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O9390

Sigma-Aldrich

N-Oxalylglycine

≥98% (HPLC)

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99,70 €
50 MG
395,00 €

99,70 €

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10 MG
99,70 €
50 MG
395,00 €

About This Item

Formula empirica (notazione di Hill):
C4H5NO5
Numero CAS:
5262-39-5
Peso molecolare:
147.09
Numero MDL:
MFCD00913253
Codice UNSPSC:
12352209
ID PubChem:
329818940
NACRES:
NA.77

99,70 €

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Saggio

≥98% (HPLC)

Stato

solid

Condizioni di stoccaggio

desiccated

Solubilità

deionized water: >10 mg/mL

Temperatura di conservazione

2-8°C

Stringa SMILE

OC(=O)CNC(=O)C(O)=O

InChI

1S/C4H5NO5/c6-2(7)1-5-3(8)4(9)10/h1H2,(H,5,8)(H,6,7)(H,9,10)
BIMZLRFONYSTPT-UHFFFAOYSA-N

Azioni biochim/fisiol

N-Oxalylglycine is an inhibitor of α-ketoglutarate-dependent enzymes and mimics the initial steps but does not initiate the hydroxylation process. N-Oxalylglycine has been used to inhibit Jumonji C-domain-containing histone lysine demethylases.
N-Oxalylglycine is an inhibitor of α-ketoglutarate-dependent enzymes.

Caratteristiche e vantaggi

This compound is a featured product for Gene Regulation and Neuroscience research. Discover more featured Gene Regulation and Neuroscience products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound is featured on the Glutamate/GABA Synthesis and Metabolism page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.

Pittogrammi

Exclamation mark
GHS07

Avvertenze

Warning

Indicazioni di pericolo

H302

Classi di pericolo

Acute Tox. 4 Oral

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

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Certificati d'analisi (COA)

Lot/Batch Number
0000413950
0000413952
0000413952
0000413950
0000339566

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α-Ketoglutaric acid ≥98.5% (NaOH, titration)

Sigma-Aldrich

K1750

α-Ketoglutaric acid

α-Ketoglutaric acid sodium salt ≥98% (titration)

Sigma-Aldrich

K1875

α-Ketoglutaric acid sodium salt

Shan Shao et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(8), 10860-10870 (2020-06-28)
The tumor microenvironment (TME) is a crucial factor in cancer progression. In breast cancer, cancer-associated fibroblasts (CAFs) and the derived stromal components have been recognized as comprising the majority of the pathological structure of the TME. In this study, we
Gulzhan Raiymbek et al.
eLife, 9 (2020-03-21)
H3K9 methylation (H3K9me) specifies the establishment and maintenance of transcriptionally silent epigenetic states or heterochromatin. The enzymatic erasure of histone modifications is widely assumed to be the primary mechanism that reverses epigenetic silencing. Here, we reveal an inversion of this
Lisa P Elia et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 39(17), 3332-3344 (2019-01-31)
Deficient progranulin levels cause dose-dependent neurological syndromes: haploinsufficiency leads to frontotemporal lobar degeneration (FTLD) and nullizygosity produces adult-onset neuronal ceroid lipofuscinosis. Mechanisms controlling progranulin levels are largely unknown. To better understand progranulin regulation, we performed a genome-wide RNAi screen using
Nathaniel W Mabe et al.
Cell reports, 33(5), 108341-108341 (2020-11-05)
Dysregulated gene expression is a common feature of cancer and may underlie some aspects of tumor progression, including tumor relapse. Here, we show that recurrent mammary tumors exhibit global changes in gene expression and histone modifications and acquire dependence on
Xiongwen Cao et al.
Cell reports, 30(12), 4152-4164 (2020-03-27)
Histone methyl groups can be removed by demethylases. Although LSD1 and JmjC domain-containing proteins have been identified as histone demethylases, enzymes for many histone methylation states or sites are still unknown. Here, we perform a screening of a cDNA library
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