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Gene Review

TNS2  -  tensin 2

Homo sapiens

Synonyms: C1 domain-containing phosphatase and tensin homolog, C1-TEN, C1TEN, KIAA1075, TENC1, ...
 
 
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High impact information on TENC1

  • Thus, we have named the protein C1 domain-containing phosphatase and TENsin homologue (C1-TEN) [1].
  • (2) With the stimulator working on the same wrist as for TNS-1, the loading time of the opposite wrist was determined (TNS-2) [2].
  • In conclusion, C1-TEN appears to be a novel intracellular phosphatase that negatively regulates the Akt/PKB signaling cascade, and is similar to its relative PTEN in this respect [3].
  • In addition, C1-TEN-overexpressing cells showed a markedly reduced phosphorylation of Akt/PKB kinase and its substrate GSK3, as well as reduced Akt enzymatic activity [3].
  • C1-TEN is a negative regulator of the Akt/PKB signal transduction pathway and inhibits cell survival, proliferation, and migration [3].
 

Biological context of TENC1

  • Furthermore, serum starvation-induced apoptosis caused a twofold increase in caspase 3 activity in C1-TEN-overexpressing cells vs. mock cells [3].
  • Furthermore, cells expressing a C1-TEN mutant where the putative phosphatase active site cysteine at position 231 was substituted for a serine displayed full restoration of both cell proliferation and Akt activation [3].
 

Analytical, diagnostic and therapeutic context of TENC1

  • Northern blot analysis of C1-TEN in human tissues revealed highest expression in heart, kidney, and liver [1].

References

  1. Interaction of Axl receptor tyrosine kinase with C1-TEN, a novel C1 domain-containing protein with homology to tensin. Hafizi, S., Alindri, F., Karlsson, R., Dahlbäck, B. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  2. Transcutaneous nerve stimulation in rheumatoid arthritis. Kumar, V.N., Redford, J.B. Archives of physical medicine and rehabilitation. (1982) [Pubmed]
  3. C1-TEN is a negative regulator of the Akt/PKB signal transduction pathway and inhibits cell survival, proliferation, and migration. Hafizi, S., Ibraimi, F., Dahlbäck, B. FASEB J. (2005) [Pubmed]
 
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