There is no specific curative therapy for this disease
DNMT1 DNA Methyltransferase 1 DNMT3B DNA Methyltransferase 3B PRC2 Polycomb Repressive Complex 2 EZH2 Enhancer of Zeste 2 EED Embryonic Ectoderm Development IL-1b Interleukin-1 Beta IL6 Interleukin 6 EWAS Epigenome-Wide Association Study GPR56 G Protein-Coupled Receptor 56 5-aza-cytidine 5-Azacytidine RG108 A DNA Methyltransferase Inhibitor PD Parkinsons Disease SNCA Synuclein Alpha PARK7 Parkin 7 DJ-1 Parkinsonism Associated Deglycase SLC7A11 Solute Carrier Family 7 Member 11 HOTAIR HOX Transcript Antisense RNA SLC17A6 Solute Carrier Family 17 Member 6 PTPRN2 Protein Tyrosine Phosphatase Receptor Type N2 NR4A2 Nuclear Receptor Subfamily 4 Group A Member 2 PGC1-a Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha FXS Fragile X Syndrome FMR1 Fragile X Mental Retardation 1 CRISPR/Cas9 Clustered Regularly Interspaced Short Palindromic Repeats/Cas9 RRBS Reduced Representation Bisulfite Sequencing AP-1 Activator Protein 1 SOX2 SRY-Box Transcription Factor 2 5-hmC 5-Hydroxymethylcytosine YAC128 Yeast Artificial Chromosome 128 DhMRs Disease-Specific Hydroxymethylation Regions cfDNA Cell-Free DNA DMP Differentially Methylated Probes DMR Differentially Methylated Regions qPCR Quantitative Polymerase Chain Reaction References 1 WisselBDDwivediAKMerolaAChinDJacobCDukerAPet al
Georgia : Atlanta
Mokhtari, E., Rafiei, S., Shokri-Mashhadi, N., & Saneei, P
GLS inhibition does show some selectivity in the viability of mutant cell lines at the tested concentrations, particularly in G12A and G12D cells (Fig
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