SAN DIEGO, Feb. 9 /PRNewswire/ -- Researchers at University of California, San Diego (UCSD) have used Aviva Systems Biology's (ASB) core ChIP-DSL (Chromatin Immunoprecipitation-DNA Selection and Ligation) technology to discover unique regulatory mechanisms involved in the activation and progression of breast cancer. As reported in today's issue of CELL, Dr. Rosenfeld's laboratory has demonstrated that a cohort of Histone Methyltransferases (HMTs), and demethylases such as LSD1, work together to establish ligand-dependant regulation of gene activation by estrogen receptor alpha (ER alpha) in human breast cancer cells. In an accompanying CELL review article Dr. W. Lee Kraus from Cornell University states, "this mode of regulation is likely to represent a fundamental mechanism controlling the regulation of a wide array of signal-regulated genes."
"This publication represents a major milestone for the maturation of the ChIP-DSL technology platform. These findings clearly demonstrated ChIP-DSL's ability to provide fundamental insight about gene regulatory mechanisms that have important implications for understanding and treating breast cancer and other diseases. ChIP-DSL also has many additional applications that will be invaluable in deciphering transcription factor/DNA interactions and the role of DNA methylation in gene regulation, pathway activation, and the development of diseases states," says ASB CEO, Julian Yuan.
Based in San Diego, California, Aviva Systems Biology is dedicated to the development of reagents for transcription factor research including antibodies to all putative transcription factors. Aviva Systems Biology also generates antibodies and additional reagents for other important research areas.
Contact: To learn more about ASB or ChIP-DSL, email Jeff Falk, Director of Technology Applications, jfalk@avivasysbio.com
Web Site: http://www.avivasysbio.com
Aviva Systems BiologyCONTACT: Jeff Falk, Director of Technology Applications, +1-858-552-6979,jfalk@avivasysbio.com
Web site: http://www.avivasysbio.com/
