The cellular myelocytomatosis (c-myc) gene mapped to human chromosome 8q24, is the cellular homologue of the v-myc gene originally isolated from an avian myelocytomatosis virus. C-myc is a member of MYC gene family. c-Myc gene codes for basic helix-loop-helix/leucine zipper (bHLH/LZ) transcription factor that regulates the G1-S cell cycle transition. Increased expression of c-myc is observed in variety of human cancerous tissue.
Immunogen
Synthetic peptide sequence (AEEQKLISEEDLL) corresponding to the C-terminal region of human c-Myc
Application
Monoclonal Anti-MYC-FITC , (C-terminal) antibody produced in mouse has been used in immunofluorescence and flow cytometry.
Biochem/physiol Actions
The cellular myelocytomatosis (c-myc) oncogene plays a vital role in cellular proliferation, differentiation, apoptosis and acts as a transcriptional regulator of gene expression. c-Myc expression is essential and sufficient to assist most of the cells to enter DNA synthetic (S) phase of the cell cycle. The encoded protein plays a crucial role in vasculogenesis and angiogenesis during cancer development and progression. c-Myc interacts with its binding partner Max and activates the transcription of growth promoting genes such as cyclin D2, ornithine decarboxylase, and transcription factor E2F1 and it also represses the transcription of multiple genes, especially p21 and p27, by binding to the transcription initiator element (Inr) in a complex with Max and either Sp1 or Miz1 (transcription factors).
Features and Benefits
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Physical form
Solution in phosphate buffered saline, pH 7.4, with 15 mM sodium azide.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
Journal of immunology (Baltimore, Md. : 1950), 201(1), 202-214 (2018-05-18)
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