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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 Antibodies (122) and Nemo-Like Kinase Kits (8) and many more products for this protein.
Showing 10 out of 11 products:
the promoters of WIF1 (show WIF1 Proteins), NLK, and APC (show APC Proteins) are highly methylated in the nasopharyngeal cancers (NPC (show NPC1 Proteins)) and gastric carcinoma (GC) cell lines, and the 3 genes are also regulated by miR (show MLXIP Proteins)-BART19-3p expressed by Epstein-Barr virus (EBV); expression of the WIF1 (show WIF1 Proteins), APC (show APC Proteins), and NLK genes is strongly affected by hypermethylation, and in EBV-associated tumors, the 3 genes are also affected by miR (show MLXIP Proteins)-BART19-3p
overexpression of miR (show MLXIP Proteins)-221 decreased LEF1 (show LEF1 Proteins) phosphorylation but increased the expression of MYCN (show MYCN Proteins) via targeting of NLK and further regulated cell cycle, particularly in S-phase. This study provides a novel insight for miR (show MLXIP Proteins)-221 in the control of neuroblastoma (show ARHGEF16 Proteins) cell proliferation and tumorigenesis, suggesting potentials of miR (show MLXIP Proteins)-221 as a prognosis marker and therapeutic target for patients with MYCN (show MYCN Proteins) overexpressing neuroblastoma (show ARHGEF16 Proteins).
our data suggest that NLK/Nemo (show IKBKG Proteins) acts as an endogenous regulator of Hippo signaling by controlling nuclear localization and activity of YAP/Yorkie (show YAP1 Proteins).
NLK is a novel signaling molecule for proper lung development through the interconnection between epithelial and endothelial cells during lung morphogenesis
Our results suggest that NLK inhibits transcriptional activation of Nurr1 (show NR4A2 Proteins) gene by impeding CBP's role as a co-activator of NF-kappaB (show NFKB1 Proteins) and CREB (show CREB1 Proteins) in prostate cancer.
The expression of NLK was negatively correlated with TCF4 (show TCF4 Proteins) 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 Proteins)-92b-induced cell proliferation, and its protein level was obviously downregulated in the miR (show MLXIP Proteins)-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).
NLK can phosphorylate the mutant polyglutamine-expanded androgen receptor (show AR Proteins) protein, enhance its aggregation, and promote androgen receptor (show AR Proteins)-dependent gene transcription by regulating androgen receptor (show AR Proteins)-cofactor interactions.
Nlk is a negative regulator of skeletal homeostasis.
either reducing NLK enzymatic activity or decreasing NLK expression levels can have beneficial effects against the toxicity induced by polyglutamine-expanded ATXN1 (show ATXN1 Proteins)
NEMO (show IKBKG Proteins) 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 Proteins) and WNT (show WNT2 Proteins) canonical signaling
Wnt3a (show WNT3A Proteins) stimulation led to an increase in the interaction of TAB2 (show TAB2 Proteins) with NLK and the formation of a TAK1 (show NR2C2 Proteins).TAB2 (show TAB2 Proteins).NLK complex, suggesting that this TAK1 (show NR2C2 Proteins)-TAB2 (show TAB2 Proteins)-NLK pathway may constitute a negative feedback mechanism for canonical Wnt (show WNT2 Proteins) signaling.
NLK negatively regulates osteoblastic differentiation.
NLK negatively regulates Notch (show NOTCH1 Proteins)-dependent transcriptional activation by phosphorylating Notch1ICD. Phosphorylated Notch1ICD is impaired in its ability to form a transcriptionally active ternary complex.
Nanog (show NANOG Proteins) suppresses the expression of vasa (show DDX4 Proteins) by directly regulating nlk1 in the early zebrafish embryo
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 Proteins) specifically regulates NLK function, which is required for anterior formation in Xenopus development.
These data show that porcine epidemic diarrhea virus nsp5 (show SPECC1 Proteins) disrupts type I interferon (show IFNA Proteins) signaling by cleaving NEMO (show IKBKG Proteins).
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
, phosphoglucose isomerase
, phosphohexose isomerase
, serine/threonine-protein kinase NLK
, nemo-like kinase
, serine/threonine protein kinase NLK
, nemo like kinase b
, nemo-like kinase 2
, Nemo-like kinase
, Serine/threonine-protein kinase NLK
, nemo like kinase
, Nemo-Like kinase
, serine/threonine-protein kinase NLK-like