Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.1.3.16 extracted from

  • Baek, K.H.; Zaslavsky, A.; Lynch, R.C.; Britt, C.; Okada, Y.; Siarey, R.J.; Lensch, M.W.; Park, I.H.; Yoon, S.S.; Minami, T.; Korenberg, J.R.; Folkman, J.; Daley, G.Q.; Aird, W.C.; Galdzicki, Z.; Ryeom, S.
    Downs syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1 (2009), Nature, 459, 1126-1130.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.1.3.16

Inhibitors

Inhibitors Comment Organism Structure
DSCR1 a calcineurin inhibitor, encoded by gene Dscr1 on chromosome 21, is elevated in Down syndrome individuals. Increased dosage of Dyrk1A, appears to act in concert with Dscr1 to suppress tumor angiogenesis by further attenuating VEGF-calcineurin-NFAT signalling in endothelial cells, mechanism, overview. DSCR1-dependent inhibition of the VEGF-calcineurin-NFAT pathway in endothelial cells as a key component of the reduced cancer incidence in Down syndrome individuals Homo sapiens
DSCR1 a calcineurin inhibitor, encoded by gene Dscr1 on chromosome 21, is elevated in Down syndrome model mice Mus musculus

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
 individuals with Down syndrome
-
Mus musculus
-
 Down syndrome model Ts65Dn mice
-

Source Tissue

Source Tissue Comment Organism Textmining
endothelial cell
-
 Mus musculus
-
endothelial cell
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
calcineurin
-
 Mus musculus
calcineurin
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction DSCR1-dependent inhibition of the VEGF-calcineurin-NFAT pathway in endothelial cells as a key component of the reduced cancer incidence in Down syndrome individuals Homo sapiens
malfunction modest elevation in expression afforded by a single extra transgenic copy of Dscr1 is sufficient to confer significant suppression of tumor growth in mice and that such resistance is a consequence of a deficit in tumor angiogenesis arising from suppression of the calcineurin pathway. Attenuation of calcineurin activity by DSCR1 together with another chromosome 21 gene DYRK1A, may be sufficient to dramatically diminish angiogenesis Mus musculus