Mouse Ampd2 ELISA Kit (V2LY-0626-LY2022)

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Tested Data
Request for COA
Datasheet Target References Q & As Review & reward Protocols Associated Products

Basic Information

Sensitivity
0.009 ng/mL
Detection Range
0.02-3.5 ng/mL
Sample Type
Serum, Plasma, cell culture supernates
Specificity
Mouse
Assay Type
Sandwich
Reactivity
Mouse
Assay Time
1.5 h
Molecule Mass
92.0 kDa
Components
  • Pre-coated ELISA Plate: 12 wells * 8 detachable strips
  • Standard solution: 0.5ml x1
  • Standard diluent: 3ml x1
  • Streptavidin-HRP: 6ml x1
  • Stop solution: 6ml x1
  • Substrate solution A: 6ml x1
  • Substrate solution B: 6ml x1
  • Wash buffer concentrate (25x): 20ml x1
  • Biotinylated antibody: 1ml x1

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at 2-8°C
More Infomation

Target

Full Name
adenosine monophosphate deaminase 2 (isoform L)
Function
AMP deaminase plays a critical role in energy metabolism. Catalyzes the deamination of AMP to IMP and plays an important role in the purine nucleotide cycle.
Biological Process
AMP metabolic process Source: GO_Central
Cyclic purine nucleotide metabolic process Source: UniProtKB
Energy homeostasis Source: MGI
IMP biosynthetic process Source: MGI
IMP salvage Source: UniProtKB-UniPathway
Purine-containing compound salvage Source: Reactome
Cellular Location
Cytosol
Involvement in disease
Pontocerebellar hypoplasia 9 (PCH9): A form of pontocerebellar hypoplasia, a disorder characterized by structural defects of the pons and cerebellum, evident upon brain imaging. PCH9 features include severely delayed psychomotor development, progressive microcephaly, spasticity, seizures, and brain abnormalities, including brain atrophy, thin corpus callosum, and delayed myelination.
Spastic paraplegia 63, autosomal recessive (SPG63): A form of spastic paraplegia, a neurodegenerative disorder characterized by a slow, gradual, progressive weakness and spasticity of the lower limbs. Rate of progression and the severity of symptoms are quite variable. Initial symptoms may include difficulty with balance, weakness and stiffness in the legs, muscle spasms, and dragging the toes when walking. In some forms of the disorder, bladder symptoms (such as incontinence) may appear, or the weakness and stiffness may spread to other parts of the body.
PTM
Methylated at Gln-6 by N6AMT1.

Abnous, K., & Storey, K. B. (2021). 5′-Adenosine monophosphate deaminase regulation in ground squirrels during hibernation. Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology, 253, 110543.

Orth, M. F., Gerke, J. S., Knösel, T., Altendorf‐Hofmann, A., Musa, J., Alba‐Rubio, R., ... & Grünewald, T. G. (2019). Functional genomics identifies AMPD2 as a new prognostic marker for undifferentiated pleomorphic sarcoma. International journal of cancer, 144(4), 859-867.

Scola, E., Ganau, M., Robinson, R., Cleary, M., De Cocker, L. J., Mankad, K., ... & D’Arco, F. (2019). Neuroradiological findings in three cases of pontocerebellar hypoplasia type 9 due to AMPD2 mutation: typical MRI appearances and pearls for differential diagnosis. Quantitative imaging in medicine and surgery, 9(12), 1966.

Wang, H., & Ye, S. (2019). 301 NovelmiRNA-25 inhibits AMPD2 in peripheral blood mononuclear cells of patients with systemic lupus erythematosus and represents a promising novel biomarker.

Kortüm, F., Abou Jamra, R., Alawi, M., Berry, S. A., Borck, G., Helbig, K. L., ... & Kutsche, K. (2018). Clinical and genetic spectrum of AMPD2-related pontocerebellar hypoplasia type 9. European journal of human genetics, 26(5), 695-708.

Severino, M., Zara, F., Rossi, A., & Striano, P. (2017). Teaching NeuroImages: figure of 8: the clue to the diagnosis of AMPD2 pontocerebellar hypoplasia (PCH9). Neurology, 89(14), e172-e173.

Marsh, A. P., Yap, P., Tan, T., Pope, K., White, S. M., Chong, B., ... & Lockhart, P. J. (2017). A novel AMPD2 mutation outside the AMP deaminase domain causes pontocerebellar hypoplasia type 9. Am J Med Genet A, 173, 820-823.

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For research use only. Not intended for any clinical use.

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