Cancer can develop when cells escape normal growth control mechanisms through mutations in proto-oncogenes or tumor suppressor genes. A characteristic of most oncogene and tumor suppressor gene products is that they are components of signal transduction pathways that are essential for maintaining cellular homeostasis. PTEN (phosphatase and tensin homolog), also known as MMAC1 (mutated in multiple advanced cancers 1), is a tumor suppressor gene that is mutated at high frequency in multiple tumor types. The protein encoded by PTEN is a phosphatase that preferentially dephosphorylates phosphoinositide substrates. It is believed that a mechanism by which PTEN mutations cause tumors is the loss of its negative control on the phosphoinositide 3-kinase signaling pathway that regulates cell growth and survival. PTEN also plays a role in the maintenance of hematopoietic stem cells.
The A2B1 monoclonal antibody recognizes PTEN, regardless of phosphorylation status.
The specificity of this antibody conjugate for flow cytometric analysis was validated by confirming that RNA-mediated interference (RNAi) of the specific protein reduced the staining of the cells (see figure). Furthermore, the capacity of the RNAi to down-regulate the expression of the relevant protein was confirmed by western blot analysis (data not shown).