BIK (Phospho-Thr33) ELISA Kit (DEIA-XYA286)

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

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Size
2 x 96T
Sample
cultured cells
Species Reactivity
Human
Intended Use
The BIK (Phospho-Thr33) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor BIK protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated BIK in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on BIK phosphorylation.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL (10x)
3. Quenching Buffer: 24 mL (1x)
4. Blocking Buffer: 50 mL (1x)
5. 10x Wash Buffer: 50 mL (10x)
6. 100x Anti-BIK (Phospho-Thr33) Antibody (Rabbit Polyclonal): 60 μL (100x), Red
7. 100x Anti-BIK Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL (1x), Glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL (1x), Glass
11. Primary Antibody Diluent: 12 mL (1x)
12. Ready-to-Use Substrate: 12 mL (1x), Brown
13. Stop Solution: 12 mL (1x)
14. Crystal Violet Solution: 12 mL (1x), Glass
15. SDS Solution: 24 mL (1x)
16. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


Induced Autoimmunity against Gonadal Proteins Affects Gonadal Development in Juvenile Zebrafish

PLOS ONE

Authors: Presslauer, Christopher; Nagasawa, Kazue; Dahle, Dalia; Babiak, Joanna; Fernandes, Jorge M. O.; Babiak, Igor

A method to mitigate or possibly eliminate reproduction in farmed fish is highly demanded. The existing approaches have certain applicative limitations. So far, no immunization strategies affecting gonadal development in juvenile animals have been developed. We hypothesized that autoimmune mechanisms, occurring spontaneously in a number of diseases, could be induced by targeted immunization. We have asked whether the immunization against specific targets in a juvenile zebrafish gonad will produce an autoimmune response, and, consequently, disturbance in gonadal development. Gonadal soma-derived factor (Gsdf), growth differentiation factor (Gdf9), and lymphocyte antigen 75 (Cd205/Ly75), all essential for early gonad development, were targeted with 5 immunization tests. Zebrafish (n5329) were injected at 6 weeks post fertilization, a booster injection was applied 15 days later, and fish were sampled at 30 days. We localized transcripts encoding targeted proteins by in situ hybridization, quantified expression of immune-, apoptosis-, and gonad-related genes with quantitative real-time PCR, and performed gonadal histology and whole-mount immunohistochemistry for Bcl2-interacting-killer (Bik) pro-apoptotic protein. The treatments resulted in an autoimmune reaction, gonad developmental retardation, intensive apoptosis, cell atresia, and disturbed transcript production. Testes were remarkably underdeveloped after anti-Gsdf treatments. Anti-Gdf9 treatments promoted apoptosis in testes and abnormal development of ovaries. Anti-Cd205 treatment stimulated a strong immune response in both sexes, resulting in oocyte atresia and strong apoptosis in supporting somatic cells. The effect of immunization was FSH-independent. Furthermore, immunization against germ cell proteins disturbed somatic supporting cell development. This is the first report to demonstrate that targeted autoimmunity can disturb gonadal development in a juvenile fish. It shows a straightforward potential to develop auto-immunization-based technologies to mitigate fish reproduction before they reach maturation. However, the highly variable results between treatments and individuals suggest significant optimization should be performed to achieve the full potential of this technology.

The pro-apoptotic paradox: the BH3-only protein Bcl-2 interacting killer (Bik) is prognostic for unfavorable outcomes in breast cancer

ONCOTARGET

Authors: Pandya, Vrajesh; Glubrecht, Darryl; Vos, Larissa; Hanson, John; Damaraju, Sambasivarao; Mackey, John; Hugh, Judith; Goping, Ing Swie

Breast cancer is the leading cause of cancer-associated deaths in women worldwide. Clinical biomarkers give information on disease progression and identify relevant biological pathways. A confounding factor that uncouples markers from disease outcome is the ability of tumor cells to mutate and evade clinical intervention. Therefore, we focussed on apoptotic genes that modulate tumor regression. Using gene and tissue microarray analyses, we identified an association of Bcl-2 interacting killer (Bik) with poor breast cancer prognosis. Bik prognostic ability was independent of Estrogen Receptor/Progesterone Receptor and Her2 status. Additionally, Bik was independent of anti-apoptotic Bcl-2, Bcl-xL, Mcl-1 and Bcl-w suggesting a complex mechanism of tumor promotion identified by Bik high tumors. Bik also stimulates autophagy, which can contribute to enhanced tumor fitness. We found a significant association between the autophagy marker ATG5 and Bik. Combined high expression level of ATG5 and Bik was a stronger predictor of outcome than either alone. Thus, our study identifies Bik as a novel, independent prognostic biomarker for poor outcomes in breast cancer and suggests that Bik-mediated autophagy contributes to disease recurrence.

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