EC Number |
General Information |
Reference |
---|
3.1.4.11 | malfunction |
inhibition of PI-PLC in vivo resultes in rapid upregulation of PtdIns(4,5)P2 levels |
714877 |
3.1.4.11 | malfunction |
isoforms of PI-PLC family display different expression and/or sub cellular distribution under non-physiological conditions such as the rat astrocytes activation during neurodegeneration, the tumoural progression of some neoplasms and the inflammatory cascade activation after lipopolysaccharide administration. PI-PLC beta3 and PI-PLC gamma2 isoforms, whose expression and sub cellular localization significantly differ after U73122 inhibitor treatment |
715713 |
3.1.4.11 | malfunction |
lack of isoform PI-PLCbeta1 is linked to myelodysplastic syndrome progression toward acute myeloid leukemia. Loss of both PI-PLCbeta2 and PI-PLCbeta3 isozymes is associated with an impaired T-cell migration that is caused by an inability to increase the intracellular calcium. Isoform PI-PLCbeta 2 downregulation plays an important role in M1-M2 macrophage differentiation, whereas PI-PLCbeta3 activity is essential for promoting macrophage survival, especially in atherosclerotic plaques. Isoform PI-PLCbeta3 deficiency is also linked to the development of myeloproliferative neoplasm |
751272 |
3.1.4.11 | malfunction |
loss of enzyme function renders rice plants salt sensitive |
751706 |
3.1.4.11 | malfunction |
phosphoinositide-specific phospholipase C 4 mutant seedlings are hyposensitive to salt stress |
751845 |
3.1.4.11 | malfunction |
PLC isozymes are involved in several diseases, detailed overview |
716810 |
3.1.4.11 | malfunction |
plc2 mutants display multiple auxin-defective phenotypes in root development, including short primary root, impaired root gravitropism, and inhibited root hair growth |
751847 |
3.1.4.11 | malfunction |
possible involvement of the interstitial deletion of PLCbeta1 gene in the progression of myelodysplastic syndrome to acute myeloid leukemia in humans |
716113 |
3.1.4.11 | malfunction |
silencing of PLC4 impairs the race-specific effector Avr4 from the pathogenic fungus Cladosporium fulvum/Cladosporium fulvum-resistant Cf-4 tomato-induced hypersensitive response and results in increased colonisation of Cladosporium fulvum-resistant Cf-4 plants by Cladosporium fulvum expressing Avr4. Silencing of PLC6 does not affect hypersensitive response, whereas it causes increased colonisation of Cf-4 plants by the fungus |
710285 |
3.1.4.11 | metabolism |
the enzyme specifically binds to phosphatidylcholine and cleaves glycosylphosphatidylinositol-anchored proteins of eukaryotic plasma membranes |
750911 |