Sentence examples for binding to target enzymes from inspiring English sources

Exact(1)

Scientists are beginning to appreciate the importance of water as a possible competitor of inhibitors for binding to target enzymes.

Similar(59)

Thus ISP1 and ISP2 appear to present significant differences in the binding site to target enzymes, which are consistent with, and suggestive of, important functional diversity.

Studies of chemical shift perturbations upon chagasin contact with cruzipain identified residues in L2, L4 and L6 as candidates to comprise chagasin's binding-site to target enzymes [6].

To test the potential role of Ca2+/CaM in DC120-induced mTORC1 signaling, the cells were pretreated with N- 6-aminohexyl -5-chloro-1-naphthalenesulfonamide (W7), a cell-permeable CaM aN- 6-aminohexyl -5-chloro-1-naphthalenesulfonamideiN- 6-aminohexyl -5-chloro-1-naphthalenesulfonamide

SUMO proteins participate in an important post-translational modification called SUMOylation, which promotes SUMO proteins binding to target proteins via an ATP-consuming enzyme cascade, including SUMO-activating enzyme (SAE1/SAE2), Ubiquitin-conjugating enzyme 9 (Ubc9), and several E3 ligases [ 5].

Thus, there is no reasonable doubt that β-catenin/TCF binding to target gene promoters is definitely involved in the regulation of drug-metabolizing enzymes.

AAC(6' -Ib encodes a ciprofloxacin acetylating enzyme, while the product of qnr inhibits quinolones binding to target proteins [ 16' -Ib.

Superior to competitive inhibitors, mechanism-based inhibitors exhibit higher potency by covalent binding to the target enzymes and completely and irreversibly inactivating them.

SKF shows fluorescence, which is strongly enhanced upon binding to the target enzyme.

The establishment of the molecular basis for recognition of the adenine moiety of ATP in proteins will directly impact molecular design of ATP-binding site targeted enzyme inhibitors such as kinase inhibitors.

Mechanisms for DILI include cell stress imposed by reactive metabolites (e.g. depletion of glutathione or binding to enzymes and lipids), direct targeting of mitochondrial functions (e.g. ATP depletion or inhibition of β-oxidation causing steatosis) and immune reactions triggered by drugs or their metabolites.

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