| Autor: |
Ravindranath AK; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Kaur S; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Wernyj RP; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Kumaran MN; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Miletti-Gonzalez KE; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.; Present address: Delaware State University, Dover, DE, USA., Chan R; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Lim E; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA., Madura K; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.; Rutgers Robert Wood Johnson Medical School, Piscataway, NJ, USA., Rodriguez-Rodriguez L; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA.; Department of Obstetrics and Gynecology, New Brunswick, Rutgers Cancer Institute of New Jersey, NJ, USA. |
| Abstrakt: |
Here we demonstrate that a ubiquitin E3-ligase, FBXO21, targets the multidrug resistance transporter, ABCB1, also known as P-glycoprotein (P-gp), for proteasomal degradation. We also show that the Ser291-phosphorylated form of the multifunctional protein and stem cell marker, CD44, inhibits FBXO21-directed degradation of P-gp. Thus, CD44 increases P-gp mediated drug resistance and represents a potential therapeutic target in P-gp-positive cells. |
