Abcam, ab265001, Human NLK knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
NLK KO cell line available to order. KO validated by. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, 14 bp deletion in exon 1 and Insertion of the selection cassette in exon 1. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 14 bp deletion in exon 1 and Insertion of the selection cassette in exon 1,
Disease:Adenocarcinoma

Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-NLK, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
NLK (Nemo-Like Kinase) functions as a serine/threonine protein kinase involved in various signaling pathways. It alternatively is known as nemo-like protein or nlk. The molecular mass of NLK is approximately 54 kDa. Expression of NLK occurs in various tissues but it is highly observed in the brain and testis. This wide expression suggests that NLK may have diverse functional roles.
Biological function summary
NLK participates in regulating cellular processes such as cell cycle apoptosis and transcription. It is not part of a larger complex but works within signaling pathways to influence these processes. NLK modulates the activity of several transcription factors particularly in the Wnt/beta-catenin signaling pathway where it negatively regulates the signaling to control gene expression relevant to cell proliferation and differentiation.
Pathways
NLK is an important player in the Wnt/beta-catenin and MAPK pathways. In the Wnt/beta-catenin pathway it associates with proteins such as TCF/LEF and beta-catenin acting to modulate transcription by phosphorylating these molecules. The MAPK pathway involves NLK in response to stress signals coordinating with proteins like TAK1 to mediate cellular responses. These pathways illustrate NLK's role in transmitting signals that govern cell fate and stress responses.
NLK has links to cancer and neurodegenerative diseases. Alterations in NLK expression or function can contribute to the development and progression of cancers by affecting the regulation of cell proliferation and apoptosis. Specifically dysregulation in the Wnt/beta-catenin pathway in which NLK acts relates to colorectal cancers. In the context of neurodegenerative diseases NLK has connections with the protein TDP-43 which is implicated in diseases such as amyotrophic lateral sclerosis highlighting its role in neuronal health and potential links to neuronal degradation.