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Review
. 1999 Jan;19(1):1-11.
doi: 10.1128/MCB.19.1.1.

c-Myc target genes involved in cell growth, apoptosis, and metabolism

Affiliations
Review

c-Myc target genes involved in cell growth, apoptosis, and metabolism

C V Dang. Mol Cell Biol. 1999 Jan.
No abstract available

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Figures

FIG. 1
FIG. 1
The c-myc gene is a central oncogenic switch for oncogenes and the tumor suppressor APC. The APC tumor suppressor protein mediates the degradation of β-catenin. The Wnt oncoprotein is shown activating its receptor, which results in the stabilization of free β-catenin. β-Catenin, which sustains activating mutations in human cancers, is a cofactor for the transcription factor Tcf. Tcf activates c-myc expression through specific DNA binding sites. The oncogenic fusion protein TEL-PDGFR hypothetically activates c-src, as does native PDGFR, resulting in the activation of c-myc. The BCR-ABL oncoprotein likewise requires c-myc for its activity.
FIG. 2
FIG. 2
Association of factors to functional domains of the c-Myc protein. O-GlcNAc marks a glycosylation site. GSK3 and CDK mark phosphorylation sites. Max is depicted in association with c-Myc through the HLH-LZ motif; b is the basic region. NTS is the nuclear target signal. TRD represents the transcriptional regulatory domain. The proteins Bin1, PAM, p107, and TBP are shown associated with the TRD of c-Myc. Miz1 and TFII-I are shown associated with the HLH-LZ region of c-Myc. YY1 may associate with the central domain of c-Myc.
FIG. 3
FIG. 3
Models of c-Myc/Max and Mad/Max in transcriptional regulation. The c-Myc/Max heterodimer is shown at the top tethered to the E box 5′-CACGTG-3′. c-Myc contacts TBP, although the molecular mechanisms involved in c-Myc transactivation are not known. The bottom diagram depicts the association of the Mad/Max heterodimer with the E box, as well as with mSin3, N-Cor, and histone deacetylase (HDAC). HDAC deacetylates histones, causing the locking of nucleosomal DNA and, consequently, inhibition of transcription. POL, polymerase.
FIG. 4
FIG. 4
Links between c-Myc, selected putative target genes, cellular functions, and cell growth. This diagram illustrates the complexity of the connections between c-Myc and its putative target genes, which are shown clustered according to their functions. The various cellular functions cooperate to promote cell growth. It should be noted that this diagram does not reflect the controversies over the authentication of the various target genes.

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