EC Number   |
General Information |
Reference |
|---|
   3.1.1.32 | evolution |
evolutionary relationship and phylogenetics of isozymes Ves a 1.01-1.04, overview |
731003 |
| 3.1.1.32 | evolution |
mechanisms of activation of the ExoU family of PLAs may be evolutionarily conserved |
715386 |
| 3.1.1.32 | evolution |
the enzyme is a member of the pancreatic lipase family |
729305 |
| 3.1.1.32 | malfunction |
Because orientation of seam cell division is randomized relative to the A-P axis in ipla-1 mutants, ipla-1 mutants exhibit aberrant orientation of seam cell divisions. Acl-8 acl-9 acl-10 triple mutations also cause misorientation of seam cell divisions similar to that observed in ipla-1 mutants |
716165 |
| 3.1.1.32 | malfunction |
in enzyme mutants, in the absence of transport to the Golgi, rhodopsin 1 is aberrantly glycosylated and is mislocalized. These defects lead to decreased levels of the protein and decreased sensitivity of the photoreceptors to light. Several GPCRs, including other rhodopsins and Bride of sevenless, are similarly affected, phenotypes, overview |
730100 |
| 3.1.1.32 | malfunction |
knockdown of intracellular PLA1gamma expression by RNAi does not affect the anterograde transport of ts045 vesicular stomatitis virus protein (VSVGts045) but dramatically delays two types of Golgi-to-endoplasmic reticulum retrograde membrane transport, i.e., transfer of the Golgi membrane into the endoplasmic reticulum in the presence of brefeldin A and delivery of cholera toxin B subunit from the Golgi complex to the endoplasmic reticulum. Knockdown of intracellular PLA1gamma does not impair coat protein complex I- and Rab6-dependent retrograde transports represented by ERGIC-53 recycling and endoplasmic reticulum delivery of Shiga toxin, respectively |
709054 |
| 3.1.1.32 | malfunction |
phosphatidic acid-preferring phospholipase A1 depletion causes mitochondrial elongation, leading to a loss of motility |
730037 |
| 3.1.1.32 | malfunction |
phosphatidic acid-preferring phospholipase A1 depletion causes mitochondrial elongation. Enzyme knock-out mice have a defect in sperm formation, spermatozoa from PA-PLA1-/- mice possess an annulus that is not attached to the mitochondrial sheath, whereas that in control mice is attached. In enzyme-deficient sperm, the mitochondrial structure is disorganized, and an abnormal gap structure exists between the middle and principal pieces.A flagellum is bent at that position, leading to a loss of motility |
730037 |
| 3.1.1.32 | metabolism |
intracellular phospholipase A1 and acyltransferase are involved in Caenorhabditis elegans stem cell divisions |
716165 |
| 3.1.1.32 | more |
residue Ser11 is essential for the catalytic function of the enzyme, the active site may include residues Ser216 and His218 |
-, 729743 |
