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1 e and higher claudin-11 expression along the blood-testis barrier.
2 t spermatogenesis and create the impermeable blood-testis barrier.
3 partment, thus completing transit across the blood-testis barrier.
4 this plasma insulin cannot pass through the blood-testis barrier.
5 or male contraception may interfere with the blood-testis barrier.
6 These tight junctions form the basis of the blood-testis barrier, a structure whose function and dyn
7 ivileged site in the testis protected by the blood-testis barrier, also called the Sertoli cell (SC)
9 to the adhesion between Sertoli cells at the blood-testis barrier, as well as between Sertoli and dev
10 that it is localized in Sertoli cells at the blood-testis barrier (BTB) and at the apical ectoplasmic
11 calized to actin-based cell junctions at the blood-testis barrier (BTB) and the apical ectoplasmic sp
12 e from type B spermatogonia and traverse the blood-testis barrier (BTB) at stage VIII of the seminife
13 oss the murine blood-brain barrier (BBB) and blood-testis barrier (BTB) by a saturable transport syst
15 es permanent infertility due to irreversible blood-testis barrier (BTB) disruption even though the po
16 sforming growth factor (TGF)-beta3 regulates blood-testis barrier (BTB) dynamics in vivo, plausibly b
18 r the basement membrane, associated with the blood-testis barrier (BTB) in stage VIII-IX tubules.
19 sis, preleptotene spermatocytes traverse the blood-testis barrier (BTB) in the seminiferous epitheliu
24 Throughout spermatogenesis, the Sertoli cell blood-testis barrier (BTB) is strictly regulated by cyto
25 s, would disrupt spermatogenesis because the blood-testis barrier (BTB) must remain intact during the
27 rmore, gap and tight junctions essential for blood-testis barrier (BTB) organization are disrupted.
28 such as rats, the mechanism(s) that regulate blood-testis barrier (BTB) restructuring at stages VIII-
29 and coordinate the events of spermiation and blood-testis barrier (BTB) restructuring in the seminife
30 g apical ectoplasmic specialization (ES) and blood-testis barrier (BTB) restructuring in the testis.
31 ates the timely and selective opening of the blood-testis barrier (BTB) to migrating preleptotene/lep
34 axis between the basement membrane (BM), the blood-testis barrier (BTB), and the apical ectoplasmic s
38 ein, using an in vitro model of Sertoli cell blood-testis barrier (BTB), PFOS was found to induce Ser
45 ic antigen-presenting cells, and sustain the blood-testis barrier formed by their tight junctions.
47 nal blood-testis barrier reversibly perturbs blood-testis barrier integrity in vitro and in the rat t
49 ally, germ cell sloughing and rupture of the blood-testis barrier occur and are correlated with decre
50 ding spermatogenic failures and the impaired blood-testis barrier, recapitulated the defects found in
51 ility assessment, and overexpression of BTB (blood-testis barrier) regulatory genes such as FAK and i
52 Sertoli cells with an established functional blood-testis barrier reversibly perturbs blood-testis ba
54 tor results in increased permeability of the blood-testis barrier to biotin, suggesting claudin 3 reg
56 gh thiamin transporter expression beyond the blood-testis barrier, were more susceptible to apoptosis
57 permiation and mediates restructuring of the blood-testis barrier, which facilitates the transit of p
58 degeneration of Sertoli cells, including the blood-testis barrier, which leads to disruption of the a
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