EC Number   |
General Information |
Reference |
|---|
   3.6.4.6 | evolution |
enzyme SKD1 belongs to the AAA ATPase family |
734975 |
| 3.6.4.6 | evolution |
enzyme vacuolar protein sorting 4, Vps4, belongs to the AAA ATPases. Vps4 forms a hexameric complex that disassembles ESCRT-III, allowing recycling of its components, and also plays an active role in scission of the vesicle neck. Vps4 is required for epidermal growth factor receptor signaling even in the absence of Shibire, the Dynamin that internalizes epidermal growth factor receptor from the plasma membrane. In ovarian follicle cells, in contrast, Vps4 does not affect epidermal growth factor receptor signaling, although it is still essential for receptor degradation, Vps4 is not required for EGFR or Notch signaling in follicle cells. Enzyme Vps4 can promote epidermal growth factor receptor activity through an endocytosis-independent mechanism, a non-endocytic and cell type-dependent mechanism. Protein Vps4 is the only energy-utilizing ESCRT component |
733702 |
| 3.6.4.6 | evolution |
human and Dictyostelium p97 share 81% identity and 89% similarity on the amino acid sequence level and have an almost identical order and composition of secondary structure elements |
756637 |
| 3.6.4.6 | evolution |
the enzyme Vps4 belongs to the type I AAA ATPases |
734303 |
| 3.6.4.6 | malfunction |
deletion of Vps4p in yeast leads to the formation of crescent-like membrane structures instead of the characteristic spherule and vesicle-like structures |
-, 735147 |
| 3.6.4.6 | malfunction |
heterozygous missense mutations of p97 cause at least five human neurodegenerative disorders, i.e. R93C, R155H, and R155C mutations. All human p97 mutations lead to an increase in ATPase activity. p97 point mutations lead to differences in enzymatic activities and molecular interactions, which in the long-term result in a late-onset and progressive multisystem disease |
756637 |
| 3.6.4.6 | malfunction |
inhibition of p97, but not NSF ATPase can be associated with ER/Golgi disruption and apoptosis in alphaSNAP-depleted epithelial cells. AlphaSNAP knockdown does not affect p97 expression, it perturbes a balance between key p97-binding partners. Specifically, expression of syntaxins 5 and 18 are significantly decreased |
720048 |
| 3.6.4.6 | malfunction |
p97 point mutations lead to differences in enzymatic activities and molecularinteractions, which in the long-term result in a late-onset and progressive multisystem disease |
756637 |
| 3.6.4.6 | malfunction |
photoreceptors are largely absent from Vps4 mutant clones in the eye disc, the resulting mutant R8 photoreceptors fail to recruit surrounding cells to differentiate as R1-R7 photoreceptors. Loss of Vps4 disrupts the epidermal growth factor receptor, EGFR, pathway. In imaginal disc cells deficient for enzyme Vps4, EGFR and other receptors accumulate in endosomes, and EGFR target genes are not expressed |
733702 |
| 3.6.4.6 | malfunction |
subunit Atp6v0d2-deficient macrophages have augmented mitochondrial damage, enhanced inflammasome activation and reduced clearance of Salmonella typhimurium |
755920 |
