EC Number   |
General Information |
Reference |
|---|
   2.7.1.150 | malfunction |
a loss of enzyme function causes the release of late endosomal proteins, Ara7, and SNX1 from the endosome membrane. Downregulation of FAB1A/B or YM201636 inhibitor treatment affects the auxin distribution and and alteration of PIN2 localization in root cells. FAB1 knockdown causes relocation of the basal polarity of PIN2 in young root cortical cells |
739357 |
| 2.7.1.150 | malfunction |
CgFAB1 disruption impaires vacuole homeostasis and actin organization, and the F-actin stabilizing compound jasplakinolide rescues azole toxicity in cytoskeleton defective-mutants including the Cgfab1DELTA mutant. The actin depolymerization factor CgCof1 binds to multiple lipids including phosphatidylinositol 3,5-bisphosphate. CgCof1 distribution along with the actin filament-capping protein CgCap2 is altered upon both CgFAB1 disruption and fluconazole exposure. Actin polymerization inhibition renders fluconazole fully and partially fungicidal in azole-susceptible and azole-resistant Candida glabrata clinical isolates, respectively, thereby, underscoring the role of fluconazole-effectuated actin remodeling in azole resistance. MDR genes are activated in the Cgfab1DELTA mutant upon fluconazole exposure. Fluconazole-treated wild-type and Cgfab1DELTA cells display a 1.5fold increased efflux of the MDR pump substrate rhodamine 6G |
761922 |
| 2.7.1.150 | malfunction |
enzyme inhibition reduces contraction- and AICAriboside (5-amino-4-imidazolecarboxamide riboside)-stimulated glucose uptake. PIKfyve knockdown in C2C12 myotubes reduced AICAriboside-stimulated glucose transport |
737640 |
| 2.7.1.150 | malfunction |
loss of PPK-3, the Caenorhabditis elegans homologue of the PtdIns3P 5-kinase PIKfyve, causes accumulation of phagolysosomal vacuoles that are defective in phagocytic lysosome reformation (PLR). Loss of slc-36.1 and ppk-3 causes strong defects in autophagic lysosome reformation in adult animals. Ppk-3(n2668) strong loss-of-function mutants embryos contain many vacuolar structures of different sizes, a subset of which are positive for both LAAT-1::GFP and HIS-24::mCh, indicating that they are phagolysosomes. The double mutants of slc-36.1(yq110) with ppk-3(n2668) contain enlarged autolysosomes similar to ppk-3(n2668) single mutants |
761580 |
| 2.7.1.150 | malfunction |
Ste12PIKFYVE-deficient mutants are unable to advance the cell cycle to reduce cell size after a nitrogen downshift to poor nitrogen (proline) growth conditions. Ste12PIKFYVE mutants have enlarged vacuoles (yeast lysosomes), neither a block to autophagy or mutants that independently have enlarged vacuoles has any impact upon nitrogen control of mitotic commitment. The addition of rapamycin to Ste12PIKFYVE-deficient mutants reduces cell size at division to suggest that Ste12PIKFYVE possibly functions upstream of TORC1. Ste12 mutants display increased Torin1 (TOR inhibitor) sensitivity. No major impact on TORC1 or TORC2 activity is observed in the ste12-deficient mutants. Advancement of cell division is markedly compromised in ste12PIKFYVE.W1037STOP cells as a consequence of a reduction in the efficiency with which mitosis is advanced by the stress. Thus, ste12PIKFYVE-W1037STOP cells are deficient in their nitrogen stress response. Rapamycin rescues both the inability to advance mitosis and reduce cell size at division, suggesting that Ste12 may acts upstream of TORC1. ste12PIKFYVE-W1037STOP autophagy defect is unlikely to account for the inability to control size after nitrogen stress |
-, 762218 |
| 2.7.1.150 | malfunction |
the intracellular trafficking of pathogens, Zaire EBOV GP (VSV-MeGFPZEBOV) and SARS-CoV-2 S Wuhan-Hu-1 strain (VSV-eGFP-SARS-CoV-2), is elicited by inhibition of PIKfyve kinase via apilimod and vacuolin-1, small-molecule inhibitors of the main endosomal phosphatidylinositol-3-phosphate/phosphatidylinositol 5-kinase, PIKfyve |
762289 |
| 2.7.1.150 | malfunction |
the vacuolation phenotype in cultured Vps34 (EC 2.7.1.137)-deficient podocytes is caused by the absence of a substrate for the Vps34 downstream effector PtdIns 3-phosphate 5-kinase, which phosphorylates Vps34-generated 1-phosphatidyl-1D-myo-inositol 3-phosphate to produce + 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate. PtdIns 3-phosphate 5-kinase perturbation and 1-phosphatidyl-1D-myo-inositol 3,5-bisphosphate reduction result in massive membrane vacuolation along the endosomal system. Genetic deletion of the enzyme in endocytically active proximal tubular cells results in the development of large cytoplasmic vacuoles caused by arrested endocytic traffic progression at a late-endosome stage, while deletion of the enzyme in glomerular podocytes does not significantly alter the endosomal morphology, even in age 18-month-old mice |
738465 |
| 2.7.1.150 | metabolism |
amino acid transporter SLC-36.1 and PPK-3 function in the same genetic pathway, and they directly interact with one another. The SLC-36.1-PPK-3 axis is essential for autophagic lysosome reformation (ALR) |
761580 |
| 2.7.1.150 | more |
Gly867 and Gly1870 are required for the functioning of CgFab1 |
761922 |
| 2.7.1.150 | physiological function |
analysis of the intracellular trafficking of pathogens elicited by inhibition of PIKfyve kinase |
762289 |
