1.We have previously shown that mice with partial inactivation of both alleles of ankRD26 are morbidly obese, have diabetes and are larger than normal. We have now shown that food restriction prevents the development of obesity, diabetes and the increase in body size. We have also found that MEFs from the mutant mice have an increased propensity to differentiate into adipocytes in the presence or absence of obesity inducers. We have performed two hybrid analyses to identify proteins interacting with ankrd26 and identified 3 proteins now under study. We have examined the mutant mice as a function of age and have found old mice develop liver cancer and plan to study why this occurs. We are analyzing the brains of the mutant mice by immunohistochemistry to determine which signaling pathways are abnormal and can account for the hyperphagia. 2. We have shown that the POTE family of genes is pro-apoptotic and acts through the BAK pathway to kill target cells. We have investigated to precise location of the POTE protein in testicular cells and shown that it is present in round spermatids that are undergoing apoptosis and speculate it may have a role in spermatid editing. 3. We have generated new monoclonal antibodies to CAPC. Using these specific antibodies we found CAPC resides in the endoplasmic reticulum. Over expression of CAPC causes changes in cell motility and cell growth.
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