-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
- Cosmetic Ingredient
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Ensure that the DNA double strands do not break while efficiently replacing DNA-specific bases - a task that in the past was not possible with gene-editing technology CRISPR-Cas9.
, American scientists have developed a new type of "base editor" that makes it possible.
Since most genetic diseases are rooted in single nucleotide mutations, the emergence of this base editor helps humans fight genetic diseases.
October 26, Beijing time, the international academic journal Nature published an article by David Liu, a core member of the Broad Institute in the United States, and colleagues reporting on the adenine base editor (ABE) they developed to convert A-T base pairs to G-C base pairs.
adenine (A), ostrich (G), cytosine (C) and thymus (T) are the basic units that make up DNA.
these bases are paired in the form of A-T, C-G, forming a double helix structure of DNA.
in RNA, thymus pyneselie (T) is replaced by urinary pedicos (U).
last year, also published in nature, David Liu and colleagues first reported their "base editor", by installing rat cytosine deaminase APOBEC1 on the Cas9 protein, cas9's "scissors" function will disappear, no longer cut the double strand skid of DNA, but can still bind the target DNA fragments, while converting cytosine (C) into ulysine (U).
, a third protein is used to allow the cells to initiate a DNA repair procedure, eventually replacing the C-G base pair with the T-A base pair.
David Liu and colleagues did not stop last year's results.
scientists already know that about half of all known disease-related mono-base pair mutations are related to wild-type G-C base pairs that are converted to mutant A-T base pairs.
the time David Liu and colleagues reported that the adenine base editor could complete the task of converting the A-T base pair back to the G-C base pair, complementing last year's results.
the adenine base editor is reported to work in both bacterial and human cells.
in human cells, it is 50% efficient and has a low off-target rate, with little side effect sintofed, deletion, or other mutations.
.