EC Number   |
General Information |
Reference |
|---|
   6.3.2.61 | malfunction |
along with the loss of axonemal curvature, the axonemes and tracheal epithelial cilia from enzyme knockout mice lose beating asymmetry which results in a reduction of cilia-generated fluid flow in trachea from the knockout mice. The mice display a significant accumulation of mucus in the nasal cavity, and also emit frequent coughing- or sneezing-like noises |
763639 |
| 6.3.2.61 | malfunction |
deletion of isoform TTLL1 prevents degeneration of Purkinje cells and of myelinated axons in peripheral nerves ine mice lacking the deglutamylase CCP1. Moreover, loss of TTLL1 leads to increased mitochondria motility in neurons |
762971 |
| 6.3.2.61 | malfunction |
disruption of the TTLL1 and TTLL9 genes decreases the rates of cell multiplication and phagocytosis. Cells lacking both genes had fewer cortical microtubules and show defects in the maturation of basal bodies |
-, 750454 |
| 6.3.2.61 | malfunction |
disruption of the TTLL1 and TTLL9 genes decreases the rates of cell multiplication and phagocytosis. Cells lacking both genes have fewer cortical microtubules and show defects in the maturation of basal bodies |
-, 750454 |
| 6.3.2.61 | malfunction |
isoform TTLL5 mutant flies are viable without any defect in vesicular axonal transport, synapse morphology and larval locomotion. Moreover, isoform TTLL5 mutant flies display normal negative geotaxis behavior and their lifespan is not altered |
763711 |
| 6.3.2.61 | malfunction |
knockdown of ttll6 strongly reduces cilia tubulin glutamylation but only partially affects cilia structure and motility. Combined loss of function of ttll3 and ttll6 causes near complete loss of cilia motility and induced a variety of axonemal ultrastructural defects |
751028 |
| 6.3.2.61 | malfunction |
loss of the tubulin polyglutamylase complex leads to aberrant, enhanced assembly of microtubules that penetrate the nucleus, which in turn leads to defects in nuclear shape, and disorganization of cytoplasmic actin that disrupts the YAP/TAZ pathway and cilium disassembly |
762893 |
| 6.3.2.61 | physiological function |
enzyme-mediated ubulin polyglutamylation is essential for airway ciliary function through the regulation of beating asymmetry |
763639 |
| 6.3.2.61 | physiological function |
enzyme-meditated glutamylation of tubulin directly stimulates spastin-mediated severing of microtubules |
763301 |
| 6.3.2.61 | physiological function |
glutamylation on alpha-tubulin is not essential but is required for efficiency of assembly and function of a subset of microtubule-based organelles. Furthermore, the spatial restriction of modifying enzymes (TTLL1 and TTLL9) appears to be a major mechanism that drives differential glutamylation at the subcellular level |
-, 750454 |
