Identification of Ank(G107), a muscle-specific ankyrin-G isoform.

We previously showed that alternatively spliced ankyrins-G, the Ank3 gene products, are expressed in skeletal muscle and localize to the postsynaptic folds and to the sarcoplasmic reticulum. Here we report the molecular cloning, tissue expression, and subcellular targeting of Ank(G107), a novel ankyrin-G from rat skeletal muscle. Ank(G107) lacks the entire ANK repeat domain and contains a 76-residue sequence near the COOH terminus.

Effects of cyclic AMP on components of the cell cycle machinery regulating DNA synthesis in cultured astrocytes.

Cyclic AMP is a second messenger for various hormones that inhibits cell multiplication and DNA synthesis in cultured astrocytes. We examined the effects of increasing intracellular cyclic AMP on the catalytic (cdks) and regulatory (cyclins and ckis) components of cyclin-dependent protein kinases, which regulate progression of the cell cycle before completion of DNA synthesis, in primary cultured astrocytes and in an astrocytic cell line C.LT.

Rapid TGF beta 1 effects on actin cytoskeleton of astrocytes: comparison with other factors and implications for cell motility.

We have previously shown that long-term treatment of primary cultured astrocytes with TGF beta 1 induces morphological changes accompanied by increases in actin and GFAP synthesis, and a profound rearrangement of the cytoskeleton. The present report describes the short-term reorganization of actin filaments induced by TGF beta 1 in rat cerebellum cultured astrocytes and in an astrocytic cell line. TGF beta 1 caused the appearance of new actin and vinculin organizations, without protein synthesis.

Inhibition of G1 cyclin expression and G1 cyclin-dependent protein kinases by cAMP in an astrocytic cell line.

The effects of cAMP on cell cycle progression were examined using an astrocytic cell line. We show that forskolin and 8-bromo-cAMP block the basic Fibroblast Growth Factor-induced DNA synthesis, do not inhibit mitogen activated protein kinase activation whereas they reduce G1 cyclin (E and D1) expression without modification of cyclin A level. Furthermore, they inhibit the activation of cyclin A- and cyclin E-dependent histone H1 kinases.