LMTK2 ELISA Kit

Name: LMTK2 ELISA Kit
SKU: DEIA-XYA1142
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

cultured cells

Species Reactivity

Human

Intended Use

The LMTK2 Colorimetric Cell-Based ELISA Kit allows for the qualitative detection of LMTK2 and the effects that certain stimulation conditions have on LMTK2 expression in different cell lines.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 1 Plate.
2. 10x TBS: 24 mL (10x), Clear.
3. Quenching Buffer, 24 mL (1x), Clear.
4. Blocking Buffer, 50 mL (1x), Clear.
5. 10x Wash Buffer, 50 mL (10x), Clear.
6. 100x Anti-LMTK2 Antibody (Rabbit Polyclonal), 60 μL (100x), Purple.
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal), 60 μL (100x), Green.
8. HRP-Conjugated Anti-Rabbit IgG Antibody, 6 mL (1x), Glass.
9. HRP-Conjugated Anti-Mouse IgG Antibody, 6 mL (1x), Glass.
10. Primary Antibody Diluent, 12 mL (1x), Clear.
11. Ready-to-Use Substrate, 12 mL (1x), Brown.
12. Stop Solution, 12 mL (1x), Clear.
13. Crystal Violet Solution, 6 mL (1x), Glass.
14. SDS Solution, 24 mL (1x), Clear.
15. Adhesive Plate Seals, 4 Seals.

Storage

4°C/6 Months

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Lemur Tyrosine Kinase 2, a novel target in prostate cancer therapy

ONCOTARGET

Authors: Shah, Kalpit; Bradbury, Neil A.

Abstract

Progression from early forms of prostate cancer to castration-resistant disease is associated with an increase in signal transduction activity. The majority of castration-resistance cancers persist in the expression of the androgen receptor (AR), as well as androgen-dependent genes. The AR is regulated not only by it associated steroid hormone, but also by manifold regulatory and signaling molecules, including several kinases. We undertook evaluation of the role of Lemur Tyrosine Kinase 2 (LMTK2) in modulating AR activity, as several Genome Wide Association Studies (GWAS) have shown a marked association of LMTK2 activity with the development of prostate cancer. We confirm that not only is LMTK2 mRNA reduced in prostate cancer tissue, but also LMTK2 protein levels are markedly diminished. Knockdown of LMTK2 protein in prostate cell lines greatly increased the transcription of androgen-responsive genes. In addition, LMTK2 knockdown led to an increase in prostate cancer stem cell populations in LNCaP cells, indicative of increased tumorogenicity. Using multiple approaches, we also demonstrate that LMTK2 interacts with the AR, thus putting LMTK2 as a component of a signaling complex modulating AR activity. Our finding that LMTK2 is a negative regulator of AR activity defines a novel cellular pathway for activation of AR-responsive genes in castrate resistant-prostate cancer. Moreover, pharmacologic manipulation of LMTK2 activity will provide a novel therapeutic target for more effective treatments for patients with castrate-resistant prostate cancer.

Multiple newly identified loci associated with prostate cancer susceptibility

NATURE GENETICS

Authors: Eeles, Rosalind A.; Kote-Jarai, Zsofia; Giles, Graham G.; Al Olama, Ali Amin; Guy, Michelle; Jugurnauth, Sarah K.; Mulholland, Shani; Leongamornlert, Daniel A.; Edwards, Stephen M.; Morrison, Jonathan; Field, Helen I.; Southey, Melissa C.; Severi, Gianluca; Donovan, Jenny L.; Hamdy, Freddie C.; Dearnaley, David P.; Muir, Kenneth R.; Smith, Charmaine; Bagnato, Melisa; Ardern-Jones, Audrey T.; Hall, Amanda L.; O'Brien, Lynne T.; Gehr-Swain, Beatrice N.; Wilkinson, Rosemary A.; Cox, Angie; Lewis, Sarah; Brown, Paul M.; Jhavar, Sameer G.; Tymrakiewicz, Malgorzata; Lophatananon, Artitaya; Bryant, Sarah L.; Horwich, Alan; Huddart, Robert A.; Khoo, Vincent S.; Parker, Christopher C.; Woodhouse, Christopher J.; Thompson, Alan; Christmas, Tim; Ogden, Chris; Fisher, Cyril; Jamieson, Charles; Cooper, Colin S.; English, Dallas R.; Hopper, John L.; Neal, David E.; Easton, Douglas F.

Abstract

Prostate cancer is the most common cancer affecting males in developed countries. It shows consistent evidence of familial aggregation, but the causes of this aggregation are mostly unknown. To identify common alleles associated with prostate cancer risk, we conducted a genome-wide association study (GWAS) using blood DNA samples from 1,854 individuals with clinically detected prostate cancer diagnosed at <= 60 years or with a family history of disease, and 1,894 population-screened controls with a low prostate-specific antigen (PSA) concentration (< 0.5 ng/ml). We analyzed these samples for 541,129 SNPs using the Illumina Infinium platform. Initial putative associations were confirmed using a further 3,268 cases and 3,366 controls. We identified seven loci associated with prostate cancer on chromosomes 3, 6, 7, 10, 11, 19 and X (P = 2.7 x 10(-8) to P = 8.7 x 10(-29)). We confirmed previous reports of common loci associated with prostate cancer at 8q24 and 17q. Moreover, we found that three of the newly identified loci contain candidate susceptibility genes: MSMB, LMTK2 and KLK3.