Other Name(s): c-Myc, c-myc, Myc
Drug Target Analysis Report Drug Target Analysis Report Content

About the Target

Based on the provided context information, here are some key viewpoints about MYC:

MYC plays a crucial role in both the activation and repression of target genes [1]. It functions as a transcription factor by forming a heterodimer with MAX and binding to specific DNA sequences called E-boxes [1][2]. This interaction leads to the recruitment of chromatin-modifying complexes and the activation of transcription [2].

In transcriptional activation, MYC-MAX heterodimers recruit chromatin-modifying co-factors such as TIP60, GCN5, TRRAP, and p300/CBP [1][2]. These co-factors increase the acetylation of histones, resulting in an open chromatin conformation that allows RNA polymerase II to bind and initiate transcription [1].

MYC can also repress the transcription of non-canonical target genes by forming complexes with MAX and MIZ1 [1][2]. This interaction recruits chromatin co-repressors such as DNMT3A, HDAC1, HDAC3, and EZH2, leading to gene silencing [1][2].

The stability and activity of MYC are regulated by various factors. Phosphorylation by PIM1 and AURKA increases its stability [1]. Additionally, WDR5 is crucial for the recruitment of MYC at chromatin regions [1]. There are also specific domains within MYC, known as Myc boxes, that are involved in its functions [2].

MYC-dependent malignancies can be targeted through various approaches. Pathway inhibitors, BET bromodomain inhibitors, and complex inhibitors have been developed to disrupt MYC signaling and target its transcriptional output [4]. These inhibitors aim to halt the initiation of MYC transcription and interfere with its interactions with co-factors or DNA binding sites [4].

In summary, MYC is a key transcription factor involved in both the activation and repression of target genes. It forms heterodimers with MAX and interacts with chromatin-modifying co-factors to regulate gene expression. MYC can be targeted for therapeutic purposes in MYC-driven malignancies using specific inhibitors.
Based on the given context information, here are some key viewpoints regarding the MYC protein:

The MYC protein, encoded by the MYC gene on chromosome 8, consists of various structural regions and highly conserved MYC boxes at the N-terminal [6].
MYC is involved in gene transcription, and its accumulation at the promoter sequences of target genes enhances their transcriptional activity [6].
In hyperglycemic conditions, cancer cells exhibit upregulation of glycolysis mediated by c-Myc, which makes them less sensitive to the energetic stress induced by metformin [7].
In normoglycemic conditions, metformin inhibits c-Myc expression, preventing the survival-promoting metabolic mechanism associated with increased glycolysis [7].
Certain deubiquitinating enzymes, such as USP36, USP28, USP22, and USP37, are known to stabilize MYC through deubiquitination processes [8].
The deregulation of MYC intensifies the expression of both target genes and aberrant nontarget genes, contributing to tumorigenesis [9].
Physiological Myc is tightly controlled by both transcriptional and post-transcriptional components, while deregulated Myc leads to the upregulation of target genes, including low-affinity ones, and additional nontarget genes, promoting further tumorigenesis [9].
Knockout of IGF2BPs, in conjunction with depletion of MYC, inhibits cell proliferation, and colony formation in HepG2 cells [10].
IGF2BPs play a role in the regulation of m6A modified mRNAs, protecting target mRNAs from degradation in the P-body and facilitating translation in the cytoplasm [10].

Note: The provided context information is limited, and additional sources may provide a more comprehensive understanding of the topic.

Figure [1]

Figure [2]

Figure [3]

Figure [4]

Figure [5]

Figure [6]

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Note: If you are interested in the full version of this target analysis report, or if you'd like to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the MYC target at a cost 90% lower than traditional approaches, please feel free to contact us at BD@silexon.ai.

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