Protein Kinase C and Calcium/Calmodulin-activated Protein Kinase II (CaMK II) Suppress Nicotinic Acetylcholine Receptor Gene Expression in Mammalian Muscle

This publication has 36 references indexed in Scilit:

• CaM Kinase II-dependent Suppression of Nicotinic Acetylcholine Receptor δ-Subunit Promoter Activity
  Journal of Biological Chemistry, 2001
• Electrical activity regulates AChR gene expression via JNK, PKCζ and Sp1 in skeletal chick muscle
  FEBS Letters, 2001
• DEVELOPMENT OF THE VERTEBRATE NEUROMUSCULAR JUNCTION
  Annual Review of Neuroscience, 1999
• Characterization of the Functional Role of E‐box Elements for the Transcriptional Activity of Rat Acetylcholine Receptor ε‐Subunit and γ‐Subunit Gene Promoters in Primary Muscle Cell Cultures
  European Journal of Biochemistry, 1994
• Depolarization-transcription signals in skeletal muscle use calcium flux through L channels, but bypass the sarcoplasmic reticulum
  Neuron, 1994
• Phosphorylation of myogenin in chick myotubes: regulation by electrical activity and by protein kinase C. Implications for acetylcholine receptor gene expression
  Biochemistry, 1994
• Two adjacent E box elements and a M‐CAT box are involved in the muscle‐specific regulation of the rat acetylcholine receptor β subunit gene
  European Journal of Biochemistry, 1993
• Deletion of the regulatory domain of protein kinase C alpha exposes regions in the hinge and catalytic domains that mediate nuclear targeting.
  The Journal of cell biology, 1992
• Induction of adult-type nicotinic acetylcholine receptor gene expression in noninnervated regenerating muscle
  Neuron, 1991
• Denervation supersensitivity in skeletal muscle: analysis with a cloned cDNA probe.
  The Journal of cell biology, 1984