Out of these six different compounds, dichloromethane is a selective substrate for human GST T1-1, whereas 1-menaphthyl sulfate and 1-chloro-2,4-dinitrobenzene are substrates for rat GST T2-2.
Because p62/SQSTM1 is a selective substrate of autophagy and, hence, monitoring endogenous p62 protein levels indirectly measures autophagic degradation, we concurrently monitored how acquisition of breast cancer auto-resistance to Tzb affected cellular distribution of both p62 and LC3 (Figure 5).
SQSTM1/sequristome/p62 protein or p62, an ubiquitin-binding protein, is a selective substrate of autophagy and an accumulation of both p62 and ubiquinated proteins serves as an indicator of autophagy inhibition [ 20- 22].
For a number of tumour cell lines it has been shown that TK1 activity exceeds TS activity by a factor of at least 16 [ 14]. 3′-Deoxy-3′-[F]-fluorothymidine (F-FLT), an analogue of thymidine, is a selective substrate for TK1, that is for the salvage pathway.
Autophagy is typically activated under conditions of amino acid starvation, and autophagy marker proteins include light chain 3 (LC3) and p62 [ 5]. p62 (also called SQSTM1) is a selective substrate of autophagy, and its accumulation is observed when autophagy is inhibited [ 7].
Three subjects in each group received ritonavir 100 mg or placebo in order to evaluate and compare the inhibitory potential of either ritonavir or cobicistat on concomitantly administered midazolam, which is known to be a selective CYP3A substrate.
NBR1 itself is also a selective substrate of autophagy., The early senescence phenotypes of loss-of-function atg mutants indicate that autophagy is required to maintain cellular homeostasis in response to internal and external cues (Fig. S1)., However, the concurrent functions of autophagy complicate analyses of its contributions to responses to different stimuli.
The p62 protein is a selective autophagy substrate that accumulates when autophagy is reduced.
The endogenous molecule α-ketoglutarate is a selective PHD substrate and agonist [ 312], and it is able to reactivate PHDs to inhibit HIF-1 regardless of intracellular oxygen tension [ 141].
