mProX™ Human NEK6 Stable Cell Line

Sub Cat	Product Name	Target Protein Species	Host Cell Type	Assay Types	Inquiry	Datasheet
S01YF-1222-KX402	Magic™ Human NEK6 in Vitro Assay	Human		Kinase Assay

Product Information

Target Family

Kinases/Enzyme

Target Protein Species

Human

Host Cell Type

HEK293;CHO-K1;HeLa

Target Classification

Kinase Cell Lines

Gene ID

Human:10783

UniProt ID

Human:Q9HC98

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

NEK6, a member of the NEK (Never in mitosis A (NIMA) related kinase) gene family, has been found to be differentially expressed in various diseases and has implications in tumorigenesis, tumor progression, drug resistance, neurodevelopmental disorders, and macrophage polarization. In esophageal adenocarcinoma (EAC) and its precancerous condition, NEK6 was found to be significantly upregulated. NEK6 also plays a role in promoting axon targeting in neural development. In macrophages, NEK6 knockdown polarized them into a pro-inflammatory phenotype. Additionally, NEK6 was found to promote the progression of osteosarcoma by activating the STAT3 signaling pathway and was identified as a potential therapeutic target for hepatocellular carcinoma (HCC). These studies highlight the diverse applications of NEK6 in various diseases and biological processes.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Alex Miller (Verified Customer)

How does NEK6 contribute to tumorigenesis? Sep 18 2022

chat Patrick Liam (Creative Biolabs Scientific Support)

NEK6 is involved in cell cycle control and plays significant roles in tumorigenesis. Sep 18 2022

chat Taylor Miller (Verified Customer)

What is the relationship between NEK6 and castration-resistant prostate cancer (CRPC)? May 29 2023

chat Patrick Liam (Creative Biolabs Scientific Support)

NEK6 is a central kinase in developing CRPC, influencing cancer cell adaptation to high reactive oxygen species (ROS) levels and avoiding cell death by increasing antioxidant defenses. May 29 2023

Published Data

Fig.1 Endogenous Nek6 knockdown causes M phase arrest.

Western blot analysis was conducted to assess endogenous Nek6 protein levels following siRNA transfection, using 40 μg of total protein per lane. Immunoblotting employed anti-α-tubulin antibody as a loading control and anti-Nek6 anti-serum. The experimental groups included control lamin A/C siRNA transfection (Group 1) and Nek6-specific siRNA transfections (Groups 2 and 3). Cellular samples were split and retransfected on the fifth day, and subsequent harvests were performed at various days post-transfection as indicated. HeLa cells transfected with control and Nek6-specific siRNA were subjected to FACS analysis on day 7 post-transfection, with Sub-G1 and M phase cell populations quantified and presented as percentages.

Ref: Yin, Min-Jean, et al. "The serine/threonine kinase Nek6 is required for cell cycle progression through mitosis." Journal of Biological Chemistry 278.52 (2003): 52454-52460.

Pubmed: 14563848

DOI: 10.1074/jbc.M308080200

Research Highlights

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 drastically over the past four decades, making it the most prevalent form of esophageal cancer in the United States and Western countries. The NEK (Never in mitosis A (NIMA) related kinase) gene family, which includes 11 members, has been linked to various human cancers and plays a critical role in tumorigenesis, progression, and drug resistance. However, the expression of NEKs in EAC and its precursor condition, Barrett's esophagus (BE), has not been thoroughly investigated. In this study, multiple bioinformatic analyses were performed to examine the expression of NEKs in EAC and BE using data from 10 databases (TCGA and 9 GEO databases, including 8 with EAC and 6 with BE). Results showed a significant upregulation of NEK2 (7/8), NEK3 (6/8), and NEK6 (6/8) in EAC compared to normal esophagus samples. In contrast, NEK1 was downregulated in EAC samples. However, alterations in the genomic sequence of these NEKs were not frequently observed in EAC. These findings were confirmed using qRT-PCR, Western blotting, and immunohistochemistry and immunofluorescence on EAC cell lines and primary EAC tissues. Overall, the study suggests that the frequent upregulation of NEK2, NEK3, and NEK7 may hold significant implications for 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

J, Cody; C, Christopher. "UNC-116 and UNC-16 function with the NEKL-3 kinase to promote axon targeting." Development (Cambridge, England), 2023.
The study focuses on the role of KIF5C, a kinesin-1 heavy chain, in axon targeting. Through genetic analysis and imaging experiments in Caenorhabditis elegans, the researchers demonstrate that UNC-116/KIF5C works with the NEKL-3/NEK6/7 kinase to promote axon targeting. Furthermore, they find that the UNC-16/JIP3 kinesin-1 cargo adaptor is necessary for proper axon termination, while the kinesin-1 light chain does not play a significant role. The results suggest a model in which UNC-116 and UNC-16 collaborate to localize NEKL-3, which then works with the RPM-1 ubiquitin ligase to facilitate axon termination.
J, Cody; C, Christopher. "UNC-116 and UNC-16 function with the NEKL-3 kinase to promote axon targeting." Development (Cambridge, England), 2023.
Pubmed: 37756604 DOI: 10.1242/dev.201654