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ATM/ATR
Both ATM and ATR can be activated by DNA damage, although it is not known exactly how these two kinases sense such damage. However, ATM responds primarily to doublestrand breaks (DSBs) induced by IR, while ATR also reacts to UV or stalled replication forks.Nevertheless,there is no clean-cut differentiation between the signals for the two kinases, as ATM also functions in some UV responses, mediating the repair of UV-induced DNA damage and the phosphorylation of STAT3. ATM is also involved in UVA-induced signaling and apoptosis, whereas ATR functions in UVC-induced signaling and apoptosis. It was previously thought that ATM and ATR might be activated both through interactions with DNA and with members of the repair complexes.ATM can bind directly to DNA and pre-treatment of DNA±cellulose matrix with IR or restriction enzymes stimulates ATM binding, suggesting that ATM binds to DNA ends.
ATR also binds to DNA and with higher affinity to UV-damaged than to undamaged DNA. In addition, damaged DNA stimulates the kinase activity of ATR to a significantly higher level than does undamaged DNA. ATM and ATR also interact with many proteins that co-localize at the site of DNA damage to form `foci' .ATM/ATR can usually be found in these areas several minutes after the damage occurs, supporting a role for these two kinases in the damage sensing process. The other proteins involved include structural proteins of chromatin, proteins that function in chromosomal repair and maintenance and, on some occasions, transcription factors, for exmaple BRCA-1, H2AX, MDC1, WRN, 53BP1 and E2F1.
References
1.Yang J, et al. Carcinogenesis. 2003 Oct;24(10):1571-80.
ATR also binds to DNA and with higher affinity to UV-damaged than to undamaged DNA. In addition, damaged DNA stimulates the kinase activity of ATR to a significantly higher level than does undamaged DNA. ATM and ATR also interact with many proteins that co-localize at the site of DNA damage to form `foci' .ATM/ATR can usually be found in these areas several minutes after the damage occurs, supporting a role for these two kinases in the damage sensing process. The other proteins involved include structural proteins of chromatin, proteins that function in chromosomal repair and maintenance and, on some occasions, transcription factors, for exmaple BRCA-1, H2AX, MDC1, WRN, 53BP1 and E2F1.
References
1.Yang J, et al. Carcinogenesis. 2003 Oct;24(10):1571-80.
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)
ATM/ATR
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Lartesertib
产品货号 : M35661
cas no: 2495096-26-7
Lartesertib (M4076) 是一种有效的丝氨酸/苏氨酸蛋白激酶 ATM 的抑制剂 (信息提取自专利 WO2022058351A1)。
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Camonsertib
产品货号 : M35617
cas no: 2417489-10-0
Camonsertib (RP-3500) 是一种口服有效的，选择性 ATR 激酶抑制剂 (ATRi)，在生化试验中的 IC50 为 1.00 nM。Camonsertib 对 ATR 的选择性是 mTOR 的 30 倍 (IC50=120 nM)，是 ATM、DNA-PK 和 PI3Kα 激酶的 > 2,000 倍。Camonsertib 具有有效的抗肿瘤活性。
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Ro 90-7501
产品货号 : M33482
cas no: 293762-45-5
Ro 90-7501 是一种淀粉样 β42 (Aβ42) 原纤维组装抑制剂，可降低 Aβ42 诱导的细胞毒性 (EC50 为 2 μM)。Ro 90-7501 抑制 ATM 磷酸化和 DNA 修复。RO 90-7501选择性增强 TLR3和 RLR 配体诱导的 IFN-β 基因表达和抗病毒反应。Ro 90-7501 还以 TPR 依赖性方式抑制蛋白磷酸酶 5 (PP5)，并对宫颈癌细胞具有显着的放射增敏作用。
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KU 59403
产品货号 : M33395
cas no: 845932-30-1
KU 59403 是 ATM 的一个有效抑制剂，其对 ATM、DNA-PK 和 PI3K 的 IC50 值分别为 3 nM、9.1 μM 和 10 μM。
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AZ-32
产品货号 : M22388
cas no: 2288709-96-4
AZ32 是一种具有口服生物利用度和血脑屏障穿透性的 ATM 抑制剂（ATM 酶和细胞内的 IC50 分别为 <6.2 nM 和 0.31 μM）。
