Product Name: LKB1 (295-309)
Product Number: PE-01ASP90
Size: | 200 µg | | Price: | 45.00 |
| 1 mg | | $US | 90.00 |
| 5 mg | | | 211.00 |
Peptide Name: LKB1 (295-309)
Product Use: Services as a blocking peptide for use with the LKB1-3 rabbit polyclonal antibody (Cat. No.: AB-NK227-4) that is also available from Kinexus. The peptide sequence is located in the kinase catalytic domain last alpha-chain.
Peptide Production Method: Solid-phase peptide synthesis
Peptide Origin: Homo sapiens
Peptide Sequence: CAKRFSIRQIRQHSWF
Peptide Modifications N Terminus: Free amino
Peptide Modifications C Terminus: Amide
Peptide Molecular Mass Calculated: 2062.4 Da
Peptide Purity Percent after Synthesis and Purification: 90
Scientific Background: LKB1 (STK11) is a protein-serine/threonine kinase of the CAMK group and CAMKL family. LKB1 has important roles in the regulation of cell metabolism, cell polarity, apoptosis, and the response to DNA damage. LKB1 promotes recruitment of p53/TP53 to the CDKN1A/WAF1 promoter to activate transcription. in addition, LKB1 regulates p53/TP53-dependent apotosis pathways. The LKB1 protein is found in the nucleus and cytoplasm of cells and translocates to the mitochondria during apoptosis. LKB1 is activated by binding of a complex consisting of CAB39 and STRAD or CAB39 and ALS2CR2. Phosphorylation at S307 induces interaction with AMPK1, STLK5 and exportin 1. Phosphorylation at S428 increases phosphotransferase activity. Phosphorylation at T336 inhibits LKB1. It displays tumour suppressor activity that functions in the regulation of AMP-activated protein kinase (AMPK) family members through phosphorylation of their activation T-loop. LKB1 appears to be a tumour suppressor protein (TSP). Cancer-related mutations in human tumours point to a loss of function of the protein kinase. In particularly, cancer-associated mutations are found in the substrate recognition domain of the protein or result in protein truncation. Significantly reduced LKB1 expression has been observed in benign intestinal polyps, which correlated with reduced apoptosis, which may potentially contribute to the development of malignant intestinal tumours. Additionally, LKB1 protein in tumour cells is restricted to the nucleus, compared to the normal distribution of the protein in both the nucleus and cytoplasm. The introduction of LKB1 protein into LKB1-deficient cancer cell lines results in G1 phase cell cycle arrest. This effect is still seen for LKB1 proteins that lack nuclear localization signals, indicating that the tumour suppressive effects of the kinase are mediated in the cytoplasm. The proposed mechanism of LKB1-mediated cell cycle arrest is a p53-dependent induction of p21. Analysis of gene expression in human lung cancer cell lines and mouse lung tumours revealed that repression of LKB1 results in the activation of various metastasis-promoting genes, such as NEDD9, VEGFC, and CD24.