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ME2 was involved in glioblastoma multiforme growth, invasion, migration, Reactive oxygen species and ATP production.
The chromosome 18q21 deletion in nearly one third of pancreatic adenocarcinomas eliminates not only the tumor suppressor SMAD4, but also neighboring genes with important cellular roles, such as ME2
deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
ME1/ME2 expression phenotype may have a potential to be a valuable marker for sebaceous differentiation in sebaceous lesions.
Data indicate that malic enzyme 2 knockdown impacts phosphatidylinositol 3-kinases/proto-oncogene protein akt (PI3K/AKT) signaling.
ME2 might be an important factor in melanoma progression and a novel biomarker of invasion.
Three SNP alleles in BRD2, Cx-36, and ME2 and microdeletions in 15q13.3, 15q11.2, and 16p13.11 also contribute risk to juvenile myclonic epilepsy.
p53 represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 and ME2 in human and mouse cells
Depletion of malic enzyme 2 induced erythroid differentiation in human erythroleukemia cells.
An ME2-centered nine-SNP haplotype, when present homozygously, increases the risk for IGE (odds ratio 6.1; 95% confidence interval 2.9-12.7) compared with any other genotype
Site directed mutagenesis was used to detrmine which amino acids in the active site of human mitochondrial NAD+-dependent malic enzyme are necessary for the inhibitory effects of ATP.
These findings provide a molecular rationale for the role of hS14 in TR-dependent transcriptional activation of the expression of specific genes.
Schizophrenic subjects are identified with mitochondrial genes involved in oxidative metabolism as showing consistently decreased expression, including ME2.
Single nucleotide polymorphism in ME2 gene is associated with acute lymphoblastic leukemia.
ME2 activity in Islets of Langerhans cells was measured by a spectrophotometric enzyme assay by utilizing the distinct kinetic properties.
Me2 activity in Islet of Langerhans cells was measured by a spectrophotometric enzyme assay by utilizing the distinct kinetic properties of Me2.
This gene encodes a mitochondrial NAD-dependent malic enzyme, a homotetrameric protein, that catalyzes the oxidative decarboxylation of malate to pyruvate. It had previously been weakly linked to a syndrome known as Friedreich ataxia that has since been shown to be the result of mutation in a completely different gene. Certain single-nucleotide polymorphism haplotypes of this gene have been shown to increase the risk for idiopathic generalized epilepsy. Alternatively spliced transcript variants encoding different isoforms found for this gene.
, NAD-dependent malic enzyme, mitochondrial
, malate dehydrogenase
, pyruvic-malic carboxylase
, malic enzyme 2