expression profile of the enzyme in cancer cell lines, overview. Splice variant ek2beta exhibits a markedly low mRNA transcript level in all three of the cancer cell lines
expression profile of the enzyme in cancer cell lines, overview. Splice variant ek2beta exhibits a markedly low mRNA transcript level in all three of the cancer cell lines
human ethanolamine kinase exists as three isoforms: EK1, EK2alpha and EK2beta, encoded by two separate genes; ek1, which produces the ek1 transcript variant 1, and ek2, which undergoes alternative splicing to produce ek2alpha (NCBI reference: NM_018208.2) and ek2beta (GenBank reference: AK001623.1) transcript variants. ek2alpha and ek2beta are respectively translated into EK2alpha and EK2beta
choline kinase and ethanolamine kinase are enzymes that initiate the first step in the Kennedy pathway, resulting in the biosynthesis of phosphatidylcholine and phosphatidylethanolamine. Expression profiling of ethanolamine kinase in MCF-7, HCT-116 and Hep-G2 cells, and the transcriptional regulation by epigenetic modification
splicing variant ek2beta exhibits a markedly low mRNA transcript level in all three of the cancer cell lines examined, thus suggesting that transcription of the ek2beta gene may be negligible and this isoform may not have a significant role in phosphatidyletanolamine synthesis in the three cancer cell lines
human ethanolamine kinase exists as three isoforms: EK1, EK2alpha and EK2beta, encoded by two separate genes; ek1, which produces the ek1 transcript variant 1, and ek2, which undergoes alternative splicing to produce ek2alpha (NCBI reference: NM_018208.2) and ek2beta (GenBank reference: AK001623.1) transcript variants. ek2alpha and ek2beta are respectively translated into EK2alpha and EK2beta
somatic enzyme mutations targeted to two contiguous amino acids in the ETNK1 kinase domain are involved in systemic mastocytosis with eosinophilia and chronic myelomonocytic leukemia, phenotypes, overview
choline kinase and ethanolamine kinase are enzymes that initiate the first step in the Kennedy pathway, resulting in the biosynthesis of phosphatidylcholine and phosphatidylethanolamine. Expression profiling of ethanolamine kinase in MCF-7, HCT-116 and Hep-G2 cells, and the transcriptional regulation by epigenetic modification
gene eki1, a Sp site at position (-40/-31) is essential for the basal transcription of this gene, quantitative real-time PCR transcription analysis of ek1 mRNA, Identification of important regulatory regions in the ek1 gene promoter by analysis of 4 promoter constructs, trichostatin A activates basal ek1 promoter activity via Sp(-40/-31) site
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EXPRESSION
ORGANISM
UNIPROT
LITERATURE
substantial induction of splicing variant ek2alpha mRNA expression in response to trichostatin A treatment in Hep-G2 cells, the elevated ek2alpha mRNA expression may be due to the accumulation of acetylated histones H3 and H4, located around the promoter regions. Trichostatin A may also induce the recruitment of euchromatic markers and RNA polymerase II to the transcription factor complex that binds to the promoter, thus facilitating gene transcription
treatment of HCT-116 cells with trichostatin A (TSA), a histone deacetylase inhibitor, significantly upregulates the eki1 promoter activity through the Sp(-40/-31) site and increases the endogenous expression of gene eki1. Trichostatin A increases the binding of Sp1, Sp3 and RNA polymerase II to the ek1 promoter in HCT116 cells, molecular mechanism, overview. The effect of TSA on ek1 promoter activity is cell-line specific as TSA treatment does not affect ek1 promoter activity in Hep-G2 cells
Expression profiling of choline and ethanolamine kinases in MCF7, HCT116 and HepG2 cells, and the transcriptional regulation by epigenetic modification