NLK

Official Full Name

nemo like kinase

Organism

Homo sapiens

Gene ID

51701

Background

Enables DNA-binding transcription factor binding activity; protein serine/threonine kinase activity; and ubiquitin protein ligase binding activity. Involved in several processes, including negative regulation of TORC1 signaling; protein stabilization; and transforming growth factor beta receptor signaling pathway. Predicted to be located in cytosol and nucleoplasm. Predicted to be active in cytoplasm and nucleus. [provided by Alliance of Genome Resources, Feb 2025]

Synonyms

Or10g9b; Olfr980; MOR223-2

Cat.No.	Product Name	Price
CSC-DC010427	Panoply™ Human NLK Knockdown Stable Cell Line	Inquiry
CSC-SC010427	Panoply™ Human NLK Over-expressing Stable Cell Line	Inquiry
CSC-RT0821	Human NLK Knockout Cell Line-HeLa	Inquiry
CLOE-0848	Human NLK Insect Cell Lysate	Inquiry
CLKO-0324	NLK KO Cell Lysate-HeLa	Inquiry

Cat.No.	Product Name	Price
AD00211Z	Human NLK(DN) adenoviral particles	Inquiry
AD00212Z	Human NLK adenoviral particles	Inquiry
AD10828Z	Human NLK adenoviral particles	Inquiry
LV19619L	human NLK (NM_016231) lentivirus particles	Inquiry

Cat.No.	Product Name	Price
SHH352836	shRNA set against Human NLK (NM_016231.4)	Inquiry
SHH352840	shRNA set against Mouse NLK (NM_008702.3)	Inquiry
SHH352844	shRNA set against Rat NLK (NM_001191924.1)	Inquiry
SHR012640	shRNA set against Human NLK(NM_016231.4)	Inquiry
SHR012658	shRNA set against Mouse Nlk(NM_008702.3)	Inquiry

Cat.No.	Product Name	Price
CDCS414225	Human NLK ORF Clone (BC064663)	Inquiry
CDFG000077	Human NLK cDNA Clone(NM_016231.4)	Inquiry
MiUTR1H-06791	NLK miRNA 3'UTR clone	Inquiry
MiUTR1M-07681	NLK miRNA 3'UTR clone	Inquiry
SKO0633	NLK Validated sgRNA vector	Inquiry
CDCB188488	Rabbit NLK ORF clone (XM_002718934.2)	Inquiry
CDCL138633	Human NLK ORF clone (NM_016231.4)	Inquiry
CDCL151464	Mouse Nlk ORF clone (NM_008702.3)	Inquiry
CDCL185492	Human NLK ORF clone(NM_002946.3)	Inquiry

Detailed Information

Nemo-like kinase (NLK) is an evolutionarily highly conserved MAPK-like kinase that is widely distributed in various tissues and organs of the body. Many studies have found that NLK can participate in the growth, differentiation, proliferation and apoptosis of tumor cells by regulating a variety of signaling pathway molecules such as Wnt/β-catenin, c-Myb, and caspase-3. Abnormally expressed NLK plays an important role in the development of neoplastic diseases and in judging the prognosis of the disease.

NLK Related Signaling Pathway

NLK exists in many signal paths, the most important of which is the Wnt/Wg signal path. Studies have shown that NLK plays an important role in the regulation of cell growth, differentiation, embryo development and tumorigenesis and development by negatively regulating the classical Wnt/β-catenin pathway by phosphorylated T-cell factor/lymphocyte enhancer family members. NLK affects the phosphorylation signal transduction and activator of transcription 3 (STAT3), and is involved in transforming growth factor beta (TGF-β)-induced Xenopus embryos. It plays an important role in the development of mesoderm. Phosphorylation of the c-Myb-related site leads to ubiquitination of c-Myb and degradation of the proteasome. In addition, NLK is also involved in the Notch/Delta signaling pathway and is closely related to the development of the animal mesoderm blood system.

It was found that NLK inhibits the transcriptional activity of the β-catenin/TCF complex by phosphorylating T cell factor (TCF) and inhibits the classical Wnt signal. The Wnt/β-catenin signaling pathway plays an important role in tumor formation, suggesting that NLK, a negative regulator of the Wnt/β-catenin signaling pathway, may be a tumor suppressor. Other studies have shown that NLK acts as a tumor suppressor gene in breast cancer tissues and inhibits tumors by inhibiting the Wnt/βcatenin signal pathway. In the cascade of TAK1-NLK signaling, TGF-β-activated kinase 1 (TAK1) is a downstream agonist of NLK kinase activity, and the TAK1-NLK pathway is regulated negatively. The classical Wnt/β-catenin pathway plays an important role. NLK phosphorylates T cell factor/lymphocyte potentiating factor and inhibits its activity. NLK is able to directly phosphorylate lymphocyte enhancer factor 1/T cytokines (LEF1/TCFs) to block beta-catenin LEF1/TCFs complex binding to DNA. NLK phosphorylation of LEF1/TCFs simultaneously promotes ubiquitination of LEF1/TCFs, leading to degradation of LEF1/TCFs, thereby inhibiting β-catenin-dependent transcription.

Nlk Figure 1. Schematic representation of the proposed signaling pathways for NLK-inhibited Nurr1 expression in PCa cells. (Wang, J., et al. 2016)

NLK and Tumor

The study used immunohistochemistry (IHC) staining to find that NLK was only expressed in the nucleus of ovarian cancer tissue, which was significantly reduced compared with normal ovarian tissue. The down-regulated NLK was not associated with malignant cells, age, cytopathology, residual tumor, ascites, and ascites, but was closely related to clinical stage and pathological grade. In a 5-year follow-up study, abnormally expressed NLK was significantly associated with prognosis in patients. The high overall survival rate of patients with low expression of NLK was significantly lower in patients, suggesting that NLK is one of the indicators for predicting the prognosis of patients with ovarian cancer. Furthermore, in vitro studies have found that NLK plays an important role in the chemotherapy of ovarian cancer. Overexpression of NLK promoted cisplatin-induced apoptosis in ovarian cancer SKOV3 cells and inhibited their growth; inhibition of NLK reversed cisplatin-induced apoptosis and growth of SKOV3 cells.

Studies have confirmed that NLK expression is significantly up-regulated in human hepatocellular carcinoma tissues compared with corresponding normal liver tissues, and significant NLK overexpression in hepatocellular carcinoma occurs. Targeting cleavage of NLK inhibits both cyclin D1 and cyclin-dependent protein kinase 2, thereby inhibiting hepatoma cell growth and cell cycle transition. NLK can be used as a target protein of miRNA, and participates in the process of miRNA regulating tumor cell growth and proliferation.

References:

Wang, J. , Yang, Z. H. , Chen, H. , Li, H. H. , Chen, L. Y. , & Zhu, Z. , et al. (2016). Nemo-like kinase as a negative regulator of nuclear receptor nurr1 gene transcription in prostate cancer. BMC Cancer, 16(1), 257.
Todd, T. W. , Kokubu, H. , Miranda, H. C. , Cortes, C. J. , & Spada, A. R. L. . (2015). Nemo-like kinase is a novel regulator of spinal and bulbar muscular atrophy. eLife, 4, (2015-08-24), 4.
Shawhallgren, G., Chmielarska, M. K., Zarrizi, R., Hellman, U., Karlsson, P., & Helou, K., et al. (2014). Association of nuclear-localized nemo-like kinase with heat-shock protein 27 inhibits apoptosis in human breast cancer cells. Plos One, 9(5), e96506.

Quick Inquiry

NLK

You might be looking for:

Detailed Information