Examples of using C-myc in English and their translations into Chinese
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This“oncoprotein” is called c-MYC.
Again, c-Myc seems to be the key to I-BET-762's success.
This"oncoprotein" is called c-MYC.
C-myc as a novel fetal DNA epigenetic marker for pre-eclampsia.
But until now,the drugs hadn't been tested on a live C-MYC model.
The cancer-causing gene c-Myc paradoxically activates both cell proliferation and death.
The scientists also found that these proteins activate c-Myc(a well-known cancer gene), and it.
Using mice, Oliver's team created the first known replica of asmall cell tumor subgroup called C-MYC.
When the cell becomes cancerous, c-Myc- induced death is bypassed, promoting tumor formation.
SRT 2183 induces growth arrest and apoptosis, concomitant with deacetylation of STAT3 and NF-κB,and reduction of c-Myc protein levels.
Epigenetic mechanisms regulate placental c-myc and hTERT in normal and pathological pregnancies;
Nudging c-Myc in one direction or the other could make vaccines more effective or advance immunotherapies for cancer treatment.
Known messy proteins that can promote cancer- including c-myc, p53 and K-RAS- have proven elusive.
The biological function of c-MYC is to regulate the expression of over 15 percent of all the genes of the human body.
Well-known disordered proteins that can contribute to cancer- including c-Myc, p53 and K-RAS- have proved too elusive.
Now that we know the mechanism by which c-Myc acts, we can go after the components of that mechanism as potential drug targets.
Well-known disordered proteinsthat can contribute to cancer--including c-Myc, p53 and K-RAS--have proved too elusive.
But in cancer cells in which c-Myc is overproduced, this suicide pathway is compromised, allowing the cell to survive and proliferate.
Large-scale screening tests to evaluate thousands of drug candidates fortherapeutic potential have revealed several that inhibit c-Myc, and some are moving toward clinical development.
It turns out that high levels of c-Myc send a tumor cell's gene expression program into overdrive.
The scientists also found that these proteins activate c-Myc(a well-known cancer gene) and its regulatory network.
Although cancer cells that overproduce c-Myc are associated with poor clinical outcomes, their reliance on c-Myc for survival may represent an Achilles' heel.
Previous research from Green and his colleagues showed that c-Myc also drives metabolic changes following T cell activation.
ACTL6/BAF53 has been shown to interact with c-Myc, where it functions as a cofactor and is important in the transformation process(16).
Although their findings have to be confirmed by further studies,Djouder believes that c-MYC inhibitors might be useful to mitigate radiation-induced gastrointestinal syndrome in patients.
Since the downstream genes of NF-kB include CyclinD1 and c-Myc, sustained activation of NF-kB stimulates cell growth, leading to uncontrolled cell proliferation.
When these“Myc-addicted” cells are deprived of c-Myc in vitro, even for a short period of time, they quickly die.