Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Serine/threonine-protein kinase that regulates a number of transcription factors with key roles in cell fate determination. Additionally we are shipping Nemo-Like Kinase Proteins (11) and Nemo-Like Kinase Kits (5) and many more products for this protein.
Showing 10 out of 112 products:
Human Monoclonal NLK Primary Antibody for WB - ABIN1882269
Ohkawara, Shirakabe, Hyodo-Miura, Matsuo, Ueno, Matsumoto, Shibuya: Role of the TAK1-NLK-STAT3 pathway in TGF-beta-mediated mesoderm induction. in Genes & development 2004
Show all 4 Pubmed References
our data suggest that NLK/Nemo (show IKBKG Antibodies) acts as an endogenous regulator of Hippo signaling by controlling nuclear localization and activity of YAP/Yorkie (show YAP1 Antibodies).
NLK is a novel signaling molecule for proper lung development through the interconnection between epithelial and endothelial cells during lung morphogenesis
NLK can phosphorylate the mutant polyglutamine-expanded androgen receptor (show AR Antibodies) protein, enhance its aggregation, and promote androgen receptor (show AR Antibodies)-dependent gene transcription by regulating androgen receptor (show AR Antibodies)-cofactor interactions.
Nlk is a negative regulator of skeletal homeostasis.
PGI (show BGN Antibodies) is a moonlighting protein that functions as a cytosolic enzyme involved in glycolysis and gluconeogenesis, and as cytokine through binding to its cell surface receptor.
The mGPI-transgenic mice presented GPI (show GPI Antibodies) more efficiently and showed a dramatic increase in negative selection and an inhibition of arthritis.
either reducing NLK enzymatic activity or decreasing NLK expression levels can have beneficial effects against the toxicity induced by polyglutamine-expanded ATXN1 (show ATXN1 Antibodies)
Increased red cell turnover in a line of CD22 (show CD22 Antibodies)-deficient mice is caused by Gpi1c: a model for hereditary haemolytic anaemia.
NEMO (show IKBKG Antibodies) binding domain peptide treatment results in improved generation of specific force and greater resistance to lengthening activations in dystrophic diaphragm muscle ex vivo.
Nlk suppresses osteoblastogenesis by opposing BMP/Smad (show SMAD1 Antibodies) and WNT (show WNT2 Antibodies) canonical signaling
NLK negatively regulates Notch (show NOTCH1 Antibodies)-dependent transcriptional activation by phosphorylating Notch1ICD. Phosphorylated Notch1ICD is impaired in its ability to form a transcriptionally active ternary complex.
nlk strongly enhances convergent/extension phenotypes, suggesting a role in modulating cell movements as well as cell fate.
NLK1 acts as a kinase by catalyzing phosphorylation of pumilio (Pum)1, Pum2, and cytoplasmic polyadenylation element binding protein 1 (CPEB) to regulate translation of mRNAs, including cyclin B1 mRNA, stored in oocytes.
These results provide the first evidence that p38 (show MAPK14 Antibodies) specifically regulates NLK function, which is required for anterior formation in Xenopus development.
Our results suggest that NLK inhibits transcriptional activation of Nurr1 (show NR4A2 Antibodies) gene by impeding CBP's role as a co-activator of NF-kappaB (show NFKB1 Antibodies) and CREB (show CREB1 Antibodies) in prostate cancer.
The expression of NLK was negatively correlated with TCF4 (show TCF4 Antibodies) expression in lung cancers
NLK overexpression is an independent prognostic factor in colorectal cancer and knockdown of NLK expression inhibits colorectal cancer progression and metastasis.
Further experiments demonstrated that the overexpression of miR3623p resulted in decrease expression levels of nemo-like kinase
NLK was involved in miR (show MLXIP Antibodies)-92b-induced cell proliferation, and its protein level was obviously downregulated in the miR (show MLXIP Antibodies)-92b-overexpressing xenograft tumors.
Data show that metformin inhibits nemo like kinase (NLK) expression and might be a potential treatment strategy for non-small cell lung cancer (NSCLC).
Down-regulation of NLK inhibited tumorigenesis and up-regulated the expression of cell cycle proteins in laryngeal cancer cells.
In this review, we will make a summary on the comprehensive roles of NLK in the regulation of various cancers
These data show that porcine epidemic diarrhea virus nsp5 (show SPECC1 Antibodies) disrupts type I interferon (show IFNA Antibodies) signaling by cleaving NEMO (show IKBKG Antibodies).
Serine/threonine-protein kinase that regulates a number of transcription factors with key roles in cell fate determination. Positive effector of the non-canonical Wnt signaling pathway, acting downstream of WNT5A, MAP3K7/TAK1 and HIPK2. Activation of this pathway causes binding to and phosphorylation of the histone methyltransferase SETDB1. The NLK- SETDB1 complex subsequently interacts with PPARG, leading to methylation of PPARG target promoters at histone H3K9 and transcriptional silencing. The resulting loss of PPARG target gene transcription inhibits adipogenesis and promotes osteoblastogenesis in mesenchymal stem cells (MSCs). Negative regulator of the canonical Wnt/beta-catenin signaling pathway. Binds to and phosphorylates TCF7L2/TCF4 and LEF1, promoting the dissociation of the TCF7L2/LEF1/beta-catenin complex from DNA, as well as the ubiquitination and subsequent proteolysis of LEF1. Together these effects inhibit the transcriptional activation of canonical Wnt/beta-catenin target genes. Negative regulator of the Notch signaling pathway. Binds to and phosphorylates NOTCH1, thereby preventing the formation of a transcriptionally active ternary complex of NOTCH1, RBPJ/RBPSUH and MAML1. Negative regulator of the MYB family of transcription factors. Phosphorylation of MYB leads to its subsequent proteolysis while phosphorylation of MYBL1 and MYBL2 inhibits their interaction with the coactivator CREBBP. Other transcription factors may also be inhibited by direct phosphorylation of CREBBP itself. Acts downstream of IL6 and MAP3K7/TAK1 to phosphorylate STAT3, which is in turn required for activation of NLK by MAP3K7/TAK1 (By similarity).
, autocrine motility factor
, glucose phosphate isomerase 1 complex
, glucose phosphate isomerase 1, regulatory
, glucose phosphate isomerase 1, structural
, glucose phosphate isomerase 1, temporal
, glucose-6-phosphate isomerase
, maturation factor
, phosphoglucose isomerase
, phosphohexose isomerase
, structural glucose phosphate isomerase 1
, nemo like kinase b
, nemo-like kinase
, nemo-like kinase 2
, Nemo-like kinase
, nemo like kinase
, Nemo-Like kinase
, serine/threonine-protein kinase NLK-like
, glucose phosphate isomerase
, serine/threonine protein kinase NLK
, serine/threonine-protein kinase NLK
, Serine/threonine-protein kinase NLK