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Human Polyclonal NAD-ME Primary Antibody pour ICC, IF - ABIN4333385
Tsuyuguchi, Kawasumi, Takashima, Tsuyuguchi, Kishimoto: Mycobacterium avium-Mycobacterium intracellular complex-induced suppression of T-cell proliferation in vitro by regulation of monocyte accessory cell activity. dans Infection and immunity 1990
Show all 4 Pubmed References
ME2 (Montrer CELSR1 Anticorps) 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 Anticorps), but also neighboring genes with important cellular roles, such as ME2 (Montrer CELSR1 Anticorps)
deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
ME1 (Montrer ME1 Anticorps)/ME2 (Montrer CELSR1 Anticorps) 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 Anticorps) protein akt (Montrer AKT1 Anticorps) (PI3K (Montrer PIK3CA Anticorps)/AKT (Montrer AKT1 Anticorps)) signaling.
ME2 (Montrer CELSR1 Anticorps) might be an important factor in melanoma progression and a novel biomarker of invasion.
Three SNP alleles in BRD2 (Montrer BRD2 Anticorps), Cx-36 (Montrer GJD2 Anticorps), and ME2 (Montrer CELSR1 Anticorps) and microdeletions in 15q13.3, 15q11.2, and 16p13.11 also contribute risk to juvenile myclonic epilepsy.
p53 (Montrer TP53 Anticorps) represses the expression of the tricarboxylic-acid-cycle-associated malic enzymes ME1 (Montrer ME1 Anticorps) and ME2 (Montrer CELSR1 Anticorps) 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
Mechanistic analysis indicated that E47 (Montrer TCF3 Anticorps) activated expression of the transcription factor Spi-B (Montrer SPIB Anticorps) and the suppressor of cytokine signaling 3 (SOCS3 (Montrer SOCS3 Anticorps)), which both downregulated Foxp3 (Montrer FOXP3 Anticorps) expression. These findings demonstrate that the balance of Id3 (Montrer ID3 Anticorps) and E47 (Montrer TCF3 Anticorps) controls the maintenance of Foxp3 (Montrer FOXP3 Anticorps) expression in Treg cells and, thus, contributes to Treg cell plasticity.
this study identifies E2A (Montrer TCF3 Anticorps) target genes in embryonic neural stem cells and demonstrates that E47 (Montrer TCF3 Anticorps) regulates neuronal differentiation via p57(KIP2 (Montrer CDKN1C Anticorps)).
If Gfi1 (Montrer ZNF163 Anticorps) levels fall below a threshold, Id1 (Montrer ID1 Anticorps) expression increases and renders E2A (Montrer TCF3 Anticorps) unable to function, which prevents hematopoietic progenitors from engaging along the B lymphoid lineage
these data identified E2A (Montrer TCF3 Anticorps) and E2-2 (Montrer TCF4 Anticorps) as central regulators of B cell immunity.
down-regulation of Id3 (Montrer ID3 Anticorps) in B cells is essential for releasing E2A (Montrer TCF3 Anticorps) and E2-2 (Montrer TCF4 Anticorps), which in a redundant manner are required for antigen-induced B cell differentiation.
Data suggest a novel mechanism of drug resistance in which E2a (Montrer TCF3 Anticorps) and PRC2 drive changes in the B-cell epigenome; these alterations attenuate alkylating agent treatment-induced apoptosis.
These findings suggest that miR (Montrer MLXIP Anticorps)-506-3p played an important role in regulating NSC proliferation and differentiation via targeting TCF3 (Montrer TCF7L1 Anticorps), and provide a promising avenue for future in-depth research into the functions of miR (Montrer MLXIP Anticorps)-506-3p and TCF3 (Montrer TCF7L1 Anticorps) in nervous system development.
Conditional expression of E2A (Montrer TCF3 Anticorps)-HLF (Montrer HLF Anticorps) induces B-cell precursor death and myeloproliferative-like disease in knock-in mice.
Upregulation of E12/E47 by HBx ultimately and concomitant repression of E-cadherin (Montrer CDH1 Anticorps) expression led to epithelial-mesenchymal transition in human hepatocytes.
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
, immunoglobulin enhancer-binding factor E12/E47
, transcription factor A1
, transcription factor E2-alpha
, transcription factor E2a