EC Number   |
Application |
Reference |
|---|
    6.3.2.2 | agriculture |
comparison of three transgenic poplar lines over-expressing the Escherichia coli gamma-glutamylcysteine synthetase. The three lines differ in their expression levels of the transgene and in the accumulation of gamma-glutamylcysteine and glutathione in leaves, roots and phloem exudates. The lowest transgene expression level is observed in line Lggs6 which shows an increased growth, an enhanced rate of photosynthesis and a decreased excitation pressure. Line Lggs12 shows the highest transgene expression level, highest gamma-glutamylcysteine accumulation in leaves and highest glutathione enrichment in phloem exudates and roots. This line also exhibits a reduced growth, and after a prolonged growth of 4.5 months, symptoms of leaf injury |
706163 |
| 6.3.2.2 | agriculture |
expression of GCS via agroinfection in the heavy metal intolerant grass Agrostis palustris. GCS and phytochelatin synthase are up-regulated in the transgenic lines. All the transgenic lines accumulate more Cd2+ and phytochelatins than the wild-type line, and three of five lines grow more effectively than the wild-type after either five or 21 days of Cd2+ stress. Variation among the transgenics is observed for the distribution of Cd2+ in the root, shoot and leaf. The malondialdehyde content of all the transgenic lines is lower than that of the wild type under Cd2+ treatment, while the activity of both superoxide dismutase and peroxidase present in the transgenic lines increases markedly 24 h after Cd2+ stress, and then rapidly declines |
706167 |
| 6.3.2.2 | agriculture |
transformation of GCS gene via agroinfection into the heavy metal intolerant grass Agrostis palustris results in upregulation of GCS and phytochelatin synthase in the transgenic lines. Transgenic lines accumulate more Cd2+ and phytochelatins than the wild-type line, and three of five lines grow more effectively than the wild-type after either five or 21 d of Cd2+ stress. Variation among the transgenics is observed for the distribution of Cd2+ in the root, shoot and leaf. The malondialdehyde content of all the transgenic lines is lower than that of the wild type under Cd2+ treatment, while the activity of both superoxide dismutase and peroxidase present in the transgenic lines increases markedly 24 h after Cd2+ stress, and then rapidly declines |
706167 |
| 6.3.2.2 | biotechnology |
a protein transduction approach whereby recombinant GCL protein can be rapidly and directly transferred into cells when coupled to the HIV TAT protein transduction domain. The TAT-GCL fusion proteins are capable of heterodimerization and formation of functional GCL holoenzyme in vitro. Exposure of Hepa-1c1c7 cells to the TAT-GCL fusion proteins results in the time- and dose-dependent transduction of both GCL subunits and increased cellular GCL activity and glutathione levels. A heterodimerization-competent, enzymatically deficient GCLC-TAT mutant was also generated in an attempt to create a dominant-negative suppressor of GCL |
706829 |
| 6.3.2.2 | drug development |
the enzyme is a target for development of specific enzyme inhibitors in the treatment of ancylostomiasis |
745734 |
| 6.3.2.2 | medicine |
activation of glycogen synthase kinase 3beta is a key mediator of the initial phase of acetaminophen-induced liver injury through modulating GCL and Mcl-1 degradation, as well as JNK activation in liver. The silencing of glycogen synthase kinase 3beta decreases the loss of hepatic GCL, and promotes greater GSH recovery in liver following acetaminophen treatment |
704707 |
| 6.3.2.2 | medicine |
enzyme inhibitor L-buthionine-S-sulfoximine is used to modulate GSH levels in cancer patients, overview |
649263 |
| 6.3.2.2 | medicine |
gamma-GCS gene is the downstream target of c-Myc oncoprotein, driving the response to ROS-inducing drugs. gamma-GCS impairment might specifically sensitize high c-Myc tumor cells to chemotherapy |
676099 |
| 6.3.2.2 | medicine |
mice lacking the glutamate-cysteine ligase modifier subunit are susceptible to myocardial ischaemia-reperfusion injury partly through an increased vulnerability of mitochondria to oxidative damage owing to mitochondrial glutathione reduction |
703091 |
| 6.3.2.2 | medicine |
model to explain adenosine triphosphate depletion during cystinosis. In the absence of cysteine, enzyme gamma-glutamyl cysteine synthetase forms 5-oxoproline, and the 5-oxoproline is converted into glutamate by the ATP-dependant enzyme, 5-oxoprolinase. Thus, in cysteine-limiting conditions, glutamate is cycled back into glutamate via 5-oxoproline at the cost of two ATP molecules without production of glutathione and this is the cause of the decreased levels of glutathione synthesis, as well as the ATP depletion observed in these cells. The model is also compatible with the differences seen in the human patients and the mouse model of cystinosis, where renal failure is not observed |
704751 |
