Myc

<h2 id="discovery">Discovery</h2>
The Myc family was first established after discovery of <a href="/facts/Homology_(biology)/muctKlyT">homology</a> between an oncogene carried by the Avian virus, Myelocytomatosis (v-myc; <a href="https://www.uniprot.org/uniprot/P10395">P10395</a>) and a human gene over-expressed in various cancers, cellular Myc (c-Myc). Later, discovery of further homologous genes in humans led to the addition of n-Myc and l-Myc to the family of genes.<a class="footnote-ref" id="fnref:10" href="#fn:10">10</a>
The most frequently discussed example of c-Myc as a proto-oncogene is its implication in <a href="/facts/Burkitt%2527s_lymphoma/Ita1VmGg">Burkitt's lymphoma</a>. In Burkitt's lymphoma, cancer cells show <a href="/facts/Chromosomal_translocation/MKEwqpQw">chromosomal translocations</a>, most commonly between <a href="/facts/Chromosome_8/lHe695JV">chromosome 8</a> and <a href="/facts/Chromosome_14/9a08SWux">chromosome 14</a> [t(8;14)]. This causes c-Myc to be placed downstream of the highly active immunoglobulin (Ig) promoter region, leading to overexpression of Myc.

<h2 id="structure">Structure</h2>
The protein products of Myc family genes all belong to the Myc family of transcription factors, which contain <a href="/facts/BHLH/yqfuWejn">bHLH</a> (basic helix-loop-helix) and LZ (<a href="/facts/Leucine_zipper/tlAMv6Ul">leucine zipper</a>) structural motifs. The bHLH motif allows Myc proteins to bind with <a href="/facts/DNA/nB89Iauz">DNA</a>, while the leucine zipper TF-binding motif allows dimerization with <a href="/facts/MAX_(gene)/gsxQkIzN">Max</a>, another bHLH transcription factor.
Myc <a href="/facts/MRNA/oUL6qxQn">mRNA</a> contains an <a href="/facts/Internal_ribosome_entry_site/5lVqcu4I">IRES</a> (internal ribosome entry site) that allows the RNA to be translated into protein when <a href="/facts/5%2527_cap/cWUeEBJ6">5' cap</a>-dependent translation is inhibited, such as during viral infection.

<h2 id="function">Function</h2>
Myc proteins are <a href="/facts/Transcription_factor/wro0DPHe">transcription factors</a> that activate expression of many pro-proliferative genes through binding enhancer box sequences (<a href="/facts/E-box/Kme7EgfY">E-boxes</a>) and recruiting <a href="/facts/Histone_acetyltransferase/gIzJY5fn">histone acetyltransferases</a> (HATs). Myc is thought to function by upregulating transcript elongation of actively transcribed genes through the recruitment of <a href="/facts/Transcriptional_elongation/bDgp9HDN">transcriptional elongation</a> factors.<a class="footnote-ref" id="fnref:11" href="#fn:11">11</a> It can also act as a transcriptional repressor. By binding Miz-1 transcription factor and displacing the <a href="/facts/EP300/7WU3jvjy">p300</a> <a href="/facts/Co-activator/0lVABmQx">co-activator</a>, it inhibits expression of Miz-1 target genes. In addition, myc has a direct role in the control of DNA replication.<a class="footnote-ref" id="fnref:12" href="#fn:12">12</a> This activity could contribute to DNA amplification in cancer cells.<a class="footnote-ref" id="fnref:13" href="#fn:13">13</a>
Myc is activated upon various <a href="/facts/Mitogen/AyjRuS2a">mitogenic signals</a> such as serum stimulation or by <a href="/facts/Wnt_signalling_pathway/7wxpKrjy">Wnt</a>, <a href="/facts/Sonic_hedgehog/Rgp34KCx">Shh</a> and <a href="/facts/Epidermal_growth_factor/CpyH5tYs">EGF</a> (via the <a href="/facts/MAPK%2fERK_pathway/jfpd0YvE">MAPK/ERK pathway</a>).<a class="footnote-ref" id="fnref:14" href="#fn:14">14</a>
By modifying the expression of its target genes, Myc activation results in numerous biological effects. The first to be discovered was its capability to drive <a href="/facts/Cell_proliferation/Jp3hWo2t">cell proliferation</a> (upregulates cyclins, downregulates p21), but it also plays a very important role in regulating <a href="/facts/Cell_growth/wbArMaJU">cell growth</a> (upregulates ribosomal RNA and proteins), <a href="/facts/Apoptosis/8dVzSm4y">apoptosis</a> (downregulates <a href="/facts/Bcl-2/I34R1guW">Bcl-2</a>), differentiation, and <a href="/facts/Stem_cell/qgB9dFrI">stem cell</a> self-renewal. Nucleotide metabolism genes are upregulated by Myc,<a class="footnote-ref" id="fnref:15" href="#fn:15">15</a> which are necessary for Myc induced proliferation<a class="footnote-ref" id="fnref:16" href="#fn:16">16</a> or cell growth.<a class="footnote-ref" id="fnref:17" href="#fn:17">17</a>
There have been several studies that have clearly indicated Myc's role in cell competition.<a class="footnote-ref" id="fnref:18" href="#fn:18">18</a>
A major effect of c-myc is <a href="/facts/B_cell/6Y1tgwwp">B cell</a> proliferation, and gain of MYC has been associated with B cell malignancies and their increased aggressiveness, including histological transformation.<a class="footnote-ref" id="fnref:19" href="#fn:19">19</a> In B cells, Myc acts as a classical oncogene by regulating a number of pro-proliferative and anti-apoptotic pathways, this also includes tuning of BCR signaling and CD40 signaling in regulation of microRNAs (miR-29, miR-150, miR-17-92).<a class="footnote-ref" id="fnref:20" href="#fn:20">20</a>
c-Myc induces <a href="/facts/MTDH/u1WvxId7">MTDH</a>(AEG-1) gene expression and in turn itself requires AEG-1 oncogene for its expression.

<h2 id="myc-nick">Myc-nick</h2>

Myc-nick is a cytoplasmic form of Myc produced by a partial proteolytic cleavage of full-length c-Myc and N-Myc.<a class="footnote-ref" id="fnref:21" href="#fn:21">21</a> Myc cleavage is mediated by the <a href="/facts/Calpain/vebGUShd">calpain</a> family of calcium-dependent cytosolic proteases.
The cleavage of Myc by calpains is a constitutive process but is enhanced under conditions that require rapid downregulation of Myc levels, such as during terminal differentiation. Upon cleavage, the <a href="/facts/C-terminus/ws4scHgT">C-terminus</a> of Myc (containing the <a href="/facts/DNA_binding_domain/x2vlHUKl">DNA binding domain</a>) is degraded, while Myc-nick, the <a href="/facts/N-terminal/yKYpuaBJ">N-terminal</a> segment 298-residue segment remains in the <a href="/facts/Cytoplasm/Wa0sE6xf">cytoplasm</a>. Myc-nick contains binding domains for <a href="/facts/Histone_acetyltransferase/gIzJY5fn">histone acetyltransferases</a> and for <a href="/facts/Ubiquitin_ligase/8xmNaWW3">ubiquitin ligases</a>.
The functions of Myc-nick are currently under investigation, but this new Myc family member was found to regulate cell morphology, at least in part, by interacting with <a href="/facts/Acyltransferase/vwfM9UCv">acetyl transferases</a> to promote the acetylation of <a href="/facts/%25CE%2591-tubulin/j4Bk2wcL">α-tubulin</a>. <a href="/facts/Ectopic_expression/9XuMR5wc">Ectopic expression</a> of Myc-nick accelerates the differentiation of committed <a href="/facts/Myoblast/Vc6sxQvR">myoblasts</a> into muscle cells.

<h2 id="clinical-significance">Clinical significance</h2>
A large body of evidence shows that Myc genes and proteins are highly relevant for treating tumors.<a class="footnote-ref" id="fnref:22" href="#fn:22">22</a> Except for early response genes, Myc universally upregulates gene expression. Furthermore, the upregulation is nonlinear. Genes for which expression is already significantly upregulated in the absence of Myc are strongly boosted in the presence of Myc, whereas genes for which expression is low in the absence Myc get only a small boost when Myc is present.<a class="footnote-ref" id="fnref:23" href="#fn:23">23</a>
Inactivation of SUMO-activating enzyme (<a href="/facts/SAE1/bvd6eBxs">SAE1</a> / <a href="/facts/UBA2/9fEEnzc0">SAE2</a>) in the presence of Myc hyperactivation results in mitotic catastrophe and cell death in cancer cells. Hence inhibitors of <a href="/facts/SUMOylation/T5vYKlQd">SUMOylation</a> may be a possible treatment for cancer.<a class="footnote-ref" id="fnref:24" href="#fn:24">24</a>
Amplification of the MYC gene was found in a significant number of epithelial <a href="/facts/Ovarian_cancer/fsWbh3Tn">ovarian cancer</a> cases.<a class="footnote-ref" id="fnref:25" href="#fn:25">25</a> In TCGA datasets, the amplification of Myc occurs in several cancer types, including breast, colorectal, pancreatic, gastric, and uterine cancers.<a class="footnote-ref" id="fnref:26" href="#fn:26">26</a>
In the experimental transformation process of normal cells into cancer cells, the MYC gene can cooperate with the RAS gene.<a class="footnote-ref" id="fnref:27" href="#fn:27">27</a><a class="footnote-ref" id="fnref:28" href="#fn:28">28</a>
Expression of Myc is highly dependent on <a href="/facts/BRD4/mhA40pBP">BRD4</a> function in some cancers.<a class="footnote-ref" id="fnref:29" href="#fn:29">29</a><a class="footnote-ref" id="fnref:30" href="#fn:30">30</a> <a href="/facts/BET_inhibitors/3LHotnPv">BET inhibitors</a> have been used to successfully block Myc function in pre-clinical cancer models and are currently being evaluated in clinical trials.<a class="footnote-ref" id="fnref:31" href="#fn:31">31</a>
MYC expression is controlled by a wide variety of noncoding RNAs, including <a href="/facts/MiRNA/UjqbYYpe">miRNA</a>, <a href="/facts/LncRNA/FHyAb6hP">lncRNA</a>, and <a href="/facts/CircRNA/SN4vBHDk">circRNA</a>. Some of these RNAs have been shown to be specific for certain types of human tissues and tumors.<a class="footnote-ref" id="fnref:32" href="#fn:32">32</a> Changes in the expression of such RNAs can potentially be used to develop targeted tumor therapy.

<h2 id="myc-rearrangements">MYC rearrangements</h2>
MYC <a href="/facts/Chromosomal_rearrangement/zM3swLsh">chromosomal rearrangements</a> (MYC-R) occur in 10% to 15% of <a href="/facts/Diffuse_large_B-cell_lymphoma/7FSQMurk">diffuse large B-cell lymphoma</a> (DLBCLs), an aggressive <a href="/facts/Non-Hodgkin_Lymphoma/KIFxt74F">Non-Hodgkin Lymphoma</a> (NHL). Patients with MYC-R have inferior outcomes and can be classified as single-hit, when they only have MYC-R; as double hit when the rearrangement is accompanied by a translocation of <a href="/facts/Bcl-2/I34R1guW">BCL2</a> or <a href="/facts/BCL6/ykKDaTBg">BCL6</a>; and as triple hit when MYC-R includes both BCL2 and BCL6. Double and triple hit lymphoma have been recently classified as high-grade B-cell lymphoma (HGBCL) and it is associated with a poor prognosis.<a class="footnote-ref" id="fnref:33" href="#fn:33">33</a>
MYC-R in DLBCL/HGBCL is believed to arise through the aberrant activity of activation-induced cytidine deaminase (AICDA), which facilitates somatic hypermutation (SHM) and class-switch recombination (CSR).<a class="footnote-ref" id="fnref:34" href="#fn:34">34</a> Although AICDA primarily targets IG loci for SHM and CSR, its off-target mutagenic effects can impact lymphoma-associated oncogenes like MYC, potentially leading to oncogenic rearrangements. The breakpoints in MYC rearrangements show considerable variability within the MYC region. These breakpoints may occur within the so-called “genic cluster,” a region spanning approximately 1.5 kb upstream of the transcription start site, as well as the first exon and intron of MYC.<a class="footnote-ref" id="fnref:35" href="#fn:35">35</a> 
<a href="/facts/Fluorescence_in_situ_hybridization/L4juqPoq">Fluorescence in situ hybridization</a> (FISH) has become a routine practice in many clinical laboratories for lymphoma characterization. A break-apart (BAP) FISH probe is commonly utilized for the detection of MYC-R due to the variability of breakpoints in the MYC locus and the diversity of rearrangement partners, including immunoglobulin (IG) and non-IG partners (i.e. BCL2/BCL6). The MYC BAP probe includes a red and a green probe which hybridize 5’ and 3’ to the MYC gen, respectively. In an intact MYC locus, these probes yield a fusion signal. When MYC-R occur, two types of signals can be observed:

<ul><li>Balanced patterns: These patterns present separate red and green signals.</li></ul>
<ul><li>Unbalanced patterns: When isolated red or green signals in the absence of the corresponding green or red signal is observed. Unbalanced MYC-R are frequently associated with increased MYC expression.</li></ul>
There is a large variability in the interpretation of unbalanced MYC BAP results among the scientists, which can impact diagnostic classification and therapeutic management of the patients.<a class="footnote-ref" id="fnref:36" href="#fn:36">36</a><a class="footnote-ref" id="fnref:37" href="#fn:37">37</a>

<h2 id="animal-models">Animal models</h2>
In <a href="/facts/Drosophila_melanogaster/KtnHVCcB">Drosophila</a> Myc is encoded by the diminutive locus, (which was known to geneticists prior to 1935).<a class="footnote-ref" id="fnref:38" href="#fn:38">38</a> Classical diminutive alleles resulted in a viable animal with small body size. Drosophila has subsequently been used to implicate Myc in cell competition,<a class="footnote-ref" id="fnref:39" href="#fn:39">39</a> endoreplication,<a class="footnote-ref" id="fnref:40" href="#fn:40">40</a> and cell growth.<a class="footnote-ref" id="fnref:41" href="#fn:41">41</a>
During the discovery of Myc gene, it was realized that chromosomes that reciprocally translocate to chromosome 8 contained <a href="/facts/Immunoglobulin/MX8pdTdP">immunoglobulin</a> genes at the break-point. To study the mechanism of tumorigenesis in Burkitt lymphoma by mimicking expression pattern of Myc in these cancer cells, transgenic mouse models were developed. Myc gene placed under the control of <a href="/facts/IgM/23PjpgIQ">IgM</a> heavy chain enhancer in transgenic mice gives rise to mainly lymphomas. Later on, in order to study effects of Myc in other types of cancer, transgenic mice that overexpress Myc in different tissues (liver, breast) were also made. In all these mouse models overexpression of Myc causes tumorigenesis, illustrating the potency of Myc oncogene.
In a study with mice, reduced expression of Myc was shown to induce longevity, with significantly extended median and maximum lifespans in both sexes and a reduced mortality rate across all ages, better health, cancer progression was slower, better metabolism and they had smaller bodies. Also, Less TOR, AKT, S6K and other changes in energy and metabolic pathways (such as AMPK, more oxygen consumption, more body movements, etc.). The study by John M. Sedivy and others used Cre-Loxp -recombinase to knockout one copy of Myc and this resulted in a "Haplo-insufficient" genotype noted as Myc+/-. The phenotypes seen oppose the effects of normal aging and are shared with many other long-lived mouse models such as CR (calorie restriction) ames dwarf, rapamycin, metformin and resveratrol. One study found that Myc and <a href="/facts/P53/YEGULLgM">p53</a> genes were key to the survival of <a href="/facts/Chronic_myeloid_leukaemia/FA9TdgQn">chronic myeloid leukaemia</a> (CML) cells. Targeting Myc and p53 proteins with drugs gave positive results on mice with CML.<a class="footnote-ref" id="fnref:42" href="#fn:42">42</a><a class="footnote-ref" id="fnref:43" href="#fn:43">43</a>

<h2 id="relationship-to-stem-cells">Relationship to stem cells</h2>
Myc genes play a number of normal roles in stem cells including pluripotent stem cells. In neural stem cells, N-Myc promotes a rapidly proliferative stem cell and precursor-like state in the developing brain, while inhibiting differentiation.<a class="footnote-ref" id="fnref:44" href="#fn:44">44</a> In hematopoietic stem cells, Myc controls the balance between self-renewal and differentiation.<a class="footnote-ref" id="fnref:45" href="#fn:45">45</a> In particular, long-term hematopoietic stem cells (LT-HSCs) express low levels of c-Myc, ensuring self-renewal. Enforced expression of c-Myc in LT-HSCs promotes differentiation at the expense of self-renewal, resulting in stem cell exhaustion.<a class="footnote-ref" id="fnref:46" href="#fn:46">46</a> In pathological states and specifically in acute myeloid leukemia, oxidant stress can trigger higher levels of Myc expression that affects the behavior of leukemia stem cells.<a class="footnote-ref" id="fnref:47" href="#fn:47">47</a>
c-Myc plays a major role in the generation of <a href="/facts/Induced_pluripotent_stem_cell/bGItax29">induced pluripotent stem cells</a> (iPSCs). It is one of the original factors discovered by Yamanaka et al. to encourage cells to return to a 'stem-like' state alongside transcription factors <a href="/facts/Oct4/Vee10vjH">Oct4</a>, <a href="/facts/Sox2/uKRxbGml">Sox2</a> and <a href="/facts/Klf4/v8bzjrWR">Klf4</a>. It has since been shown that it is possible to generate iPSCs without c-Myc.<a class="footnote-ref" id="fnref:48" href="#fn:48">48</a>

<h2 id="interactions">Interactions</h2>
Myc has been shown to <a href="/facts/Protein-protein_interaction/etvm9Wmg">interact</a> with:

<ul><li><a href="/facts/ACTL6A/TJ2WCWe8">ACTL6A</a><a class="footnote-ref" id="fnref:49" href="#fn:49">49</a></li>
<li><a href="/facts/BRCA1/xHDwxARA">BRCA1</a><a class="footnote-ref" id="fnref:50" href="#fn:50">50</a><a class="footnote-ref" id="fnref:51" href="#fn:51">51</a><a class="footnote-ref" id="fnref:52" href="#fn:52">52</a><a class="footnote-ref" id="fnref:53" href="#fn:53">53</a></li>
<li><a href="/facts/Bcl-2/I34R1guW">Bcl-2</a><a class="footnote-ref" id="fnref:54" href="#fn:54">54</a></li>
<li><a href="/facts/Cyclin_T1/HTHzCgME">Cyclin T1</a><a class="footnote-ref" id="fnref:55" href="#fn:55">55</a></li>
<li><a href="/facts/CHD8/sREz3pKq">CHD8</a><a class="footnote-ref" id="fnref:56" href="#fn:56">56</a></li>
<li><a href="/facts/DNMT3A/1gWkklau">DNMT3A</a><a class="footnote-ref" id="fnref:57" href="#fn:57">57</a></li>
<li><a href="/facts/EP400/3zQHsXL9">EP400</a><a class="footnote-ref" id="fnref:58" href="#fn:58">58</a></li>
<li><a href="/facts/GTF2I/DonMzdX9">GTF2I</a><a class="footnote-ref" id="fnref:59" href="#fn:59">59</a></li>
<li><a href="/facts/HTATIP/UkyldBkS">HTATIP</a><a class="footnote-ref" id="fnref:60" href="#fn:60">60</a></li>
<li><a href="/facts/Let-7_microRNA_precursor/wkh6NAon">let-7</a><a class="footnote-ref" id="fnref:61" href="#fn:61">61</a><a class="footnote-ref" id="fnref:62" href="#fn:62">62</a><a class="footnote-ref" id="fnref:63" href="#fn:63">63</a></li>
<li><a href="/facts/MAPK1/VNLaNRdQ">MAPK1</a><a class="footnote-ref" id="fnref:64" href="#fn:64">64</a><a class="footnote-ref" id="fnref:65" href="#fn:65">65</a><a class="footnote-ref" id="fnref:66" href="#fn:66">66</a></li>
<li><a href="/facts/MAPK8/fbUM7qyf">MAPK8</a><a class="footnote-ref" id="fnref:67" href="#fn:67">67</a></li>
<li><a href="/facts/MAX_(gene)/gsxQkIzN">MAX</a><a class="footnote-ref" id="fnref:68" href="#fn:68">68</a><a class="footnote-ref" id="fnref:69" href="#fn:69">69</a><a class="footnote-ref" id="fnref:70" href="#fn:70">70</a><a class="footnote-ref" id="fnref:71" href="#fn:71">71</a><a class="footnote-ref" id="fnref:72" href="#fn:72">72</a><a class="footnote-ref" id="fnref:73" href="#fn:73">73</a><a class="footnote-ref" id="fnref:74" href="#fn:74">74</a><a class="footnote-ref" id="fnref:75" href="#fn:75">75</a><a class="footnote-ref" id="fnref:76" href="#fn:76">76</a><a class="footnote-ref" id="fnref:77" href="#fn:77">77</a><a class="footnote-ref" id="fnref:78" href="#fn:78">78</a><a class="footnote-ref" id="fnref:79" href="#fn:79">79</a><a class="footnote-ref" id="fnref:80" href="#fn:80">80</a></li>
<li><a href="/facts/MLH1/6oFIzNLS">MLH1</a><a class="footnote-ref" id="fnref:81" href="#fn:81">81</a></li>
<li><a href="/facts/MYCBP2/VcDaQugg">MYCBP2</a><a class="footnote-ref" id="fnref:82" href="#fn:82">82</a></li>
<li><a href="/facts/MYCBP/mAXp8Blt">MYCBP</a><a class="footnote-ref" id="fnref:83" href="#fn:83">83</a></li>
<li><a href="/facts/N-myc-interactor/BJDN82Ic">NMI</a><a class="footnote-ref" id="fnref:84" href="#fn:84">84</a></li>
<li><a href="/facts/NFYB/pYr4beA7">NFYB</a><a class="footnote-ref" id="fnref:85" href="#fn:85">85</a></li>
<li><a href="/facts/NFYC/7r17fgYX">NFYC</a><a class="footnote-ref" id="fnref:86" href="#fn:86">86</a></li>
<li><a href="/facts/P73/DM92hxht">P73</a><a class="footnote-ref" id="fnref:87" href="#fn:87">87</a></li>
<li><a href="/facts/PCAF/mzYyuY6Q">PCAF</a><a class="footnote-ref" id="fnref:88" href="#fn:88">88</a></li>
<li><a href="/facts/PFDN5/rn3gDq9L">PFDN5</a><a class="footnote-ref" id="fnref:89" href="#fn:89">89</a><a class="footnote-ref" id="fnref:90" href="#fn:90">90</a></li>
<li><a href="/facts/RuvB-like_1/Cexgyl0H">RuvB-like 1</a><a class="footnote-ref" id="fnref:91" href="#fn:91">91</a><a class="footnote-ref" id="fnref:92" href="#fn:92">92</a></li>
<li><a href="/facts/SAP130/0G3RC29j">SAP130</a><a class="footnote-ref" id="fnref:93" href="#fn:93">93</a></li>
<li><a href="/facts/Mothers_against_decapentaplegic_homolog_2/xlS5oygm">SMAD2</a><a class="footnote-ref" id="fnref:94" href="#fn:94">94</a></li>
<li><a href="/facts/Mothers_against_decapentaplegic_homolog_3/6j6Go6va">SMAD3</a><a class="footnote-ref" id="fnref:95" href="#fn:95">95</a></li>
<li><a href="/facts/SMARCA4/tTMYE8oQ">SMARCA4</a><a class="footnote-ref" id="fnref:96" href="#fn:96">96</a><a class="footnote-ref" id="fnref:97" href="#fn:97">97</a></li>
<li><a href="/facts/SMARCB1/rUDQTneh">SMARCB1</a><a class="footnote-ref" id="fnref:98" href="#fn:98">98</a></li>
<li><a href="/facts/Transcription_initiation_protein_SPT3_homolog/UHqj9UTh">SUPT3H</a><a class="footnote-ref" id="fnref:99" href="#fn:99">99</a></li>
<li><a href="/facts/T-cell_lymphoma_invasion_and_metastasis-inducing_protein_1/3tCqQjd6">TIAM1</a><a class="footnote-ref" id="fnref:100" href="#fn:100">100</a></li>
<li><a href="/facts/TADA2L/vLnueKn1">TADA2L</a><a class="footnote-ref" id="fnref:101" href="#fn:101">101</a></li>
<li><a href="/facts/TAF9/f0IsaLs1">TAF9</a><a class="footnote-ref" id="fnref:102" href="#fn:102">102</a></li>
<li><a href="/facts/TFAP2A/4dHgDFkA">TFAP2A</a><a class="footnote-ref" id="fnref:103" href="#fn:103">103</a></li>
<li><a href="/facts/Transformation%2ftranscription_domain-associated_protein/bSpGKYkH">TRRAP</a><a class="footnote-ref" id="fnref:104" href="#fn:104">104</a><a class="footnote-ref" id="fnref:105" href="#fn:105">105</a><a class="footnote-ref" id="fnref:106" href="#fn:106">106</a><a class="footnote-ref" id="fnref:107" href="#fn:107">107</a></li>
<li><a href="/facts/WDR5/WK1FpIpH">WDR5</a><a class="footnote-ref" id="fnref:108" href="#fn:108">108</a></li>
<li><a href="/facts/YY1/Ec4E5UXR">YY1</a><a class="footnote-ref" id="fnref:109" href="#fn:109">109</a> and</li>
<li><a href="/facts/ZBTB17/Jeser7jt">ZBTB17</a>.<a class="footnote-ref" id="fnref:110" href="#fn:110">110</a><a class="footnote-ref" id="fnref:111" href="#fn:111">111</a></li>
<li><a href="/facts/C2orf16/SkmE9vFK">C2orf16</a><a class="footnote-ref" id="fnref:112" href="#fn:112">112</a></li></ul>

<h2 id="further-reading">Further reading</h2>

<ul><li>Ruf IK, Rhyne PW, Yang H, Borza CM, Hutt-Fletcher LM, Cleveland JL, Sample JT (2001). "EBV Regulates c-MYC, Apoptosis, and Tumorigenicity in Burkitt's Lymphoma". Epstein-Barr Virus and Human Cancer. Current Topics in Microbiology and Immunology. Vol. 258. pp. 153–60. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1007%2F978-3-642-56515-1_10">10.1007/978-3-642-56515-1_10</a>. <a href="/facts/ISBN_(identifier)/15AdSPa9">ISBN</a> 978-3-642-62568-8. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/11443860">11443860</a>.</li>
<li>Lüscher B (October 2001). "Function and regulation of the transcription factors of the Myc/Max/Mad network". Gene. 277 (1–2): 1–14. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1016%2FS0378-1119%2801%2900697-7">10.1016/S0378-1119(01)00697-7</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/11602341">11602341</a>.</li>
<li>Hoffman B, Amanullah A, Shafarenko M, Liebermann DA (May 2002). "The proto-oncogene c-myc in hematopoietic development and leukemogenesis". Oncogene. 21 (21): 3414–21. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fsj.onc.1205400">10.1038/sj.onc.1205400</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/12032779">12032779</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:8720539">8720539</a>.</li>
<li>Pelengaris S, Khan M, Evan G (October 2002). "c-MYC: more than just a matter of life and death". Nature Reviews. Cancer. 2 (10): 764–76. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fnrc904">10.1038/nrc904</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/12360279">12360279</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:13226062">13226062</a>.</li>
<li>Nilsson JA, Cleveland JL (December 2003). "Myc pathways provoking cell suicide and cancer". Oncogene. 22 (56): 9007–21. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1038%2Fsj.onc.1207261">10.1038/sj.onc.1207261</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/14663479">14663479</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:24758874">24758874</a>.</li>
<li>Dang CV, O'donnell KA, Juopperi T (September 2005). <a href="https://doi.org/10.1016%2Fj.ccr.2005.08.005">"The great MYC escape in tumorigenesis"</a>. Cancer Cell. 8 (3): 177–8. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1016%2Fj.ccr.2005.08.005">10.1016/j.ccr.2005.08.005</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/16169462">16169462</a>.</li>
<li>Dang CV, Li F, Lee LA (November 2005). <a href="https://doi.org/10.4161%2Fcc.4.11.2121">"Could MYC induction of mitochondrial biogenesis be linked to ROS production and genomic instability?"</a>. Cell Cycle. 4 (11): 1465–6. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.4161%2Fcc.4.11.2121">10.4161/cc.4.11.2121</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/16205115">16205115</a>.</li>
<li>Coller HA, Forman JJ, Legesse-Miller A (August 2007). <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1959363">""Myc'ed messages": myc induces transcription of E2F1 while inhibiting its translation via a microRNA polycistron"</a>. PLOS Genetics. 3 (8): e146. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1371%2Fjournal.pgen.0030146">10.1371/journal.pgen.0030146</a>. <a href="/facts/PMC_(identifier)/dX1zMt71">PMC</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1959363">1959363</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/17784791">17784791</a>.</li>
<li>Astrin SM, Laurence J (May 1992). "Human immunodeficiency virus activates c-myc and Epstein-Barr virus in human B lymphocytes". Annals of the New York Academy of Sciences. 651 (1): 422–32. <a href="/facts/Bibcode_(identifier)/9HtdQSGB">Bibcode</a>:<a href="https://ui.adsabs.harvard.edu/abs/1992NYASA.651..422A">1992NYASA.651..422A</a>. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1111%2Fj.1749-6632.1992.tb24642.x">10.1111/j.1749-6632.1992.tb24642.x</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/1318011">1318011</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:31980333">31980333</a>.</li>
<li>Bernstein PL, Herrick DJ, Prokipcak RD, Ross J (April 1992). <a href="https://doi.org/10.1101%2Fgad.6.4.642">"Control of c-myc mRNA half-life in vitro by a protein capable of binding to a coding region stability determinant"</a>. Genes & Development. 6 (4): 642–54. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1101%2Fgad.6.4.642">10.1101/gad.6.4.642</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/1559612">1559612</a>.</li>
<li>Iijima S, Teraoka H, Date T, Tsukada K (June 1992). <a href="https://doi.org/10.1111%2Fj.1432-1033.1992.tb16964.x">"DNA-activated protein kinase in Raji Burkitt's lymphoma cells. Phosphorylation of c-Myc oncoprotein"</a>. European Journal of Biochemistry. 206 (2): 595–603. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1111%2Fj.1432-1033.1992.tb16964.x">10.1111/j.1432-1033.1992.tb16964.x</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/1597196">1597196</a>.</li>
<li>Seth A, Alvarez E, Gupta S, Davis RJ (December 1991). <a href="https://doi.org/10.1016%2FS0021-9258%2818%2954312-X">"A phosphorylation site located in the NH2-terminal domain of c-Myc increases transactivation of gene expression"</a>. The Journal of Biological Chemistry. 266 (35): 23521–4. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1016%2FS0021-9258%2818%2954312-X">10.1016/S0021-9258(18)54312-X</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/1748630">1748630</a>.</li>
<li>Takahashi E, Hori T, O'Connell P, Leppert M, White R (1991). "Mapping of the MYC gene to band 8q24.12----q24.13 by R-banding and distal to fra(8)(q24.11), FRA8E, by fluorescence in situ hybridization". Cytogenetics and Cell Genetics. 57 (2–3): 109–11. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1159%2F000133124">10.1159/000133124</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/1914517">1914517</a>.</li>
<li>Blackwood EM, Eisenman RN (March 1991). "Max: a helix-loop-helix zipper protein that forms a sequence-specific DNA-binding complex with Myc". Science. 251 (4998): 1211–7. <a href="/facts/Bibcode_(identifier)/9HtdQSGB">Bibcode</a>:<a href="https://ui.adsabs.harvard.edu/abs/1991Sci...251.1211B">1991Sci...251.1211B</a>. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1126%2Fscience.2006410">10.1126/science.2006410</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/2006410">2006410</a>.</li>
<li>Gazin C, Rigolet M, Briand JP, Van Regenmortel MH, Galibert F (September 1986). <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1167107">"Immunochemical detection of proteins related to the human c-myc exon 1"</a>. The EMBO Journal. 5 (9): 2241–50. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1002%2Fj.1460-2075.1986.tb04491.x">10.1002/j.1460-2075.1986.tb04491.x</a>. <a href="/facts/PMC_(identifier)/dX1zMt71">PMC</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1167107">1167107</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/2430795">2430795</a>.</li>
<li>Lüscher B, Kuenzel EA, Krebs EG, Eisenman RN (April 1989). <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC400922">"Myc oncoproteins are phosphorylated by casein kinase II"</a>. The EMBO Journal. 8 (4): 1111–9. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1002%2Fj.1460-2075.1989.tb03481.x">10.1002/j.1460-2075.1989.tb03481.x</a>. <a href="/facts/PMC_(identifier)/dX1zMt71">PMC</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC400922">400922</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/2663470">2663470</a>.</li>
<li>Finver SN, Nishikura K, Finger LR, Haluska FG, Finan J, Nowell PC, Croce CM (May 1988). <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC280141">"Sequence analysis of the MYC oncogene involved in the t(8;14)(q24;q11) chromosome translocation in a human leukemia T-cell line indicates that putative regulatory regions are not altered"</a>. Proceedings of the National Academy of Sciences of the United States of America. 85 (9): 3052–6. <a href="/facts/Bibcode_(identifier)/9HtdQSGB">Bibcode</a>:<a href="https://ui.adsabs.harvard.edu/abs/1988PNAS...85.3052F">1988PNAS...85.3052F</a>. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1073%2Fpnas.85.9.3052">10.1073/pnas.85.9.3052</a>. <a href="/facts/PMC_(identifier)/dX1zMt71">PMC</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC280141">280141</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/2834731">2834731</a>.</li>
<li>Showe LC, Moore RC, Erikson J, Croce CM (May 1987). <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC304752">"MYC oncogene involved in a t(8;22) chromosome translocation is not altered in its putative regulatory regions"</a>. Proceedings of the National Academy of Sciences of the United States of America. 84 (9): 2824–8. <a href="/facts/Bibcode_(identifier)/9HtdQSGB">Bibcode</a>:<a href="https://ui.adsabs.harvard.edu/abs/1987PNAS...84.2824S">1987PNAS...84.2824S</a>. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1073%2Fpnas.84.9.2824">10.1073/pnas.84.9.2824</a>. <a href="/facts/PMC_(identifier)/dX1zMt71">PMC</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC304752">304752</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/3033665">3033665</a>.</li>
<li>Guilhot S, Petridou B, Syed-Hussain S, Galibert F (December 1988). "Nucleotide sequence 3' to the human c-myc oncogene; presence of a long inverted repeat". Gene. 72 (1–2): 105–8. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1016%2F0378-1119%2888%2990131-X">10.1016/0378-1119(88)90131-X</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/3243428">3243428</a>.</li>
<li>Hann SR, King MW, Bentley DL, Anderson CW, Eisenman RN (January 1988). "A non-AUG translational initiation in c-myc exon 1 generates an N-terminally distinct protein whose synthesis is disrupted in Burkitt's lymphomas". Cell. 52 (2): 185–95. <a href="/facts/Doi_(identifier)/muM9Etpq">doi</a>:<a href="https://doi.org/10.1016%2F0092-8674%2888%2990507-7">10.1016/0092-8674(88)90507-7</a>. <a href="/facts/PMID_(identifier)/JlHAvMHt">PMID</a> <a href="https://pubmed.ncbi.nlm.nih.gov/3277717">3277717</a>. <a href="/facts/S2CID_(identifier)/ldJsHa2Y">S2CID</a> <a href="https://api.semanticscholar.org/CorpusID:3012009">3012009</a>.</li></ul>

<h2 id="external-links">External links</h2>
<ul><li><a href="/facts/InterPro/pKwNm8t7">InterPro</a> signatures for protein family: <a href="https://www.ebi.ac.uk/interpro/entry/IPR002418">IPR002418</a>, <a href="https://www.ebi.ac.uk/interpro/entry/IPR011598">IPR011598</a>, <a href="https://www.ebi.ac.uk/interpro/entry/IPR003327">IPR003327</a></li>
<li><a href="https://web.archive.org/web/20071016065223/http://macromoleculeinsights.com/myc.php">The Myc Protein</a>[usurped]</li>
<li><a href="https://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?db=protein&val=71774083">NCBI Human Myc protein</a></li>
<li><a href="http://www.myccancergene.org">Myc cancer gene</a></li>
<li><a href="https://meshb.nlm.nih.gov/record/ui?name=myc+Proto-Oncogene+Proteins">myc+Proto-Oncogene+Proteins</a> at the U.S. National Library of Medicine <a href="/facts/Medical_Subject_Headings/C57g2JuF">Medical Subject Headings</a> (MeSH)</li>
<li><a href="http://www.jove.com/index/details.stp?ID=734">Generating iPS Cells from MEFS through Forced Expression of Sox-2, Oct-4, c-Myc, and Klf4</a> <a href="https://web.archive.org/web/20080409111706/http://www.jove.com/index/details.stp?ID=734">Archived</a> 2008-04-09 at the <a href="/facts/Wayback_Machine/nmQ3a6JC">Wayback Machine</a></li>
<li><a href="http://www.sdbonline.org/fly/dbzhnsky/myc1.htm">Drosophila Myc - The Interactive Fly</a></li>
<li><a href="/facts/ENCODE/X7hhKpsg">FactorBook</a> <a href="http://www.factorbook.org/mediawiki/index.php/C-Myc">C-Myc</a></li>
<li><a href="https://www.ebi.ac.uk/pdbe/pdbe-kb/proteins/P01106">PDBe-KB</a> provides an overview of all the structure information available in the PDB for Human Myc proto-oncogene protein</li></ul>

<h2 id="references">References</h2>

<ol>
<li id="fn:1">"Myc". NCBI. <a href="https://www.ncbi.nlm.nih.gov/gene/17869" target="_blank">https://www.ncbi.nlm.nih.gov/gene/17869</a> <a href="#fnref:1" class="footnote-back-ref">↩</a></li>
<li id="fn:2">Finver SN, Nishikura K, Finger LR, Haluska FG, Finan J, Nowell PC, Croce CM (May 1988). "Sequence analysis of the Myc oncogene involved in the t(8;14)(q24;q11) chromosome translocation in a human leukemia T-cell line indicates that putative regulatory regions are not altered". Proceedings of the National Academy of Sciences of the United States of America. 85 (9): 3052–6. Bibcode:1988PNAS...85.3052F. doi:10.1073/pnas.85.9.3052. PMC 280141. PMID 2834731. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC280141" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC280141</a> <a href="#fnref:2" class="footnote-back-ref">↩</a></li>
<li id="fn:3">"Myc". NCBI. <a href="https://www.ncbi.nlm.nih.gov/gene/17869" target="_blank">https://www.ncbi.nlm.nih.gov/gene/17869</a> <a href="#fnref:3" class="footnote-back-ref">↩</a></li>
<li id="fn:4">Begley S (2013-01-09). "DNA pioneer James Watson takes aim at cancer establishments". Reuters. <a href="https://www.reuters.com/article/us-usa-cancer-watson-idUSBRE90805N20130109" target="_blank">https://www.reuters.com/article/us-usa-cancer-watson-idUSBRE90805N20130109</a> <a href="#fnref:4" class="footnote-back-ref">↩</a></li>
<li id="fn:5">Carabet LA, Rennie PS, Cherkasov A (December 2018). "Therapeutic Inhibition of Myc in Cancer. Structural Bases and Computer-Aided Drug Discovery Approaches". International Journal of Molecular Sciences. 20 (1): 120. doi:10.3390/ijms20010120. PMC 6337544. PMID 30597997. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337544" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6337544</a> <a href="#fnref:5" class="footnote-back-ref">↩</a></li>
<li id="fn:6">Dang CV, Reddy EP, Shokat KM, Soucek L (August 2017). "Drugging the 'undruggable' cancer targets". Nature Reviews. Cancer. 17 (8): 502–508. doi:10.1038/nrc.2017.36. PMC 5945194. PMID 28643779. <a href="/wiki/Laura_Soucek" target="_blank">/wiki/Laura_Soucek</a> <a href="#fnref:6" class="footnote-back-ref">↩</a></li>
<li id="fn:7">Nie Z, Hu G, Wei G, Cui K, Yamane A, Resch W, Wang R, Green DR, Tessarollo L, Casellas R, Zhao K, Levens D (September 2012). "c-Myc is a universal amplifier of expressed genes in lymphocytes and embryonic stem cells". Cell. 151 (1): 68–79. doi:10.1016/j.cell.2012.08.033. PMC 3471363. PMID 23021216. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471363" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471363</a> <a href="#fnref:7" class="footnote-back-ref">↩</a></li>
<li id="fn:8">Gearhart J, Pashos EE, Prasad MK (October 2007). "Pluripotency redux--advances in stem-cell research". The New England Journal of Medicine. 357 (15): 1469–72. doi:10.1056/NEJMp078126. PMID 17928593. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:8" class="footnote-back-ref">↩</a></li>
<li id="fn:9">Cotterman R, Jin VX, Krig SR, Lemen JM, Wey A, Farnham PJ, Knoepfler PS (December 2008). "N-Myc regulates a widespread euchromatic program in the human genome partially independent of its role as a classical transcription factor". Cancer Research. 68 (23): 9654–62. doi:10.1158/0008-5472.CAN-08-1961. PMC 2637654. PMID 19047142. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637654" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2637654</a> <a href="#fnref:9" class="footnote-back-ref">↩</a></li>
<li id="fn:10">Wolf E, Eilers M (2020). "Targeting MYC Proteins for Tumor Therapy". Annual Review of Cancer Biology. 4: 61–75. doi:10.1146/annurev-cancerbio-030518-055826. <a href="https://doi.org/10.1146%2Fannurev-cancerbio-030518-055826" target="_blank">https://doi.org/10.1146%2Fannurev-cancerbio-030518-055826</a> <a href="#fnref:10" class="footnote-back-ref">↩</a></li>
<li id="fn:11">Rahl PB, Young RA (January 2014). "MYC and transcription elongation". Cold Spring Harbor Perspectives in Medicine. 4 (1): a020990. doi:10.1101/cshperspect.a020990. PMC 3869279. PMID 24384817. <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869279" target="_blank">https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869279</a> <a href="#fnref:11" class="footnote-back-ref">↩</a></li>
<li id="fn:12">Dominguez-Sola D, Ying CY, Grandori C, Ruggiero L, Chen B, Li M, Galloway DA, Gu W, Gautier J, Dalla-Favera R (July 2007). "Non-transcriptional control of DNA replication by c-Myc". Nature. 448 (7152): 445–51. Bibcode:2007Natur.448..445D. doi:10.1038/nature05953. PMID 17597761. S2CID 4422771. <a href="/wiki/Bibcode_(identifier)" target="_blank">/wiki/Bibcode_(identifier)</a> <a href="#fnref:12" class="footnote-back-ref">↩</a></li>
<li id="fn:13">Denis N, Kitzis A, Kruh J, Dautry F, Corcos D (August 1991). "Stimulation of methotrexate resistance and dihydrofolate reductase gene amplification by c-myc". Oncogene. 6 (8): 1453–7. PMID 1886715. <a href="/wiki/PMID_(identifier)" target="_blank">/wiki/PMID_(identifier)</a> <a href="#fnref:13" class="footnote-back-ref">↩</a></li>
<li id="fn:14">Campisi J, Gray HE, Pardee AB, Dean M, Sonenshein GE (1984). "Cell-cycle control of c-myc but not c-ras expression is lost following chemical transformation". Cell. 36 (2): 241–7. doi:10.1016/0092-8674(84)90217-4. PMID 6692471. S2CID 29661004. <a href="/wiki/Doi_(identifier)" target="_blank">/wiki/Doi_(identifier)</a> <a href="#fnref:14" class="footnote-back-ref">↩</a></li>
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</ol>

Myc open-in-new

Myc