Human, Mouse, Rat AKT1/2 [p Ser473, p Ser474] ELISA Kit (Colorimetric)

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ELISA: Human, Mouse, Rat AKT1/2 [p Ser473, p Ser474] ELISA Kit (Colorimetric) [NBP2-61397] - AKT ELISA Kit (Colorimetric) [NBP2-61397] - These standard curves are provided for demonstration only. A standard curve should ...read more

Product Details

Summary
Reactivity Hu, Mu, RtSpecies Glossary
Applications ELISA
Suitable Sample Type
Cell lysates of human, mouse, and rat origin.
Standard Curve Range
17.5 - 560 pg/ml
Sensitivity
5.5 pg/ml

Order Details

Human, Mouse, Rat AKT1/2 [p Ser473, p Ser474] ELISA Kit (Colorimetric) Summary

Modification
p Ser473, p Ser474
Specificity
This product has been tested with AKT1 - Ser473 and AKT2 - Ser474. Possible Cross Reactivity listed below: Inactive Akt1 0.05% Inactive Akt3 <0.03% p38a, inactive 0.17% ERK1, inactive <0.03% ERK2, inactive <0.03% JNK1, inactive <0.03%
Standard Curve Range
17.5 - 560 pg/ml
Sensitivity
5.5 pg/ml
Inter-Assay
Mean 9.7%
Intra-Assay
Mean 9.4%
Spike Recovery
Jurkat Cells - 97%
3T3 Cells - 90%
C6 Cells - 100%
Sample Volume
100 uL
Kit Type
ELISA Kit (Colorimetric)
Gene
AKT1

Applications/Dilutions

Dilutions
  • ELISA

Packaging, Storage & Formulations

Storage
Store at 4°C.

Kit Components

Components
  1. Antibody
  2. Assay buffer 32
  3. Cell lysis buffer 5
  4. Conjugate
  5. Microtiter plate
  6. Standard
  7. Stop solution 2
  8. TMB Substrate
  9. Wash buffer concentrate

Alternate Names for Human, Mouse, Rat AKT1/2 [p Ser473, p Ser474] ELISA Kit (Colorimetric)

  • AKT
  • EC 2.7.11
  • EC 2.7.11.1
  • PKBMGC99656
  • PRKBA
  • Protein kinase B
  • Proto-oncogene c-Akt
  • rac protein kinase alpha
  • RAC-alpha serine/threonine-protein kinase
  • RAC-ALPHA
  • RAC-PK-alpha
  • RACPKB-ALPHA
  • v-akt murine thymoma viral oncogene homolog 1

Background

AKT (also known as protein kinase B (PKB) and RAC (related to A and C kinases)) is a critical intracellular serine/threonine kinase that translates signals from extracellular stimuli including growth factors, cytokines and neurotransmitters1. AKT signaling plays critical roles in cell growth, proliferation, survival and differentiation1. It is also involved in organogenesis, angiogenesis and metabolism. Three mammalian AKT isoforms have been identified. The AKT pathway can be activated by any of the three members who share a high level of protein homology but are independently encoded by AKT1 (PKB alpha; 14q32.32), AKT2 (PKB beta; 19q13.2), or AKT3 (PKB gamma; 1q44)1,2. Each AKT family member contains an N-terminal pleckstrin homology (PH) domain, a central kinase domain, and a C-terminal regulatory domain. AKT mediates many of the downstream events of phosphatidylinositol 3-kinase (PI3-K), a lipid kinase activated by growth factors, cytokines and insulin. PI3-K recruits AKT to the membrane, where it is activated by PDK1 phosphorylation. AKT has two main phosphorylation sites (Ser473 and Thr308, predicted molecular weight 56kD)3,4. Once phosphorylated, AKT dissociates from the membrane and phosphorylates targets in the cytoplasm and the cell nucleus including mammalian target of rapamycin (mTOR).

The main function of AKT is to control inhibition of apoptosis and promote cell proliferation. Survival factors can activate AKT Ser473 and Thr308 phosphorylation sites in a transcription-independent manner, resulting in the inactivation of apoptotic signaling transduction through the tumor suppressor PTEN, an antagonist to PI3-K5. PTEN exerts enzymatic activity as a phosphatidylinositol-3,4,5-trisphosphate (PIP3) phosphatase, opposing PI3K activity by increasing availability of PIP3 to proliferating cells, leading to overexpression and inappropriate activation of AKT noted in many types of cancer.

AKT1 function has been linked to overall physiological growth and function2. AKT1 has been correlated with proteus syndrome, a rare disorder characterized by overgrowth of various tissues caused by a mosaic variant in the AKT1 gene in humans.AKT2 is strongly correlated with Type II diabetes, including phenotypes of insulin resistance, hyperglycemia and atherosclerosis2,6.

The function of AKT3 is specifically associated to brain development, where disruptions to AKT3 are correlated with microcephaly, hemimegalencephaly, megalencephaly and intellectual disabilities2.

References

1. Ersahin, T., Tuncbag, N., & Cetin-Atalay, R. (2015). The PI3K/AKT/mTOR interactive pathway. Mol Biosyst, 11(7), 1946-1954. doi:10.1039/c5mb00101c

2. Cohen, M. M., Jr. (2013). The AKT genes and their roles in various disorders. Am J Med Genet A, 161a(12), 2931-2937. doi:10.1002/ajmg.a.36101

3. Georgescu, M. M. (2010). PTEN Tumor Suppressor Network in PI3K-Akt Pathway Control. Genes Cancer, 1(12), 1170-1177. doi:10.1177/1947601911407325

4. Mishra, P., Paital, B., Jena, S., Swain, S. S., Kumar, S., Yadav, M. K., . . . Samanta, L. (2019). Possible activation of NRF2 by Vitamin E/Curcumin against altered thyroid hormone induced oxidative stress via NFkB/AKT/mTOR/KEAP1 signalling in rat heart. Sci Rep, 9(1), 7408. doi:10.1038/s41598-019-43320-5

5. Wedel, S., Hudak, L., Seibel, J. M., Juengel, E., Oppermann, E., Haferkamp, A., & Blaheta, R. A. (2011). Critical analysis of simultaneous blockage of histone deacetylase and multiple receptor tyrosine kinase in the treatment of prostate cancer. Prostate, 71(7), 722-735. doi:10.1002/pros.21288

6. Rotllan, N., Chamorro-Jorganes, A., Araldi, E., Wanschel, A. C., Aryal, B., Aranda, J. F., . . . Fernandez-Hernando, C. (2015). Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis. Faseb j, 29(2), 597-610. doi:10.1096/fj.14-262097

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. ELISA Kits are guaranteed for 6 months from date of receipt.

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Bioinformatics

Gene Symbol AKT1