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results shed light on crucial roles of ME1-mediated production of NADPH in gastric cancer growth and metastasis
Bioinformatics analysis identified that miR612 targeted ME1, which expression was high and inversely associated with miR612 expression in bladder cancer tissues.
Findings indicate that malic enzyme 1 (ME1) is a valid target for molecular therapy in oral squamous cell carcinomas (OSCCs).
The critical roles of miR-30a and ME1 in the development of KRAS-mutant colorectal cancer indicate therapy potentials for this subtype of cancer.
these findings uncover a direct cross-talk mechanism between ME1 and PPP, may reveal an alternative model for signaling transduction via protein conformational simulation, and pave the way for better understanding how metabolic pathways are coordinated in cancer.
ME1/ME2 expression phenotype may have a potential to be a valuable marker for sebaceous differentiation in sebaceous lesions.
ME1 expression was found to be mutant-KRAS-associated in NSCLC cancer cell lines. Patients with elevated ME1 had worse outcomes after radiotherapy. Transamination generating cytosolic NADPH via ME1 may contribute to radioresistance.
ME1 overexpression associates with unfavorable prognoses in patients with HCC, suggesting that ME1 is a poor prognostic predictor of hepatocellular carcinoma.
essential role for ME1 in the production of cytosolic NADPH and maintenance of migratory and invasive abilities of nasopharyngeal carcinoma cells
the differential protein stability between dimer and tetramer interface interactions of human c-NADP-ME
p53 represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 and ME2 in human and mouse cells
cytosolic malic enzyme 1 gene polymorphism is associated with the degree of suppression of parathyroid hormone after long-term calcium supplementation; the effect is probably mediated through an increase in intestinal calcium absorption
ME1 is a functional target gene of the BACH1 transcription factor according to ChIP-seq and knockdown analysis in HEK 293 cells.
that the single mutation of Gln362 to Lys in human m-NAD-ME changes it to an NADP+-dependent enzyme, which is characteristic because it is non-allosteric, non-cooperative, and NADP+-specific
although ME1 overexpression augments anaplerosis and glucose stimulated insulin secretion in INS-1 832/13 cells, it is not likely involved in methyl succinate and glucose stimulated insulin secretion in pancreatic islets
human c-NADP-ME exists mainly as a tetramer, whereas human m-NAD(P)-ME exists as a mixture of dimers and tetramers
A series of R98/D102 mutants examined the possible interactions between Arg98 and Asp102 using double-mutant cycle analysis. Kinetic analysis revealed that the catalytic efficiency of was severely affected by mutating both Arg98 and Asp102 residues.
Data suggest that Ad4BP plays role in regulation of intracellular NADPH concentration via transcription of Me1 and Mthfd2 genes in adrenocortical cells. (Ad4BP = nuclear receptor subfamily 5 group A member 1; Me1 = malic enzyme 1; Mthfd2 = bifunctional methylenetetrahydrofolate dehydrogenase/cyclohydrolase)
This study showed that (2)H-labeled tracers enable dissection of NADPH production routes across cell types and environmental conditions.
ME1 expression was found to be mutant-KRAS-associated in an NSCLC mouse model.
cytosolic or mitochondrial isoforms of malic enzyme do not affect glucose-stimulated insulin secretion from rodent islets
This lack of consistency across families, combined with the fact that the ME1 mutation is synonymous and that the two DECR1 polymorphisms are conservative, suggests that the associations found are not causative.
Transcript level of the porcine ME1 gene is affected by SNP in its 3'UTR, which is also associated with subcutaneous fat thickness.
Malic enzyme 1 genotype is associated with backfat thickness and meat quality traits in pigs.
Six novel SNPs, five in ME1 and one in NR0B2, were identified as candidates that have effects on meat and carcass quality traits.
ME1-Dra I genotypes had a significant effect on cooking loss.
This gene encodes a cytosolic, NADP-dependent enzyme that generates NADPH for fatty acid biosynthesis. The activity of this enzyme, the reversible oxidative decarboxylation of malate, links the glycolytic and citric acid cycles. The regulation of expression for this gene is complex. Increased expression can result from elevated levels of thyroid hormones or by higher proportions of carbohydrates in the diet.
Malic enzyme, cytoplasmic
, NADP-dependent malic enzyme
, malate dehydrogenase
, malic enzyme 1, soluble
, pyruvic-malic carboxylase
, malic enzyme, supernatant
, cytosolic malic enzyme 1
, malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+)
, malate dehydrogenase decarboxylase (NADP+)
, malic enzyme 1, NADP(+)-dependent, cytoplasmic (cytosolic, soluble)
, malic enzyme 1, NADP(+)-dependent, cytosolic
, cytosolic malic enzyme 1-like
, NADP-dependent malic enzyme-like