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Carboxyl-terminal modulator protein (CTMP), a negative regulator of PKB/Akt and v-Akt at the plasma membrane.
Journal article

Carboxyl-terminal modulator protein (CTMP), a negative regulator of PKB/Akt and v-Akt at the plasma membrane.

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  • 2001-10-13
Published in:
  • Science (New York, N.Y.). - 2001
Adaptor Proteins, Signal Transducing
Amino Acid Sequence
Animals
Carrier Proteins
Cell Division
Cell Line
Cell Line, Transformed
Cell Membrane
Cell Size
Enzyme Activation
Genes, fos
Humans
Insulin
Insulin-Like Growth Factor I
Membrane Proteins
Mice
Mice, Nude
Molecular Sequence Data
Neoplasms, Experimental
Oncogene Protein v-akt
Palmitoyl-CoA Hydrolase
Phosphorylation
Promoter Regions, Genetic
Protein Binding
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-akt
Recombinant Fusion Proteins
Retroviridae Proteins, Oncogenic
Signal Transduction
Thiolester Hydrolases
Transcription, Genetic
Transfection
Tumor Cells, Cultured
Vanadates
English The PKB (protein kinase B, also called Akt) family of protein kinases plays a key role in insulin signaling, cellular survival, and transformation. PKB is activated by phosphorylation on residues threonine 308, by the protein kinase PDK1, and Serine 473, by a putative serine 473 kinase. Several protein binding partners for PKB have been identified. Here, we describe a protein partner for PKBalpha termed CTMP, or carboxyl-terminal modulator protein, that binds specifically to the carboxyl-terminal regulatory domain of PKBalpha at the plasma membrane. Binding of CTMP reduces the activity of PKBalpha by inhibiting phosphorylation on serine 473 and threonine 308. Moreover, CTMP expression reverts the phenotype of v-Akt-transformed cells examined under a number of criteria including cell morphology, growth rate, and in vivo tumorigenesis. These findings identify CTMP as a negative regulatory component of the pathway controlling PKB activity.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://sonar.ch/global/documents/15082
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