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BMC Developmental Biology BioMed Central Methodology article Open Access A tamoxifen inducible knock-in allele for investigation of E2A function Mary E Jones, Motonari Kondo and Yuan Zhuang* Address: Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA Email: Mary E Jones - mj5@; Motonari Kondo - motonari.kondo@; Yuan Zhuang* - yzhuang@ * Corresponding author Published: 12 October 2009 Received: 9 February 2009 Accepted: 12 October 2009 BMC Developmental Biology 2009, 9:51 doi:10.1186/1471-213X-9-51 This article is available from: /1471-213X/9/51 © 2009 Jones et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: E-proteins are transcription factors important for the development of a variety of cell types, including neural, muscle and lymphocytes of the immune system. E2A, the best characterized E-protein family member in mammals, has been shown to have stage specific roles in cell differentiation, lineage commitment, proliferation, and survival. However, due to the complexity of E2A function, it is often difficult to separate these roles using conventional genetic approaches. Here, we have developed a new genetic model for reversible control of E2A protein a