Broadening Participation in Biology Education Research: Engaging Community College Students and Faculty.

Nearly half of all undergraduates are enrolled at community colleges (CCs), including the majority of U.S. students who represent groups underserved in the sciences.

Retinoic acid induced downregulation of MYCN is not mediated through changes in Sp1/Sp3.

Background: Use of retinoic acid (RA) has become the standard of care in the treatment of high risk neuroblastoma (NB). In vitro, RA induces growth arrest and differentiation, an effect that likely underlies its activity in the clinical setting. An important event in differentiation is the transcriptional downregulation of the MYCN oncogene, which is frequently activated in aggressive tumors.

Differential effects of bryostatin 1 and 12-O-tetradecanoylphorbol-13-acetate on the regulation and activation of RasGRP1 in mouse epidermal keratinocytes.

The antitumor agent bryostatin 1 and the tumor-promoting phorbol esters function as structural mimetics of the second lipid messenger diacylglycerol (DAG) by binding to the C1 domain of DAG receptors. However, bryostatin 1 and the phorbol esters often differ in their cellular actions. In mouse skin, the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) is a potent tumor promoter, whereas bryostatin 1 lacks this activity and antagonizes the tumor-promoting effects of TPA.

N-myc oncogene expression in neuroblastoma is driven by Sp1 and Sp3.

Regulation of N-myc oncogene expression is an important determinant of the biological behavior of neuroblastoma. The N-myc promoter contains several potential binding sites for transcription factors of the Sp1 family. Mutation of a CT-box motif contained within a 26 bp region required for N-myc downregulation by retinoic acid decreased basal transcriptional activity and altered DNA-protein interactions of the promoter, while mutations flanking this motif did neither.