Polymorphisms in the genes encoding members of the tristetraprolin family of human tandem CCCH zinc finger proteins.

The three known mammalian CCCH tandem zinc finger proteins of the tristetraprolin (TTP) class have recently been demonstrated to be mRNA-binding proteins. The prototype, TTP, functions in normal physiology to promote the instability of the tumor necrosis factor alpha (TNFalpha) and granulocyte-macrophage colony-stimulating factor mRNAs. Conversely, these mRNAs are stabilized in TTP-deficient mice, leading to an inflammatory phenotype characterized by overproduction of these cytokines.

Neuroanatomical development in the absence of PKC phosphorylation of the myristoylated alanine-rich C-kinase substrate (MARCKS) protein.

The myristoylated alanine-rich C-kinase substrate protein (MARCKS) is a widely expressed target of protein kinase C (PKC) phosphorylation. Disruption of Marcks in mice leads to a number of developmental defects within the central nervous system that are completely prevented by expression of an epitope-tagged wild-type human MARCKS transgene. In the present study, we investigated whether PKC phosphorylation of MARCKS is necessary for normal central nervous system development and postnatal survival.