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Menebar Ilmu Pengetahuan

c-Myc

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Onkogen Myc diisoalasi pada awal tahun 1980an. Setelah itu muncul konsep-konspe yang mencoba menjelaskan hubungan faktor transkripsi ini dalam berkontribusi pada tumorigenesis. Konsep kunci MYC bisa berfungsi sebagai onkogen, mungkin juga relevan dengan onkogen dan faktor transkripsi lain, mungkin memiliki relevansi terapeutik.

Myc endogen ada macam-macam yaitu LMYC, NMYC, dan MYC dan secara keseluruhan disebut MYC. Penekanan aktivitas MYC dapat menekan perkembangan tumor baik pada sel tumor maupun tumor microenvironment.

Penelitian sebelumnya diungkap bahwa, Omomyc (inhibitor Myc) dapat menghambat perkembangan tumor pada model tikus tergantung KRAS. Berikutnya peneliti ingin mengetahui efek penghambatan Myc terhadap sel tumor dan tumor microenvironemnt yang diinduksi KRAS.

MYC as a regulator of ribosome biogenesis and protein synthesis

MYC regulates the transcription of thousands of genes required to coordinate a range of cellular processes, including those essential for proliferation, growth, differentiation, apoptosis and self-renewal. Recently, MYC has also been shown to serve as a direct regulator of ribosome biogenesis. MYC coordinates protein synthesis through the transcriptional control of RNA and protein components of ribosomes, and of gene products required for the processing of ribosomal RNA, the nuclear export of ribosomal subunits and the initiation of mRNA translation. We discuss how the modulation of ribosome biogenesis by MYC may be essential to its physiological functions as well as its pathological role in tumorigenesis.

The role of supercoiling in transcriptional control of MYC and its importance in molecular therapeutics

MYC is deregulated in most tumour types, but an effective means to selectively target its aberrant expression is not yet available. Supercoiling that is induced by transcription has been demonstrated to have dynamic effects on DNA in the MYC promoter element: it converts duplex DNA to non-duplex DNA structures, even at considerable distances from the transcriptional start site. These non-duplex DNA structures, which control both turning on and off of transcription and the rate of transcription firing, are amenable to small-molecule targeting. This dynamic system provides a unique opportunity for the treatment of tumours in which MYC is an important oncogene.

Referensi

NCBI

MCB

c-Myc Cancer Gene

Author: admin

menebar ilmu pengetahuan

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