FAK (Phospho-Tyr861) ELISA Kit

Name: FAK (Phospho-Tyr861) ELISA Kit
SKU: DEIA-XYA643
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; Mouse; Rat

Detection Method

Indirect ELISA

Intended Use

The FAK (Phospho-Tyr861) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor FAK protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated FAK in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on FAK phosphorylation.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL
3. Quenching Buffer: 24 mL
4. Blocking Buffer: 50 mL
5. 10x Wash Buffer: 50 mL
6. 100x Anti-FAK (Phospho-Tyr861) Antibody (Rabbit Polyclonal): 60 μL, red
7. 100x Anti-FAK Antibody (Rabbit Polyclonal): 60 μL, purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL, green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL, glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL, glass
11. Primary Antibody Diluent: 12 mL
12. Ready-to-Use Substrate: 12 mL
13. Stop Solution: 12 mL
14. Crystal Violet Solution: 12 mL
15. SDS Solution: 24 mL
16. 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

Targeting telomere-containing chromosome ends with a near-infrared femtosecond laser to study the activation of the DNA damage response and DNA damage repair pathways

JOURNAL OF BIOMEDICAL OPTICS

Authors: Silva, Barbara Alcaraz; Stambaugh, Jessica R.; Berns, Michael W.

Abstract

Telomeres are at the ends of chromosomes. Previous evidence suggests that laser-induced deoxyribose nucleic acid (DNA) breaks at chromosome ends during anaphase results in delayed cytokinesis. A possible explanation for this delay is that the DNA damage response (DDR) mechanism has been activated. We describe a live imaging method to study the effects of DDR activation following focal point near-infrared femtosecond laser micro-irradiation either at a single chromosome end or at a chromosome arm in mitotic anaphase cells. Laser microirradiation is used in combination with dual fluorescent labeling to monitor the co-localization of double-strand break marker gamma H2AX along with the DDR factors in PtK2 (Potorous tridactylus) cells. Laser-induced DNA breaks in chromosome ends as well as in chromosome arms results in recruitment of the following: poly(ADP-ribose) polymerase 1, checkpoint sensors (p-Chk1, p-Chk2), DNA repair protein Ku70/Ku80, and proliferating cell nuclear antigen. However, phosphorylated p53 at serine 15 is detected only at chromosome ends and not at chromosome arms. Full activation of DDR on damaged chromosome ends may explain previously published results that showed the delay of cytokinesis. (C) 2013 Society of Photo-Optical Instrumentation Engineers (SPIE)

The downregulation of miR-3173 in B-cell acute lymphoblastic leukaemia promotes cell invasion via PTK2

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS

Authors: Tian, Lijun; Cao, Junhua; Ji, Qiang; Zhang, Chuanling; Qian, Tong; Song, Xianchuan; Huang, Baoshan; Tian, Xinyi

Abstract

MicroRNAs are important regulators of the pathogenesis of B-cell acute lymphoblastic leukaemia (B-ALL). In this study, we identified miR-3173 and its predicted target gene PTK2 were correspondingly differentially expressed in B-ALL patients. In B-ALL cell lines, CCK-8 proliferation assay revealed that miR-3173 could inhibit the cell proliferation. Moreover, transwell assay revealed that miR-3173 could also inhibit cell migration and invasion in B-ALL cell lines. Luciferase assays revealed that miR-3173 directly bound to the 3'untranslated region of PTK2, and western blotting showed that miR-3173 suppressed the expression of PTK2 at the protein level. Generally, this study indicates that miR-3173 negatively regulates PTK2 and inhibits proliferation and invasion of B-ALL cell lines. Thus, miR-3173 may represent a potential therapeutic molecule for B-ALL intervention. (C) 2017 Elsevier Inc. All rights reserved.