Myc

(redirected from C-myc)
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Myc

 (mĭk)
n.
Any of several genes encoding DNA-binding proteins that can promote the development of various cancers when present at high concentrations.

[Possibly from my(elo)c(ytomatosis virus).]
References in periodicals archive ?
Los niveles de la proteina Mad, que son opuestos a los de c-Myc, aumentan durante la diferenciacion celular, mientras que una baja expresion de la proteina Mad2 (Mxi-1) se asocia con el desarrollo de tumores en modelos murinos.
Detection of gene amplification in MYCN, C-MYC, MYCL1, ERBB2, EGFR, AKT2, and human papilloma virus in samples from cervical smear normal cytology, intraepithelial cervical neoplasia (CIN I, II, III), and cervical cancer
This protein, called c-MYC oncoprotein, can initiate and promote almost all human cancers and discovering the role it plays in cancer treatment resistance may lead to advances that save lives.
In a study published in Cell Death & Differentiation, researchers showed that THAP11 is frequently downregulated in several human tumor tissues and is able to suppress transcription of c-Myc (PMID: 19008924).
Since C-myc is known to regulate hTERT, expression of C-myc was also determined.
The other topics are polyunsaturated fatty acid deficiency, the correlation between vascular endothelial growth factor and proto-oncogene c-fos and c-myc, and the expression of neural cell adhesion molecules and osteonectin.
Furthermore, it was shown that the target RNA, from the c-myc gene, one of the main causes of restenosis, was effectively inhibited by the antisense compound AVI-5126 developed by Cook Medical's partner AVI BioPharma, Inc.
Common to all Burkitt lymphomas, endemic or sporadic, are distinctive chromosomal translocations that reactivate expression of the c-myc protooncogene and comprise the primary oncogenic mechanism.
C-myc is believed to regulate the many downstream genes that produce the pathology of restenosis, including cell migration and adhesion, collagen formation, secretion of extra-cellular matrix, and cell proliferation.
However, all the mice with the extra c-myc and microRNA, developed lymphoma within about 50 days and died 2 weeks later, Hammond's team reports.
The hypothesis addressed in this research states that there is a unique set of genes related to the c-myc basic/Helix/Loop/Helix, MyoD1, involved in the repair process of skeletal muscle atrophy.
The University of Warwick experts behind the five year research have compared the role of the protein, c-Myc, to that of Bin Laden in international terrorism.