Human NKAP (NF-kappa-B-activating protein) ELISA Kit

Name: Human NKAP (NF-kappa-B-activating protein) ELISA Kit
SKU: DEIA-FN993
Rating: 5 (1 reviews)

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

COA

SDS

Datasheet

Summary

Sample

serum, plasma, cell culture supernatants, tissue homogenate

Species Reactivity

Human

Detection Method

Sandwich ELISA

Intended Use

For quantitative detection of Human NKAP (NF-kappa-B-activating protein) in serum, plasma, tissue homogenates and other biological fluids.

Contents of Kit

1. 96-well strip plate (Dismountable), 1 plate
2. Lyophilized Standard, 2 vials
3. Sample/Standard dilution buffer, 20 mL
4. Biotin-detection antibody (Concentrated), 120 uL
5. Antibody dilution buffer, 10 mL
6. HRP-Streptavidin Conjugate(SABC), 120 uL
7. SABC dilution buffer, 10 mL
8. TMB substrate, 10 mL
9. Stop solution, 10 mL
10. Wash buffer (25X), 30 mL
11. Plate Sealer, 5 pieces
12. Product Manual, 1 copy

Storage

Store the unopened product at 2 - 8 °C. Do not use past expiration date.

Precision

Intra-Assay: CV<8%
Inter-Assay: CV<10%

Detection Range

0.156-10 ng/mL

Sensitivity

0.094 ng/mL

Standard Curve

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Synthetic Essentiality of Metabolic Regulator PDHK1 in PTEN-Deficient Cells and Cancers

CELL REPORTS

Authors: Chatterjee, Nilanjana; Pazarentzos, Evangelos; Mayekar, Manasi K.; Gui, Philippe; Allegakoen, David V.; Hrustanovic, Gorjan; Olivas, Victor; Lin, Luping; Verschueren, Erik; Johnson, Jeffrey R.; Hofree, Matan; Yan, Jenny J.; Newton, Billy W.; Dollen, John V.; Earnshaw, Charles H.; Flanagan, Jennifer; Chan, Elton; Asthana, Saurabh; Ideker, Trey; Wu, Wei; Suzuki, Junji; Barad, Benjamin A.; Kirichok, Yuriy; Fraser, James S.; Weiss, William A.; Krogan, Nevan J.; Tulpule, Asmin; Sabnis, Amit J.; Bivona, Trever G.

Abstract

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a tumor suppressor and bi-functional lipid and protein phosphatase. We report that the metabolic regulator pyruvate dehydrogenase kinasel (PDHK1) is a synthetic-essential gene in PTEN-deficient cancer and normal cells. The PTEN protein phosphatase dephosphorylates nuclear factor kappa B (NF-kappa B)-activating protein (NKAP) and limits NF kappa B activation to suppress expression of PDHK1, a NF-kappa B target gene. Loss of the PTEN protein phosphatase upregulates PDHK1 to induce aerobic glycolysis and PDHK1 cellular dependence. PTEN-deficient human tumors harbor increased PDHK1, a biomarker of decreased patient survival. This study uncovers a PTEN-regulated signaling pathway and reveals PDHK1 as a potential target in PTEN-deficient cancers.

The oncogenic role of NKAP in the growth and invasion of colon cancer cells

ONCOLOGY REPORTS

Authors: Shu, Weibin; Liu, Guoqin; Dai, Yunpeng; Feng, Alei; Chen, Zheng; Han, Junqing; Li, Xinyu

Abstract

It has been reported that NF-kappa B activating protein (NKAP) is a transcriptional repressor of the Notch signaling pathway and is involved in the proliferation and survival of hematopoietic stem cells. In the present study, we aimed to investigate the effect of NKAP on the progression and metastasis of colon cancer. The results of immunohistochemical staining and western blot analysis showed that NKAP was upregulated in colon cancer tissues, and its expression was associated with colon cancer stages. CCK-8, colony formation, Transwell, and flow cytometry assays were used to demonstrate that NKAP knockdown significantly suppressed the proliferation and invasion of HCT116 and HT-29 cells, and also induced apoptosis and autophagy. By contrast, NKAP overexpression markedly promoted the proliferation and invasion of HCT-15 cells, and inhibited cell apoptosis and autophagy. Moreover, we observed that NKAP knockdown inhibited the epithelial-mesenchymal transition (EMT) process in HCT116 and HT-29 cells, while NKAP overexpression promoted EMT in HCT-15 cells. Furthermore, NKAP knockdown inhibited activation of the Akt/mTOR signaling pathway by downregulating the phosphorylation of Akt and mTOR, as well as their downstream proteins, whereas NKAP overexpression promoted the Akt/mTOR signaling pathway. Additionally, expression of P65 was downregulated by silencing of NKAP and upregulated by NKAP overexpression. These data suggest that NKAP functions as an oncogene in the growth and invasion of colon cancer in vitro.