The roles of multifunctional protein ErbB3 binding protein 1 (EBP1) isoforms from development to disease

摘要

The roles of the two isoforms of ErbB3-binding protein 1 (Ebp1) in cellular function and its regulation in disease and development is a stimulating area in current fields of biology, such as neuroscience, cancer biology, and structural biology. Over the last two decades, a growing body of studies suggests have suggested different functions for the EBP1 isoforms in various cancers, along with their specific binding partners in the ubiquitin-proteasome system. Owing to the specific cellular context or spatial/temporal expression of the EBP1 isoforms, either transcriptional repression or the activation function of EBP1 has been proposed, and epigenetic regulation by p48 EBP1 has also been observed during in the embryo development, including in brain development and neurologic disorders, such as schizophrenia, in using an Ebp1 knockout mouse model. Here, we review recent findings that have shaped our current understanding of the emerging function of EBP1 isoforms in cellular events and gene expression, from development to disease. Cell biology: deciphering differences between “sibling” proteins A pair of proteins that originate from a common gene exert strikingly different effects on embryonic development as well as tumor growth and progression. RNA transcripts generated from the PA2G4 gene can undergo enzymatic processing to yield two different protein products, p42 EB1 and p48 EB1. These proteins differ by the presence or absence of 54 amino acids at one end, and Jee-Yin Ahn at the Sungkyunkwan University School of Medicine, Suwon, South Korea, and colleagues have reviewed current insights into the functional consequences of this difference. The two proteins bind to distinct sets of molecular partners. The p48 form appears to regulate a host of genes involved in brain development, but also appears to drive cancerous growth in various tumors. In contrast, p42 is scarcer during development, and appears to inhibit tumor formation.