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Merck

A7154

Sigma-Aldrich

Adenosine, periodate oxidized

≥93%

Sinónimos:

ADOX, Adenosine-2′,3′-dialdehyde

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About This Item

Fórmula empírica (notación de Hill):
C10H11N5O4
Número de CAS:
Peso molecular:
265.23
Número MDL:
Código UNSPSC:
41106305
ID de la sustancia en PubChem:
NACRES:
NA.51

origen biológico

synthetic (organic)

Nivel de calidad

Ensayo

≥93%

Formulario

powder

solubilidad

0.2 M HCl: 50 mg/mL, clear, colorless to faintly yellow

temp. de almacenamiento

−20°C

cadena SMILES

Nc1ncnc2n(cnc12)C(OC(CO)C=O)C=O

InChI

1S/C10H11N5O4/c11-9-8-10(13-4-12-9)15(5-14-8)7(3-18)19-6(1-16)2-17/h1,3-7,17H,2H2,(H2,11,12,13)

Clave InChI

ILMNSCQOSGKTNZ-UHFFFAOYSA-N

Aplicación

Adenosine, periodate oxidized has been used:
  • as a methylarginine transferase inhibitor in the human embryonic kidney (HEK)-293 T cells
  • as a methylase inhibitor in H4 neuroglioma
  • as a broad inhibitor of S-adenosylmethionine (AdoMet)-dependent methyltransferases in mouse embryo fibroblast NIH3T3 cells

Acciones bioquímicas o fisiológicas

Adenosine, periodate oxidized (Adox) is a protein arginine methyltransferases (PRMTs) inhibitor. It also inhibits the enzyme S-adenosylhomocysteine hydrolase and induces apoptosis. Its inhibitory effect on histone methyltransferases prevents histone methylation. Adox also elicits intrinsic cytotoxic properties.

Código de clase de almacenamiento

11 - Combustible Solids

Clase de riesgo para el agua (WGK)

WGK 3

Punto de inflamabilidad (°F)

Not applicable

Punto de inflamabilidad (°C)

Not applicable

Equipo de protección personal

Eyeshields, Faceshields, Gloves, type N95 (US)


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Yinghong He et al.
Journal of translational medicine, 11, 14-14 (2013-01-16)
Pharmacologic reactivation of fetal hemoglobin expression is a promising strategy for treatment of sickle cell disease and β-thalassemia. The objective of this study was to investigate the effect of the methyl transferase inhibitor adenosine-2',3'-dialdehyde (Adox) on induction of human fetal
Jin-Ah Park et al.
Molecules and cells, 31(4), 343-349 (2011-03-02)
Interphasic chromatin condenses into the chromosomes in order to facilitate the correct segregation of genetic information. It has been previously reported that the phosphorylation and methylation of the N-terminal tail of histone H3 are responsible for chromosome condensation. In this
Ryan Heit et al.
Journal of cell science, 122(Pt 16), 2957-2968 (2009-07-30)
Trimethylation of lysine 9 on histone H3 (H3K9me3) is known both to be necessary for proper chromosome segregation and to increase in late G2. We investigated the role of late G2 methylation, specifically in mitotic progression, by inhibiting methylation for
Malin Hultberg et al.
Clinical biochemistry, 39(2), 160-163 (2005-12-07)
The metabolism of homocysteine is influenced by several dietary factors, including folate, cobalamin and possibly also the intake of polyhydroxylated phenolic compounds (polyphenols), which were shown to increase plasma homocysteine (tHcy) concentration. In order to reveal the cause of the
Ivon J M van der Linden et al.
Birth defects research. Part A, Clinical and molecular teratology, 82(10), 676-683 (2008-10-22)
An impaired DNA methylation has been suggested to underlie the complex etiology of neural tube defects (NTDs). Previously, we have demonstrated that inhibition of methylation by periodate oxidized adenosine (Adox) results in a widening of the anterior neuropore (ANP) in

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