mProX™ Human NEK7 Stable Cell Line

Chen, Lei. et al. "Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett's Esophagus." Cancers, 2023.
The incidence of esophageal adenocarcinoma (EAC) has increased in the past four decades, making it the most prevalent type of esophageal cancer in the USA and Western countries. The NEK (Never in mitosis A (NIMA) related kinase) gene family is a group of serine/threonine kinases with 11 members. Recent studies have revealed aberrant expression of NEKs in various human cancers, contributing to tumorigenesis, progression, and drug-resistance. However, the expression of NEKs in EAC and its precursor condition, Barrett's esophagus (BE), has not been studied. Through bioinformatic analyses of 10 databases, including TCGA and 9 GEO, it was found that NEK2, NEK3, and NEK6 were upregulated, while NEK1 was downregulated in EAC compared to normal esophagus samples. These findings were validated through qRT-PCR, Western blotting, and immunohistochemistry/immunofluorescence in EAC cell lines and primary EAC tissues. The results suggest that NEK2, NEK3, and NEK7 may play significant roles in EAC development.
Chen, Lei. et al. "Differential Expression of NEK Kinase Family Members in Esophageal Adenocarcinoma and Barrett's Esophagus." Cancers, 2023.
Pubmed: 37835513   DOI: 10.3390/cancers15194821

Lin, Yuanbang. et al. "Caspase 6 promotes innate immune activation by functional crosstalk between RIPK1-IκBα axis in liver inflammation." Cell communication and signaling : CCS, 2023.
Caspase 6 plays a critical role in innate immunity, inflammasome activation, and host defense, particularly in liver sterile inflammatory injury. The study utilized human liver tissues from ischemia-related hepatectomy patients and Caspase 6-knockout (Caspase 6KO) mice to investigate Caspase 6's involvement in liver ischemia/reperfusion (IR) injury. In human liver biopsies, Caspase 6 expression correlated with severe histopathological injury and elevated ALT/AST levels postoperatively. Interestingly, Caspase 6 was primarily elevated in macrophages, not hepatocytes, in ischemic livers. Caspase 6 deficiency in mice protected against IR injury, suppressing inflammation, oxidative stress, and iron overload. Disrupting macrophage NF-κB essential modulator (NEMO) in Caspase 6-deficient livers exacerbated liver inflammation and ferroptosis. Mechanistically, Caspase 6 deficiency induced NEMO-mediated IκBα phosphorylation in macrophages, leading to RIPK1 degradation and subsequent activation of NEK7/NLRP3. Furthermore, targeting macrophage RIPK1 or ASK1 reduced NEK7/NLRP3-driven inflammation and mitigated hepatocyte ferroptosis by reducing HMGB1 release from macrophages. These findings unveil a novel Caspase 6-mediated mechanism involving RIPK1-IκBα interaction that regulates macrophage NEK7/NLRP3 function and hepatocyte ferroptosis, offering potential therapeutic targets for clinical liver IR injury.
Lin, Yuanbang. et al. "Caspase 6 promotes innate immune activation by functional crosstalk between RIPK1-IκBα axis in liver inflammation." Cell communication and signaling : CCS, 2023.
Pubmed: 37828624   DOI: 10.1186/s12964-023-01287-x