Genetic and acute CPEB1 depletion ameliorate fragile X pathophysiology.
Worcester, United States. In Nat Med, 2013
FMRP and cytoplasmic polyadenylation element-binding protein (CPEB), an activator of translation, are present in neuronal dendrites, are predicted to bind many of the same mRNAs and may mediate a translational homeostasis that, when imbalanced, results in FXS.
Specificity factors in cytoplasmic polyadenylation.
Denver, United States. In Wiley Interdiscip Rev Rna, 2013
In addition to describing the role of general polyadenylation factors, we discuss the specific RNA binding protein families associated with cytoplasmic polyadenylation elements, including CPEB (CPEB1, CPEB2, CPEB3, and CPEB4), Pumilio (PUM2), Musashi (MSI1, MSI2), zygote arrest (ZAR2), ELAV like proteins (ELAVL1, HuR), poly(C) binding proteins (PCBP2, αCP2, hnRNP-E2), and Bicaudal C (BICC1).
Connecting cis-elements and trans-factors with mechanisms of developmental regulation of mRNA translation in meiotic and haploid mammalian spermatogenic cells.
Boston, United States. In Reproduction, 2013
As a result, the mechanisms involving well-studied mRNAs (Ddx4/Mvh, Prm1, Prm2, and Sycp3) and factors (DICER1, CPEB1, DAZL, DDX4/MVH, DDX25/GRTH, translin, and ELAV1/HuR) are incompletely understood.
Cytoplasmic RNA-binding proteins and the control of complex brain function.
New York City, United States. In Cold Spring Harb Perspect Biol, 2012
Although translation in the CNS is regulated by multiple mechanisms and factors, we focus this review on regulatory mRNA-binding proteins with particular emphasis on fragile X mental retardation protein (FMRP) and cytoplasmic polyadenylation element binding (CPEB) because they have been shown to be at the nexus of translational control and brain function in health and disease.