ECDYSONELESS, A NOVEL REGULATOR OF CALCIUM INFLUX
Abstract
Cell proliferation produces two cells from one and is required for cell growth, and is most critical in embryonic development as well as in normal adult organ function, whereas uncontrolled cell proliferation is a hallmark of cancer. Consequently, understanding the regulatory controls of cell cycle progression is of utmost importance. Ecdysoneless (ECD), an evolutionary conserved protein, was first identified in Drosophila melanogaster regulating larval development. Our lab established the importance of mammalian ECD by demonstrating that Ecd germline knockout mice is embryonically lethal, and deletion in cells causes G1/G0 arrest, which can be rescued by exogenous ECD, affirming the requirement of ECD for normal mammalian cell cycle progression. Importantly, ECD is overexpressed in ErbB2‐positive breast cancers and its overexpression correlates to poor prognosis and short survival. We also demonstrated the co‐oncogenic role of ECD with Ras to induce oncogenic transformation of mammary cells. Recently, our lab has also elucidated that ECD binds to a co‐chaperonic complex called R2TP, and this interaction is required for cell cycle progression.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Apr 01, 2017
- Source ID
- 10.1096/fasebj.31.1_supplement.lb154
Entities
People
- Aniruddha Sarkar
Organizations
- Congressionally Directed Medical Research Programs
- University of Nebraska Medical Center