Uracil CAS NO.66-22-8

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
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Chemical Properties of Uracil

Source of Uracil

The herbs of Heracleum stenopterum

Biological Activity of Uracil

Protocol of Uracil

Preparing Stock Solutions of Uracil

References on Uracil

Anionic derivatives of uracil: fragmentation and reactivity.[Pubmed:25036757]

Phys Chem Chem Phys. 2014 Sep 7;16(33):17835-44.

Uracil is an essential biomolecule for terrestrial life, yet its prebiotic formation mechanisms have proven elusive for decades. Meteorites have been shown to contain Uracil and the interstellar abundance of aromatic species and nitrogen-containing molecules is well established, providing support for Uracil's presence in the interstellar medium (ISM). The ion chemistry of Uracil may provide clues to its prebiotic synthesis and role in the origin of life. The fragmentation of biomolecules provides valuable insights into their formation. Previous research focused primarily on the fragmentation and reactivity of cations derived from Uracil. In this study, we explore deprotonated Uracil-5-carboxylic acid and its anionic fragments to elucidate novel reagents of Uracil formation and to characterize the reactivity of Uracil's anionic derivatives. The structures of these fragments are identified through theoretical calculations, further fragmentation, experimental acidity bracketing, and reactivity with several detected and potential interstellar species (SO2, OCS, CS2, NO, N2O, CO, NH3, O2, and C2H4). Fragmentation is achieved through collision induced dissociation (CID) in a commercial ion trap mass spectrometer, and all reaction rate constants are measured using a modification of this instrument. Experimental data are supported by theoretical calculations at the B3LYP/6-311++G(d,p) level of theory. Lastly, the astrochemical implications of the observed fragmentation and reaction processes are discussed.

Excision of uracil from transcribed DNA negatively affects gene expression.[Pubmed:24951587]

J Biol Chem. 2014 Aug 8;289(32):22008-18.

Uracil is an unavoidable aberrant base in DNA, the repair of which takes place by a highly efficient base excision repair mechanism. The removal of Uracil from the genome requires a succession of intermediate products, including an abasic site and a single strand break, before the original DNA structure can be reconstituted. These repair intermediates are harmful for DNA replication and also interfere with transcription under cell-free conditions. However, their relevance for cellular transcription has not been proved. Here we investigated the influence of Uracil incorporated into a reporter vector on gene expression in human cells. The expression constructs contained a single Uracil opposite an adenine (to mimic dUTP misincorporation during DNA synthesis) or a guanine (imitating a product of spontaneous cytosine deamination). We found no evidence for a direct transcription arrest by Uracil in either of the two settings because the vectors containing the base modification exhibited unaltered levels of enhanced GFP reporter gene expression at early times after delivery to cells. However, the gene expression showed a progressive decline during subsequent hours. In the case of U:A pairs, this effect was retarded significantly by knockdown of UNG1/2 but not by knockdown of SMUG1 or thymine-DNA glycosylase Uracil-DNA glycosylases, proving that it is base excision by UNG1/2 that perturbs transcription of the affected gene. By contrast, the decline of expression of the U:G constructs was not influenced by either UNG1/2, SMUG1, or thymine-DNA glycosylase knockdown, strongly suggesting that there are substantial mechanistic or kinetic differences between the processing of U:A and U:G lesions in cells.

Defective repair of uracil causes telomere defects in mouse hematopoietic cells.[Pubmed:25572391]

J Biol Chem. 2015 Feb 27;290(9):5502-11.

Uracil in the genome can result from misincorporation of dUTP instead of dTTP during DNA synthesis, and is primarily removed by Uracil DNA glycosylase (UNG) during base excision repair. Telomeres contain long arrays of TTAGGG repeats and may be susceptible to Uracil misincorporation. Using model telomeric DNA substrates, we showed that the position and number of Uracil substitutions of thymine in telomeric DNA decreased recognition by the telomere single-strand binding protein, POT1. In primary mouse hematopoietic cells, Uracil was detectable at telomeres, and UNG deficiency further increased Uracil loads and led to abnormal telomere lengthening. In UNG-deficient cells, the frequencies of sister chromatid exchange and fragility in telomeres also significantly increased in the absence of telomerase. Thus, accumulation of Uracil and/or UNG deficiency interferes with telomere maintenance, thereby underscoring the necessity of UNG-initiated base excision repair for the preservation of telomere integrity.

Description

Uracil is one of the four nucleobases in the nucleic acid of RNA can be used for drug delivery and as a pharmaceutical.

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