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Myc is thought to function by upregulating transcript elongation of actively transcribed genes through the recruitment of transcriptional elongation factors. [10] It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the p300 co-activator, it inhibits expression
Several transcription factors are implicated in the process of transcriptional addiction in cancer. These factors bind to promoter regions of DNA and regulate the transcription of oncogenic genes: MYC The MYC family of transcription factors is one of the most well-known drivers of transcriptional addiction.
The MYC gene codes for widely used transcription factors. When the enhancer sequence is wrongly placed, these transcription factors are produced at much higher rates. Another example of an oncogene is the Bcr-Abl gene found on the Philadelphia chromosome , a piece of genetic material seen in Chronic Myelogenous Leukemia caused by the ...
Expression of the c-myc gene, which produces an oncogenic transcription factor, is tightly regulated in normal cells but is frequently deregulated in human cancers. The protein encoded by this gene is a transcriptional repressor thought to negatively regulate MYC function, and is therefore a potential tumor suppressor.
One example of tissue function rewiring in cancer is the activity of transcription factor NF-κB. [88] NF-κB activates the expression of numerous genes involved in the transition between inflammation and regeneration, which encode cytokines, adhesion factors, and other molecules that can change cell fate. [89]
ERG can fuse with TMPRSS2 protein to form an oncogenic fusion gene that is commonly found in human prostate cancer, especially in hormone-refractory prostate cancer. This suggests that ERG overexpression may contribute to development of androgen-independence in prostate cancer through disruption of androgen receptor signaling. [ 19 ]
The Janus kinase (JAK)/signal transducer and the activator of the transcription pathway were at the centre of attention for driving hyperinflammation in COVID-19, i.e., the SARS-CoV-2 infection triggers hyperinflammation through the JAK/STAT pathway, resulting in the recruitment of dendritic cells, macrophages, and natural killer (NK) cells, as ...
Transcription factor Jun is a protein that in humans is encoded by the JUN gene. c-Jun, in combination with protein c-Fos, forms the AP-1 early response transcription factor. It was first identified as the Fos-binding protein p39 and only later rediscovered as the product of the JUN gene. c-jun was the first oncogenic transcription factor ...