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                        MYC Diagnostic Standard
                        2020-12-08 [1324]

                        MYC proteins include c-MYC, MYCL and MYCN, which encode c-Myc, N-Myc and L-Myc, respectively. Myc protein belongs to the "super transcription factor" family, which may regulate at least 15% of the transcription of the entire genome. There are many main downstream effectors of Myc, which are involved in regulating ribosomal biosynthesis, protein translation, cell cycle and metabolism, and coordinate various biological functions, such as cell proliferation, differentiation, survival and immune surveillance. It plays an important role in tumorigenesis and resistance therapy. Several oncogenic signaling pathways, such as Wnt, Ras and phosphatidylinositol 3-kinase/Akt, may mediate their tumor-promoting effects through MYC. MYC heterodimer and MAX bind to a consensus sequence DNA element, E-box and regulating downstream target genes are involved in proliferation, differentiation, cell cycle progression, metabolism, apoptosis and angiogenesis. Silencing MYC expression in multiple tumor models can lead to tumor regression associated with tumor microenvironment remodeling. MYC is considered to be the most attractive cancer treatment target.




                        MYC family oncogenes are dysregulated in more than 50% of human cancers, and this dysregulation is often associated with poor prognosis and unfavorable patient survival. Myc plays a key role in almost every aspect of the carcinogenic process, coordinating proliferation, apoptosis, differentiation and metabolism.


                        Under normal circumstances, the expression of Myc family members is strictly controlled. However, in cancer, Myc is often out of control. Various factors can induce the overexpression of Myc, such as retroviral promoter insertion, chromosome translocation/amplification, activation of super enhancer in Myc gene, and enhancement of Myc stability. Mutations in sexual upstream signaling pathways, etc. Studies on transgenic mouse models have shown that Myc inactivation can trigger tumor regression, indicating that the regulation of oncogenic Myc can be used to treat cancer.


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                        We can provide diagnostic standards for multiple types of MYC mutations to ensure the detection limit, sensitivity and stability of the diagnostic method.





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