties. We show that overexpression of parafibromin inhibits colony formation and cellular proliferation, and induces cell cycle arrest in the G1 phase. Moreover, HPT-JT syndrome-derived mutations in HRPT2 behave in a dominant-negative manner by abolishing the ability of parafibromin to suppress cell proliferation. These findings suggest that parafibromin has a critical role in cell growth, and mutations in HRPT2 can directly inhibit this role.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0006291X06019607; http://dx.doi.org/10.1016/j.bbrc.2006.08.169; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=33749045892&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/16989776; https://linkinghub.elsevier.com/retrieve/pii/S0006291X06019607; https://dx.doi.org/10.1016/j.bbrc.2006.08.169
Elsevier BV
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