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c-Myc
The proto-oncogene, MYC, lies at the crossroads of many growth promoting signal transduction pathways and is an immediate early response gene downstream of many ligand-membrane receptor complexes. MYC expression is highly regulated, such that its level of expression is tightly control by a number of mechanisms involving many transcriptional regulatory motifs found within its proximal promoter region. Mammary carcinoma triggered by transgenic Myc expression acquired K-ras mutations that rendered tumors aggressive. Acute overexpression of MYC in normal cells triggers checkpoints including ARF or p53, such that many MYC-induced transgenic lymphomas lacks functional Arf or p53.
Among the vast numbers of targets that are repressed by Myc, a fraction is linked to Miz-1, which activates these genes. TGFβ signaling best illustrates a role for Myc-Miz-1 interaction. In the absence of TGFβ, Myc represses CDKN2B (p15INK4b) by binding Miz-1 and displacing Miz-1 cofactors to silence CDKN2B. With TGFβ, MYC expression is suppressed, and the Smad transcription factor translocates and cooperates with Miz-1 to recruit NPM1 as a Miz-1 cofactor to stimulate CDKN2B transcription and induce cell cycle arrest. Myc, on the other hand, activates many ribosomal protein genes including Rpl23, which binds to and retains NPM1 in the nucleolus, thereby inhibiting Miz-1 activity. Myc itself is modulated by NPM1, which acts as a positive Myc coactivator.
References
1.Chi V. Dang. Cell. 2012 Mar 30; 149(1): 22–35.
Among the vast numbers of targets that are repressed by Myc, a fraction is linked to Miz-1, which activates these genes. TGFβ signaling best illustrates a role for Myc-Miz-1 interaction. In the absence of TGFβ, Myc represses CDKN2B (p15INK4b) by binding Miz-1 and displacing Miz-1 cofactors to silence CDKN2B. With TGFβ, MYC expression is suppressed, and the Smad transcription factor translocates and cooperates with Miz-1 to recruit NPM1 as a Miz-1 cofactor to stimulate CDKN2B transcription and induce cell cycle arrest. Myc, on the other hand, activates many ribosomal protein genes including Rpl23, which binds to and retains NPM1 in the nucleolus, thereby inhibiting Miz-1 activity. Myc itself is modulated by NPM1, which acts as a positive Myc coactivator.
References
1.Chi V. Dang. Cell. 2012 Mar 30; 149(1): 22–35.
Cell Cycle/DNA Damage
ABC(12)
AChR(104)
Antifolate(12)
ATM/ATR(26)
Aurora Kinase(51)
CLK(15)
c-Myc(22)
DHFR(16)
DNA Alkylator(34)
DNA gyrase(11)
DNA Repair Protein(21)
DNA/RNA Synthesis(187)
DNA-PK(15)
GPR(97)
HDAC(152)
Hec1/Nek2(9)
Integrin(77)
LIM Kinase (LIMK)(7)
Mps1/TTK(2)
Nucleoside Antimetabolite/Analog(48)
Other Targets(4)
PAK(13)
PARP(67)
PLK(26)
Potassium Channel(146)
RAD51(1)
Rho(16)
ROCK(42)
Telomerase(12)
Topoisomerase(88)
Wee1(7)
c-Myc
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10074-A4
产品货号 : M28813
cas no: 312631-87-1
10074-A4 是一种 c-Myc 结合化合物，与 c-Myc370-409 结合，其行为类似于“蛋白质云”周围的“配体云”，具有与非结合配体不同的特征。
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NY2267
产品货号 : M24905
cas no: 886053-73-2
NY2267 是 Myc-Max 相互作用的破坏者，IC50 为 36.5 μM。
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EN4 MYC inhibitor
产品货号 : M23368
cas no: 1197824-15-9
EN4 MYC 抑制剂是一种共价配体，靶向 MYC 的半胱氨酸 171 (C171)。
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APTO-253
产品货号 : M22678
cas no: 916151-99-0
APTO-253 抑制 c-Myc 表达，稳定 G-四链体 DNA，并诱导急性髓系白血病细胞的细胞周期停滞和细胞凋亡。 APTO-253 通过诱导 KLF4 肿瘤抑制因子介导抗癌活性。APTO-253 (5 μM) 可诱导 SKOV3 和 OVCAR3 细胞中 KLF4 表达并增强 NSC 119875 诱导的细胞凋亡。
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MYCi975
产品货号 : M22558
cas no: 2289691-01-4
MYCi975 是一种口服活性的 MYC 抑制剂。MYCi975 以 MYC 依赖性方式抑制 P493-6、MV411、SK-N-B2 细胞活力（IC50 分别为 3.7、3.9、6.4 μM）。初始先导物 MYC 抑制剂 361 (MYCi361)，抑制小鼠体内肿瘤生长，增加肿瘤免疫细胞浸润，上调肿瘤上的 PD-L1，并使肿瘤对抗 PD1 免疫疗法敏感。
