This study showed that the knockdown of REGγ significantly elevates the stability of the MYC protein
2021
Key concepts
- primary myelofibrosis
- transcription factor
- Sphingosine kinase 2
- ectodysplasin A receptor
- death domain
- histone acetyltransferase
- follicular lymphoma
- base excision repair
- post-translational modifications
- Platelet-derived growth factor
- Acute myelocytic leukemia
- glycogen synthase kinase
- endoplasmic reticulum
- hematopoiesis
- transactivation domain
- Apoptosis
- non-homologous end joining
- Reactive oxygen species
- tumor necrosis factor receptor
- Ornithine decarboxylase
- phosphoinositide 3-kinases
- origin recognition complex
- acute lymphoblastic leukemia
- Richter syndrome
- Regulation
- hematologic malignancy
- Chronic lymphocytic leukemia
- Philadelphia chromosome
- tyrosine kinase inhibitors
- essential thrombocythemia
- polycythemia vera
- spleen tyrosine kinase
- yeast artificial chromosome
- superoxide dismutase
- bone marrow
- Cell cycle
Scholarcy highlights
- MYC is a super-transcription factor encoded by the MYC gene located at chromosome 8 q24.21
- The chromatin-modifying complex consisting of TIP60, TRRAP, TIP48, and GCN5 recruited by MYC/ Max heterodimer propels transcription through binding to the E-box DNA region within the regulatory domain of target genes
- Studies have shown that even temporary inactivation of MYC abrogates tumor progression, implying that MYC regulation could be a potential strategy to treat MYC-involved cancers
- MYC does not possess a specific active site to be targeted by small molecules
- MYC is mainly found in the nucleus; targeting MYC with antibodies is not feasible
- Future clinical studies will have to evaluate whether MYC should be targeted directly or indirectly in order to achieve a proper therapeutic outcome
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