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1 which ENT expression was limited to ENT1 or ENT2.
2 ty of an alternative nucleoside transporter, ENT2.
3 ide transporter ENT1 and thus was designated ENT2.
4 ate had different IC(50) values for ENT1 and ENT2.
5 ient expression studies with the full-length ENT2 and a 5'-truncated construct that lacks the first s
6 r newly identified crosstalk pathway between ENT2 and alveolar epithelial Adora2b in lung protection
8 y response gene HNP36 is a truncated form of ENT2 and that the full-length open reading frame of ENT2
9 in the equilibrative nucleoside transporter ENT2, and reconstitution of ENT2 into ENT2-deficient cel
10 bits genetic interactions with both ENT1 and ENT2, and that the clathrin adaptors and Sla2p together
12 nhibitors suppressed the expression of ENT1, ENT2, and TK1 and thus decreased (18)F-FLT PET activity.
13 that equilibrative nucleoside transporter 2 (ENT2), but not ENT1, is capable of translocating BAs acr
15 77% in ENT1 cells (P = 0.0463) and by 64% in ENT2 cells (P = 0.0132), which supported computational p
16 orylation of known Akl1 substrates (Sla1 and Ent2) confirmed that Akl1 is hyperactive when not phosph
17 porter ENT2, and reconstitution of ENT2 into ENT2-deficient cells restores 3E10 Fv transport into cel
20 Studies in gene-targeted mice for Ent1 or Ent2 demonstrated selective protection from liver injury
21 ition of Ado transport is in the order ENT3>=ENT2>ENT1, which also corresponds to the intrinsic abili
22 followed by EIDD-1931 (ENT1 IC(50): 259 uM; ENT2 IC(50): 467 uM), whereas molnupiravir was a modest
23 ed [(3)H]uridine uptake (ENT1 IC(50): 39 uM; ENT2 IC(50): 77 uM), followed by EIDD-1931 (ENT1 IC(50):
25 able to interact with the endocytic adaptor Ent2 in a CBM-dependent manner, and HCs encoded by chc1-
26 d protein 9 functional knockouts of ENT1 and ENT2 in HeLa S3 cells were generated and characterized.
27 rved higher expressional levels of ENT1 than ENT2, in conjunction with repression of ENT1 and ENT2 tr
28 ve nucleoside transporters 1 and 2 (ENT1 and ENT2) inhibitory activity albeit less potent than the pr
29 side transporter ENT2, and reconstitution of ENT2 into ENT2-deficient cells restores 3E10 Fv transpor
31 d that the full-length open reading frame of ENT2 is required for production of a functional plasma m
34 t1 or Ent2 revealed a selective phenotype in Ent2(-/-) mice, including attenuated pulmonary edema and
37 singly, the carboxyl-terminal portion of the ENT2 protein was nearly identical to a smaller protein i
38 nt studies in gene-targeted mice for Ent1 or Ent2 revealed a selective phenotype in Ent2(-/-) mice, i
39 g and predicting compounds that are ENT1 and ENT2 substrates and can circumvent the blood-testis barr
40 g and predicting compounds that are ENT1 and ENT2 substrates and can thereby circumvent the BTB throu
41 hree-dimensional pharmacophores for ENT1 and ENT2 substrates and inhibitors and Bayesian machine lear
42 Clofarabine and cladribine were ENT1 and ENT2 substrates, whereas nevirapine and lexibulin were E
45 , in conjunction with repression of ENT1 and ENT2 transcript and protein levels following warm ischem
46 dual-targeting mechanism based on exDNA and ENT2 transporter expression to enhance nuclear drug deli
48 FLT is transported into the cell by ENT1 and ENT2, where it is phosphorylated by TK1 and trapped intr
49 the clathrin-binding adaptor proteins Ent1, Ent2, Yap1801, and Yap1802, we identify a second endocyt