Aliases for TNKS Gene
External Ids for TNKS Gene
GeneCards Summary for TNKS Gene
TNKS (Tankyrase, TRF1-Interacting Ankyrin-Related ADP-Ribose Polymerase) is a Protein Coding gene. Diseases associated with TNKS include cerebral atherosclerosis and diphtheria. Among its related pathways are Apoptotic Pathways in Synovial Fibroblasts and Nicotinate and nicotinamide metabolism. GO annotations related to this gene include NAD+ ADP-ribosyltransferase activity. An important paralog of this gene is ANKRD52.
UniProtKB/Swiss-Prot for TNKS Gene
Poly-ADP-ribosyltransferase involved in various processes such as Wnt signaling pathway, telomere length and vesicle trafficking. Acts as an activator of the Wnt signaling pathway by mediating poly-ADP-ribosylation (PARsylation) of AXIN1 and AXIN2, 2 key components of the beta-catenin destruction complex: poly-ADP-ribosylated target proteins are recognized by RNF146, which mediates their ubiquitination and subsequent degradation. Also mediates PARsylation of BLZF1 and CASC3, followed by recruitment of RNF146 and subsequent ubiquitination. Mediates PARsylation of TERF1, thereby contributing to the regulation of telomere length. Involved in centrosome maturation during prometaphase by mediating PARsylation of HEPACAM2/MIKI. May also regulate vesicle trafficking and modulate the subcellular distribution of SLC2A4/GLUT4-vesicles. May be involved in spindle pole assembly through PARsylation of NUMA1. Stimulates 26S proteasome activity.
Tankyrases 1 and 2 (TNKS1/PARP5A and TNKS2/PARP5B/PARP5C) are proteins with poly(ADP-ribose) polymerase activity. Human tankyrases post-translationally modify multiple proteins involved in processes including maintenance of telomere length, sister telomere association, insulin responsiveness, spindle assembly and trafficking of glut4-containing vesicles. Recently tankyrases have been shown be involved in the wnt signaling pathway. Tankyrases bind directly to axin, a member of the destruction complex involved in beta-catenin degradation. Inhibition of tankyrase stabilizes axin, increases the activity of the destruction complex and promotes degradation of beta-catenin. Tankyrases are therefore an attractive target anticancer therapies.