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Updated: Jun 20, 2026

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
05:35

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

Identification of FANCA as a protein interacting with centromere-associated protein E

Jian Du1, Lijian Chen, Jilong Shen

  • 1Department of Biochemistry and Molecular Biology, Anhui Medical University, Hefei, China. dudu@mail.ustc.edu.cn

Acta Biochimica Et Biophysica Sinica
|September 26, 2009
PubMed

Insights

Researchers identified novel proteins interacting with centromere-associated protein E (CENP-E), including Fanconi anemia complementation group A (FANCA). This discovery offers insights into CENP-E

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Centromere-associated protein E (CENP-E) plays a critical role in cell cycle control.
  • Understanding CENP-E interactions is crucial for elucidating its function in cell division and tumor pathogenesis.

Purpose of the Study:

  • To identify novel proteins that interact with CENP-E.
  • To investigate the functional implications of CENP-E interactions in cell cycle regulation and cancer.

Main Methods:

  • Yeast two-hybrid screening of a human HeLa cDNA library.
  • Molecular cloning and subcloning techniques to create CENP-E bait.
  • In vitro glutathione S-transferase pull-down assays.
  • In vivo co-immunoprecipitation assays.

Main Results:

  • Eight novel CENP-E interacting proteins were identified, including Homo sapiens Fanconi anemia complementation group A (FANCA).
  • The N-terminal 260 amino acids of FANCA were found to be essential for interaction with CENP-E.
  • The interaction between CENP-E and FANCA was confirmed using multiple biochemical assays.

Conclusions:

  • The identified interaction between CENP-E and FANCA suggests their collaborative role in the mitotic checkpoint signaling pathway.
  • This finding provides new avenues for exploring CENP-E's function in cell cycle regulation and tumor development.

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