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1 in which Zbtb20 was specifically deleted in Sertoli cells.
2 erm cells inside tubules lined by epithelial Sertoli cells.
3 to a genomic bar code of the fate of foetal Sertoli cells.
4 e, intracellular domain of NOTCH1 (NICD1) in Sertoli cells.
5 t with NSun2 in spermatogonial stem cells or Sertoli cells.
6 s would be modulated through this pathway in Sertoli cells.
7 tiated by upregulation of Sox9 by SRY in pre-Sertoli cells.
8 not exclusive, source of RA in the testes is Sertoli cells.
9 equired for the survival of trophectoderm or Sertoli cells.
10 ndent on FSH and androgen action through the Sertoli cells.
11 the actions of FSH and androgen through the Sertoli cells.
12 k180, LC3, Atg12, Becn1, Rab5 and Rubicon in Sertoli cells.
13 osa cells can reprogram granulosa cells into Sertoli cells.
14 cells through its interaction with NECL4 on Sertoli cells.
15 rget genes can differ between germ cells and Sertoli cells.
16 ia also disrupts cyclical gene expression in Sertoli cells.
17 mrt1 is selectively mutated in germ cells or Sertoli cells.
18 y increases the adhesion of CHO cells to TM4 Sertoli cells.
19 major TGF-beta protein that acts directly on Sertoli cells.
20 ired in both germ cells and their supporting Sertoli cells.
21 hormone receptor expressed at high levels in Sertoli cells.
22 these cells and in their neighboring somatic Sertoli cells.
23 onstitutively active form of beta-catenin in Sertoli cells.
24 drive expression of a transgenic reporter in Sertoli cells.
25 was sparsely expressed in germ cells and in Sertoli cells.
26 lls in the testes, but at very low levels in Sertoli cells.
27 NOD1 and NOD2 expression in human and mouse Sertoli cells.
28 ta on inflammasome expression or function in Sertoli cells.
29 lity to reproduce is completely dependent on Sertoli cells.
30 nal formation of SSCs co-cultured with SCSKO Sertoli cells.
35 , receptors, and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuri
36 -testis barrier (BTB) involved in regulating Sertoli cell adhesion via its effects on the occludin-zo
38 concomitant activation of CTNNB1 and KRAS in Sertoli cells also caused testicular granulosa cell tumo
39 on than androgen action mediated through the Sertoli cells although androgen action through other cel
40 tions in the organization of microtubules in Sertoli cells and a loss of barrier integrity despite a
41 n impaired the cell junctions of the primary Sertoli cells and failed to support the clonal formation
42 the relationship of Wt1 and beta-catenin in Sertoli cells and found Wt1 inhibits beta-catenin signal
44 pe A, Int, B spermatogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in s
47 ired phagocytosis by specialized phagocytes: Sertoli cells and the retinal pigmented epithelium (RPE)
48 interactions of other testicular cells with Sertoli cells and to test novel antivirals for clearing
49 leads to malfunction of the somatic (Leydig, Sertoli) cells and consequent downstream TDS disorders.
50 s exert deleterious effects on Leydig cells, Sertoli cells, and germ cells via very different mechani
51 o membrane trafficking pathways in embryonic Sertoli cells, and perturbing secretion in male embryoni
52 ate that Ins2 is a direct target of Rhox5 in Sertoli cells, and we show that this regulation is physi
59 led several potential modifiers expressed in Sertoli cells at the time of testis determination in mic
60 we found that Notch signaling was active in Sertoli cells at various fetal, neonatal, and adult stag
62 an testes, the blood-testis barrier (BTB) or Sertoli cell barrier created by specialized junctions be
66 L-1alpha (100 pg/ml) was shown to "open" the Sertoli cell barrier when its integrity was assessed by
72 f P-glycoprotein by RNAi was found to impede Sertoli cell BTB function, making the tight junction (TJ
73 ed by changes in F-actin organization at the Sertoli cell BTB in vitro and in vivo, associated with a
77 testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild
81 emidesmosome, knockdown of beta1-integrin in Sertoli cells by RNAi was found to associate with occlud
82 s development is solely under the control of Sertoli cells, by uncovering an active and essential rol
85 rmatid (apical ES) interface, as well as the Sertoli cell-cell (basal ES) interface at the blood-test
86 r knockdown by RNAi was also found to impede Sertoli cell-cell GJ communication, disrupting protein d
87 ecruitment of actin-related protein 3 to the Sertoli cell-cell interface, where it became more tightl
88 BTB in the rat testis and the phenotypes of Sertoli cell-conditional Cx43 knockout mice share many o
90 xt investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell injury.
96 ific siRNA duplexes was performed in primary Sertoli cell cultures with an established TJ permeabilit
99 led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation of actin microf
100 erstitial progenitors, through the action of Sertoli cell-derived Hedgehog signals, become positive f
102 beta-catenin in fetal testes did not affect Sertoli cell differentiation, testis morphogenesis or ma
104 tions in mice and humans to be essential for Sertoli cell differentiation; moreover, its abnormal exp
105 n reducing occupancy of DNA sites regulating Sertoli-cell differentiation [the testis-specific SRY-bo
106 s is initiated when expression of Sry in pre-Sertoli cells directs the gonad toward a male-specific f
107 perturbed organization of actin filaments in Sertoli cells, disruption of the blood-testis barrier an
112 To determine the function of beta-catenin in Sertoli cells during testis formation, we either deleted
113 in the re-organization of actin filaments in Sertoli cells during the epithelial cycle, participating
117 tion of this approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to dr
118 ressing its dominant-negative mutant T17N in Sertoli cell epithelium was shown to block the TGF-beta3
119 s of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and repro
120 staglandin D2 (PGD2) inhibition in SC5 mouse Sertoli cells, evidence of binding at the COX-2 active s
124 re the basal membranes of adjacent polarized Sertoli cells form a niche for the proliferating spermat
126 sites during sex determination, we subjected Sertoli cells from mouse fetal testes to DNaseI-seq and
127 does so by triggering the differentiation of Sertoli cells from supporting cell precursors, which wou
128 gnaling protein that is required to maintain Sertoli cell function and could serve as a novel target
129 e caused, at least partly, by disruptions to Sertoli cell function and increased germ cell apoptosis,
131 of testes, which implies that their roles in Sertoli cell function are to support spermatogenesis and
134 e mechanisms controlled by LKB1 signaling in Sertoli cell functions and testicular biology have not b
135 (GODZ; also known as DHHC3) and its paralog Sertoli cell gene with a zinc finger domain-beta (SERZ-b
136 tion and MNG induction appears to be loss of Sertoli cell-germ cell membrane adhesion, probably due t
137 c deletion of transcription factor Zbtb20 in Sertoli cells has no apparent influence on spermatogenes
140 beta-Catenin stabilization caused changes in Sertoli cell identity and misregulation of inter-Sertoli
146 ages revealed a normal BTB structure between Sertoli cells in the BT-IgSF-KO mice, we conclude that i
147 oncurrently at the opposing ends of adjacent Sertoli cells in the seminiferous epithelium during sper
148 ed by specialized junctions between adjacent Sertoli cells in the seminiferous epithelium near the ba
149 ted spermatogonia, primary spermatocytes and Sertoli cells in the testis, resulting in cell death and
151 cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which
153 stis barrier (BTB), PFOS was found to induce Sertoli cell injury by perturbing actin cytoskeleton thr
154 rected], was found to block the PFOS-induced Sertoli cell injury by rescuing the PFOS-induced F-actin
158 e spermatocyte stage, BSG-mediated germ cell-Sertoli cell interactions appear to be necessary for int
160 known as apical ES and possibly the Sertoli-Sertoli cell interface, known as basal ES, at the blood-
161 a redistribution of occludin at the Sertoli-Sertoli cell interface, moving from cell membrane into c
162 with occludin redistribution at the Sertoli-Sertoli cell interface, wherein occludin moved away from
165 ysis revealed that the expression program of Sertoli cells is altered upon inactivation of Sin3A in g
166 lood-testis barrier (BTB) formed by adjacent Sertoli cells is composed of coexisting tight junction (
167 gocytic clearance of apoptotic germ cells by Sertoli cells is essential for spermatogenesis, little o
169 that proper regulation of Notch signaling in Sertoli cells is required for the maintenance of gonocyt
170 gocytic clearance of apoptotic germ cells by Sertoli cells is vital for germ cell development and dif
171 unction restructuring in primary cultures of Sertoli cells isolated from rat testes that formed a TJ-
172 of the transcription factors SRY and SOX9 in Sertoli cells lead to human sex reversal diseases with a
173 constitutively activating NOTCH signaling in Sertoli cells leads to premature differentiation of all
174 central component of TGF-beta signaling, in Sertoli cells led to testis cord dysgenesis and prolifer
175 testis growth through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.
176 ing defective AREs, and (iv) incubation of a Sertoli cell line with testosterone triggered corecruitm
177 provide evidence, based on an embryonic pre-Sertoli cell line, that this domain functions at a thres
178 ending are unaffected in a rat embryonic pre-Sertoli cell line, the variants exhibited selective defe
179 of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD
181 sed to endosomes, and knock-down of Sdmg1 in Sertoli cell lines causes mis-localisation of the secret
184 permatogenesis, its specific localization in Sertoli cells makes Zbtb20 a useful marker for the ident
185 dysgenesis (Leydig cell aggregation, ectopic Sertoli cells, malformed seminiferous cords) is not evid
186 that occur in the cell biology of embryonic Sertoli cells may facilitate the communication of male s
188 uncover a selective requirement for ELMO1 in Sertoli-cell-mediated removal of apoptotic germ cells an
189 a-Catenin expression was found mainly on the Sertoli cell membrane starting from embryonic day 15.5 i
191 icrofilament, thereby failing to support the Sertoli cell morphology and adhesion protein complexes (
193 ier created by specialized junctions between Sertoli cells near the basement membrane confers an immu
196 SHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effec
199 Here we show that after ablation of Sox9 in Sertoli cells of adult, fertile Sox8(-/-) mice, testis-t
201 Arid4a and Arid4b are expressed mainly in Sertoli cells of testes, which implies that their roles
203 e found that WT1 and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryon
204 astly, the BEST1 promoter was also active in Sertoli cells of the testis in transgenic mice where SOX
209 , we observed progressive germ cell loss and Sertoli cell only tubules in Lkb1(cko) testes from mice
220 der than 10 weeks, accompanied by defects in Sertoli cell polarity and testicular junctional complexe
221 germ cell (Dazl), proliferating (PCNA), and Sertoli cell populations, and quantitated levels of apop
222 with the finding that Sox9 is upregulated in Sertoli cell precursors just after SRY expression begins
224 alpha) since germ cells are known to control Sertoli cell production of this cytokine, and if yes, ho
227 ecise organization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1
230 cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), the supporting cells of the germ cel
232 Changes in PGD2 secretion in juvenile mouse Sertoli cells (SC5 cells) were measured using an ELISA.
235 codes a core NMD factor, in murine embryonic Sertoli cells (SCs) leads to severe testicular atrophy a
238 substance (MIS), which is produced by fetal Sertoli cells shortly after commitment of the bipotentia
239 Transgenic mice expressing miR-471-5p in Sertoli cells show increased germ cell apoptosis and com
241 ing actin microfilaments and microtubules in Sertoli cells so that they failed to support cell adhesi
243 rier, recapitulated the defects found in the Sertoli cell-specific androgen receptor (AR) knockout mi
247 results suggest that the Rhox5 gene achieves Sertoli cell-specific transcription using a combinatoria
248 pecific, actin-rich adherens junction at the Sertoli cell-spermatid interface) to coordinate cellular
249 le were isolated by microdissection, whereas Sertoli cells, spermatogonia plus early spermatocytes, p
250 nuously endocytosed and recycled back to the Sertoli cell surface via the clathrin-mediated but not t
251 tor cells acquire SOX9 expression and become Sertoli cells that form testis cords, whereas the remain
252 s, SOX9 is required for the determination of Sertoli cells that orchestrate testis morphogenesis.
253 s strands of tight junctions between somatic Sertoli cells that restricts solutes from crossing the p
255 ation of plectin to the nuclear perimeter of Sertoli cells, the resulting link between the nuclear en
256 cell-cell adhesion between spermatogenic and Sertoli cells through its interaction with NECL4 on Sert
257 emonstrate that Notch signaling is active in Sertoli cells throughout development and that proper reg
258 uration, and formation of tight junctions in Sertoli cells, thus confirming a requirement for PPARD i
260 The removal of calcium by EGTA perturbed the Sertoli cell tight junction barrier, but calcium repleti
261 ha2 in Sertoli cells was shown to induce the Sertoli cell tight junction permeability barrier disrupt
262 t overexpression of Cx43 indeed resealed the Sertoli cell tight junction-permeability barrier based o
263 rmer promoting and the latter disrupting the Sertoli cell tight junction-permeability barrier functio
264 a transient loss of plastin 3 perturbed the Sertoli cell tight junction-permeability barrier, mediat
265 ed in vitro by RNAi was found to perturb the Sertoli cell tight junction-permeability function in vit
267 ter the knockdown of both Cx43 and PKP2, the Sertoli cell TJ barrier function was perturbed transient
268 nsequently, this prevented the disruption of Sertoli cell TJ permeability barrier and redistribution
269 ntation in the epithelium, and a "tightened" Sertoli cell TJ permeability barrier, supporting the rol
270 n of rictor by RNAi was found to perturb the Sertoli cell TJ-barrier function in vitro and the BTB in
271 e (FSH) acts through receptors (FSHR) on the Sertoli cell to stimulate spermatogenesis while androgen
272 mium because its knockdown would desensitize Sertoli cells to cadmium-induced TJ barrier disruption.
273 of potential feminizing genes, DMRT1 allows Sertoli cells to participate in RA signaling, which is e
275 e fetal Leydig cells that acts directly upon Sertoli cells to promote their proliferation during late
276 is-to-ovary genetic reprogramming occurs and Sertoli cells transdifferentiate into granulosa-like cel
277 sexual cell-fate reprogramming in which male Sertoli cells transdifferentiate into their female equiv
278 s, there is evidence of pregranulosa cell-to-Sertoli cell transdifferentiation near birth, following
283 estis barrier (BTB), formed between adjacent Sertoli cells, undergoes extensive remodeling to facilit
286 ficient clearance of apoptotic germ cells by Sertoli cells using LAP.Although phagocytic clearance of
287 nockout mice (SCSKO), a normal population of Sertoli cells was observed, but the blood-testis barrier
288 importance, a knockdown of laminin alpha2 in Sertoli cells was shown to induce the Sertoli cell tight
289 cal role in mammalian gonads is to determine Sertoli cells, we correlated this genomic signature with
290 a without direct contact with the supporting Sertoli cells, we show that haploid spermatids express t
293 orphology and the position of the nucleus in Sertoli cells were normal, however, in the nesprin-3-kno
294 of proliferating cellular nuclear antigen in Sertoli cells were observed in Ppard(+/+) mice as compar
296 rovide evidence that ZIKV infection of human Sertoli cells, which are an important component of the s
297 I of meiosis but does inhibit maturation of Sertoli cells, which continue to express the immaturity
298 in, or the use of a synthetic F5 peptide, in Sertoli cells with an established functional blood-testi
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