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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 (Montrer SMAD4 Protéines), but also neighboring genes with important cellular roles, such as ME2
deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
ME1 (Montrer ME1 Protéines)/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 (Montrer RAB1A Protéines) protein akt (Montrer AKT1 Protéines) (PI3K (Montrer PIK3CA Protéines)/AKT (Montrer AKT1 Protéines)) signaling.
ME2 might be an important factor in melanoma progression and a novel biomarker of invasion.
Three SNP alleles in BRD2 (Montrer BRD2 Protéines), Cx-36 (Montrer GJD2 Protéines), and ME2 and microdeletions in 15q13.3, 15q11.2, and 16p13.11 also contribute risk to juvenile myclonic epilepsy.
p53 (Montrer TP53 Protéines) represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 (Montrer ME1 Protéines) 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
p53 (Montrer TP53 Protéines) represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 (Montrer ME1 Protéines) and ME2 (Montrer TCF4 Protéines) in human and mouse cells
Me2 (Montrer TCF4 Protéines) activity in Islet of Langerhans cells was measured by a spectrophotometric enzyme assay by utilizing the distinct kinetic properties of Me2 (Montrer TCF4 Protéines).
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