-
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
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Each cell has two different "tools" to repair DNA single or double strand breaks, which can be caused
by factors such as environmental toxins, chemotherapy, or ionizing radiation.
People who carry mutations in the BRCA1 and/or BRCA2 genes are at very high risk of developing certain types of tumors, most notably breast, ovarian, and prostate cancers
.
To prevent apoptosis after DNA damage, a key signaling pathway called NF-κB comes into play
.
Obstruction of PARP1 repairs
But which one? The number of candidate genes is in the thousands—after all, the NF-κ b signaling pathway controls a wide range of cellular functions, such as immune responses
.
After that, only a small group of genes remained
.
"PARP1 is like a loaded gun," Scheidereit said
.
Amazing observation
Scheidereit explains: "PARP1 modifies itself, attracts other helper proteins for the necessary repairs, and then isolates itself
.
Scheidereit concluded: "With this study, we have shown that the use of PARP inhibitors and the turn off of TSG101 have the same effect
.
PARP inhibitors have been used in the treatment of certain cancers for several years — for example, BRCA mutations
in breast cancer patients.
Original:
