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Validated All-in-One™ qPCR Primer for STK11(NM_000455.4) Search again
Product ID:
HQP017794
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
LKB1, PJS, hLKB1
Gene Description:
serine/threonine kinase 11
Target Gene Accession:
NM_000455.4(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene, which encodes a member of the serine/threonine kinase family, regulates cell polarity and functions as a tumor suppressor. Mutations in this gene have been associated with Peutz-Jeghers syndrome, an autosomal dominant disorder characterized by the growth of polyps in the gastrointestinal tract, pigmented macules on the skin and mouth, and other neoplasms. Alternate transcriptional splice variants of this gene have been observed but have not been thoroughly characterized.
Gene References into function
- This paper describes the identification and characterization of the first binding partner of LKB1; the SWI/SNF chromatin remodeling protein Brg1.
- mutation screening at the RNA level in Peutz-Jeghers syndrome reveals complex splicing abnormalities and a novel mRNA isoform (STK11 c.597(insertion mark)598insIVS4
- STK11/LKB1 gene in IPMNs (intraductal papillary-mucinous neoplasms of the pancreas) with LOH revealed a germline mutation in one IPMN that arose in a patient with PJS (Peutz-Jeghers Syndrome) and a somatic mutation in 1 of the 20 sporadic IPMNs.
- LKB1 is phosphorylated at Ser(431), Ser(31), Ser(325) and Thr(366)
- Inactivation of LKB1/STK11 is a common event in adenocarcinomas of the lung.
- polyps arising in the Lkb1+/- mice were found to be hamartomas that were histologically indistinguishable from polyps resected from PJS patients, indicating that Lkb1+/- mice model human PJS polyposis
- These observations provide the first link between ATM and LKB1 and suggest that ATM could regulate LKB1
- Results show that Cdc37 and heat shock protein 90 bind specifically to the kinase domain of LKB1.
- mutations in the STK11 gene characterize minimal deviation adenocarcinoma of the uterine cervix
- LKB1/STK11 variants in a group of Peutz-Jeghers syndrome Italian patients lack serine/threonine kinase activity, in contrast to wild type LKB1/STK11, and are unable to suppress the growth of melanoma G361 cells in vitro.
- identification and characterization of an LKB1-specific adaptor protein and substrate, STRAD (STe20 Related ADaptor); results imply that STRAD plays a key role in regulating the tumour suppressor activities of LKB1
- LKB1 kinase, which is associated with Peutz-Jeghers cancer-susceptibility syndrome, phosphorylates and activates AMPK in vitro.
- results show that LKB1 can direct the phosphorylation of the serine-threonine kinase PAR1A
- LKB1 inactivation may play a role in the critical transition from premalignant to malignant tumor growth
- LKB1-induced apoptosis is p53 independent but might be p73-mediated in pancreatic tumors
- heteromeric complex containing the molecular chaperones Hsp90 and Cdc37/p50 interacts with the kinase domain of LKB1
- LKB1 functions as a master upstream protein kinase, regulating AMPK-related kinases as well as AMPK.
- LKB1 directly phosphorylates Thr-172 of AMPKalpha in vitro and activates its kinase activity.
- our results reveal that several important factors contribute to LKB1-mediated carcinogenesis in LADs, confirming previous observations and identifying new putative pathways that should help to elucidate the biological role of LKB1.
- the risk for developing cancer at ages 20, 30, 40, 50, 60, and 70 years was 1%, 3%, 19%, 32%, 63%, and 81%, respectively
- LKB1, the gene mutated in Peutz-Jeghers syndrome (PJS), acts as a tumor suppressor by activating TSC2, the gene mutated in Tuberous sclerosis complex
- Cases in which Peutz-Jegher Syndrome patients did not harbor mutation of STK11.
- IGF-1 induces AMPK-alpha subunit phosphorylation via an ATM-dependent and LKB1-independent pathway
- Mutations in LKB1 cause the inherited Peutz-Jeghers syndrome.
- The unusual splicing defect of LKB1 associated with this Peutz-Jeghers syndrome-causing mutation uncovers differences in splice-site recognition between the major and minor pre-mRNA splicing pathways
- report of a novel truncating-type germline mutation of the STK11 gene in a Peutz-Jeghers syndrome patient with gastric cancer
- LKB1 mutants, in Peutz-Jeghers syndrome, fail to activate GSK-3beta, preventing it from inhibiting Wnt signaling.
- promoter element sequence changes in STK11/LKB1 are unlikely to contribute to Peutz-Jeghers syndrome
- LKB1 is crucial for the regulation of cell polarity
- LKB1 interacts with and phosphorylates PTEN: a functional link between two proteins involved in cancer predisposing syndromes
- Large genomic deletions within the STK11 gene are associated with Peutz-Jeghers syndrome.
- Ectopic expression of cyclooxygenase-2 and endogenous biosynthesis of eicosanoids also inhibited LKB1 activity in MCF-7 cells.
- The role of LKB1 in the phosphorylation and activation of multiple AMP-kinase related protein kinases is reported.
- LKB1-mediated AMP-activated protein kinase (AMPK) activation may play an important role in regulating not only cellular energy metabolism but also signaling pathways that control cell growth, differentiation, and survival.
- Mutation of STK11/LKB1 gene leads to the loss of cell growth inhibition in head and neck squamous cell carcinoma
- LKB1 regulates GATA-mediated gene expression and that this activity of LKB1 may be important for its tumor suppressor function.
- Exonic STK11 deletions are a common cause of Peutz-Jeghers syndrome.
- Deletions within the LKB1 gene are associated with Peutz-Jeghers syndrome.
- loss of function mutations in LKB1 may also be frequently involved in the pathogenesis of large cell lung carcinomas
- The risk of intussusception in PJS is not influenced by STK11 mutation status.
- PEA3 stabilization due to LKB1 inactivation could lead to epithelial/mesenchymal transition and greater lung cancer invasion potential.
- Genomic DNA analysis showed a 708-bp deletion in the STK11 gene
- demonstrate that LKB1 wild-type cells are more resistant to cell death upon glucose withdrawal than their mutant counterparts
- Here we review how the substrates & cellular functions of LKB1 may be linked to Peutz-Jeghers syndrome & other diseases, & discuss how some of the molecular changes associated with altered LKB1 signaling might be used in therapeutic approaches.[review]
- most, if not all PJS, is attributable to mutations in the STK11 gene, perhaps including as yet undiscovered changes in promoter or enhancer sequences or other cryptic changes
- Increased transsfected LKB1 activity in the cardiac myocyte can decrease hypertrophy-induced protein synthesis and suggest that LKB1 activation may be a method for the prevention of pathological cardiac hypertrophy.
- Chromatin immunoprecipitation analyses show that LKB1 is recruited directly to the p21/WAF1 promoter, as well as to other p53 activated promoters, in a p53-dependent fashion.
- LKB1 plays a negative regulatory role in human breast cancer.
- expression of LKB1 protects cells from cytotoxicity induced by agents which modulate ATP/AMP ratio
- Results suggest that WDR6 is implicated in the cell growth inhibitory pathway of LKB1 via regulation of p27(Kip1).
- Phosphorylation of PAR-1 by tumor suppressor protein LKB1 is required for PAR-1 activation, which promotes tau phosphorylation.
- protein kinase B, LKB1, and AMP-activated protein kinase have roles in activation of lipoprotein lipase by glucose-dependent insulinotropic polypeptide in adipocytes
- STK11 germline mutations is associated with Peutz-Jeghers syndrome
- somatic LKB1 genetic alterations preferentially occur in a subset of poorly differentiated lung adenocarcinomas that appear to correlate with smoking males
- LKB1 is involved in the regulation of microtubule dynamics through the activation of MARKs
- LKB1 catalytically deficient mutants possess oncogenic properties. This work is the first to describe a function for LKB1 mutants; recruitment to the promoter of cyclin D1 where mutants enhance the expression of the oncogene.
- LKB1 gene is located in the short arm of chromosome 19, which is frequently deleted in many tumors of sporadic origin.
- sequencing of the STK11 gene in the probands of 3 Chinese families with Peutz-Jeghers syndrome revealed two novel mutations (c180C-->G and c998-1002delGCAGC) in exon 1 and exon 8, respectively
- N33, STK11 (19p13) and TP53 might play a role in the development of metastasis in larynx and pharynx squamous cell carcinomas.
- inactivation of LKB1 was found in 34% and 19% of 144 analysed human lung adenocarcinomas and squamous cell carcinomas, respectively
- LKB1 gene mutations were relatively rare in Japanese patients with lung cancer compared with Caucasian patients.
- A role has been identified for the polarity regulator LKB1 in the development of c-Myc- resistant cell organization.
- Several novel splice isoforms of STRADalpha that differentially affect the kinase activity, complex assembly, subcellular localization of LKB1 and the activation of the LKB1-dependent AMPK pathway were discovered.
- Recombinant LKB1 produces significant growth inhibition and cell-cycle arrest.
- genetic variants of LKB1-AMPK-TORC2 pathway components may exert a weak influence on the occurrence of type 2 diabetes in Japanese
- a polymorphism in STK11, a kinase gene expressed in liver and implicated in metformin action, is associated with ovulatory response to treatment with metformin alone.
- Marked reduction of LKB1 expression in high-grade neuroendocrine tumors of the lung suggests a possible role of LKB1 inactivation in its tumorigenesis.
- LKB1 interacts only with active form of cdc42 and PAK, but not with inactive cdc42. Taken together, these results show that LKB1 is a critical mediator of the NSCLC polarity program in lung cancer cells through a novel LKB1-cdc42-PAK pathway.
- identify a multifactored mechanism to control LKB1 localization, and they suggest that the STRADbeta-LKB1 complex might possess unique functions in the nucleus
- rosiglitazone is able to acutely stimulate NO synthesis in cultured endothelial cells by an AMP-activated protein kinase-dependent mechanism, likely to be mediated by LKB1
- PKCzeta mediates LKB1-dependent Akt inhibition in response to peroxynitrite, resulting in endothelial apoptosis.
- plays important roles in regulating metabolism in resting and contracting skeletal muscle (Review)
- LKB1 may have a role in lung cancer [review]
- Results enlarge the spectrum of mutations of the STK11 gene by identifying a novel de novo mutation in a PJS patient and further support the hypothesis that STK11 mutations are disease-causing mutations for PJS with or without a positive family history
- LKB1 mutation frequency was higher in NSCLC tumours of US origin compared with NSCLCs of Korean origin. They tended to occur more commonly in adenocarcinomas than in squamous cell carcinomas.
- Peutz-Jeghers syndrome with germline mutation of LKB1
- A polymorphism in the STK11 gene is associated with low ovulatory response to treatment with metformin alone in a prospective, randomized trial.
- LKB1 deacetylation is regulated by SIRT1 and that this in turn influences its intracellular localization, association with STRAD, kinase activity, and ability to activate AMPK.
- Suppression of LKB1 expression led to apoptosis in three cell lines in which Akt is constitutively active but not in two cell lines without Akt activation.
- STRADalpha.MO25alpha complexes containing LKB1 variants were equally effective at phosphorylating and activating AMPK, BRSK1, and BRSK2
- Role of LKB1 as a master regulator of polarity and metabolism could contribute to its tumor suppressor function.
- LKB1 and KRAS mutation is associated with lung cancers and show sensitivity to the mTOR and MEK inhibitors.
- Part of a cascade that functions as a critical determinant of hepatocyte proliferation during liver regeneration after partial hepatectomy.