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Methyltransferase-like 3 (METTL3) is the only catalytic subunit of the transferase complex responsible for m6A modification, and it has been found to play a key role in tumorigenesis, tumor growth, metastasis and tumor drug resistance. In recent years, METTL3 has attracted more and more attention as a potential target for cancer treatment.

On this basis, we established an in vitro and in vivo screening platform on METTL3/14 complex, which can realize high-throughput screening of METTL3 inhibitors in vitro experiments. High purity METTL3/14 protein complex has been successfully purified and used in develop METTL3/14 biochemical experiments. We have also established different cellular assays, including proliferation and m6A RNA Methylation quantification assay. Lastly, CDX models utilizing different Ovarian cell lines have been validated. We aim to aid the discovery of new drugs through the METTL3/14 screening cascade.

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Lysine acetyltransferase 6A (KAT6A, also called MOZ and MYST3) is a histone acetyltransferase (HAT) belonging to the MYST family. Other members include MOF(KAT8)、MORF(KAT6B)、TIP60(KAT5) and HBO1(KAT7). The histone substrates of KAT6A identified to date include H3K9, -K14, and -K23. KAT6A has been reported to play a critical role in hematopoietic stem cell maintenance, cell cycle regulation, and cell senescence. In addition, KAT6A is thought to be an oncogene in human cancers, including breast cancer, glioma and leukemia. Here, we have developed KAT6A related biochemical assays, cellular assays and in vivo pharmacology models to support novel KAT6A inhibitor discovery.

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High-throughput screening cell panel is very important tool in drug research and development, the tested sensitive cell lines can provide references for in vivo models or indication for the selection of clinical trial subjects. Cell Panel screening can be used to study the mechanism of action and selectivity of drugs, and combined with bioinformatics studies can help researchers discover biomarkers of drug response. Moreover, Cell Panel screening can be used to study whether combination therapy strategies improve cancer treatment effect and solve clinical drug resistance and other problems.

The Human RAS Oncogenes play a vital role in cancer development, including KRAS, NRAS and HRAS, KRAS is the most frequently mutated RAS isoform with a mutation incidence of >10% across all cancers, and up to 70% and 20% in pancreatic and non-small cell lung cancer (NSCLC), respectively.

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Werner Syndrome (WS) is an autosomal-recessive genetic disorder characterized by premature ageing and DNA repair defects because of mutations in the WRN gene. WRN is a RecQ family protein with helicase, strand annealing and exonuclease activities. WRN localizes to the sites of damaged DNA, interacts with several DNA repair pathways including base excision DNA repair, non-homologous end-joining (NHEJ), homologous recombination (HR) and replication re-start after DNA damage.

Here, we constructed an experimental cascade from in vitro to in vivo, which is composed of protein production, biochemical assays, cell line construction, cellular assays, and animal modeling. This WRN screening cascade can satisfy the mechanism study of WRN as well as efficient and comprehensive screen of WRN inhibitor, thus accelerate the novel drug discovery.