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.
A new collaborative report from IARC. There were almost 20 million new cases of cancer and close to 10 million deaths from cancer in 2022. Despite an estimated increase to more than 2.31 million new cases, breast cancer became the second most common cancer type, after lung cancer. The most common subtype, hormone-receptor-positive/HER2-negative (HR+ or ER+/HER2-), accounts for 69% of all cases. Cyclin-dependent kinase (CDK) 4/6 inhibition in combination with endocrine therapy is the standard-of-care treatment for patients with advanced-stage HR+HER2- breast cancer. Cell cycle regulators with promising clinical potential include CDK2, CDK4, CDK7, PLK4, WEE1, PKMYT1, AURKA and TTK. Novel inhibitors of these targets, alone or in combination, may overcome CDK4/6 inhibitor resistance. Based on this, we have established a series of in vivo and in vitro assays on CDK family targets. On this basis, we have established a series of in vitro and in vivo experiments on CDK family targets, which can achieve high-throughput screening in vitro experiments, providing a faster screening strategy for CDKs inhibitors.
The PARP (Poly(ADP-ribose) polymerase) family consists of enzymes vital for cellular functions, notably DNA repair, crucial for genomic stability. Once malfunction, these enzymes can contribute to various diseases, including cancer, neurodegenerative disorders, and inflammatory conditions. PARP inhibitors (PARPi), which target these enzymes, have shown promise as treatments for certain cancers, particularly those with DNA repair pathway defects such as BRCA-mutated cancer. Here, we have developed and validated PARP-related biochemical assays, cell-based assays, drug resistant cell line construction, and in vivo pharmacology models to support novel PARPi discovery.
Phosphodiesterases (PDEs) are enzymes that hydrolyze cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) into AMP and GMP, respectively. Inhibitors of PDEs allow the elevation of cAMP and cGMP which lead to a variety of cellular effects including airway smooth muscle relaxation and inhibition of cellular inflammation or of immune responses. PDE4 inhibitors are potent inhibitors of inflammation, and they have been approved for the treatment of inflammatory diseases ranging from arthritis to chronic obstructive pulmonary disease (COPD). In addition, PDE4 inhibitors are approved as oral or topical treatments for psoriasis and atopic dermatitis, respectively. As PDE4 is such an appealing clinical target for many additional non-dermatologic indications, additional research has continued to pursue strategies to widen the therapeutic index. Therefore, we have launched these integrated services for PDE4 screening platform from in vitro to in vivo, to get a comprehensive investigation of PDE4.
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