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1  NOD1 and NOD2 expression in human and mouse Sertoli cells.
2 ta on inflammasome expression or function in Sertoli cells.
3 lity to reproduce is completely dependent on Sertoli cells.
4 nal formation of SSCs co-cultured with SCSKO Sertoli cells.
5  in which Zbtb20 was specifically deleted in Sertoli cells.
6 erm cells inside tubules lined by epithelial Sertoli cells.
7 e, intracellular domain of NOTCH1 (NICD1) in Sertoli cells.
8 t with NSun2 in spermatogonial stem cells or Sertoli cells.
9 s would be modulated through this pathway in Sertoli cells.
10 tiated by upregulation of Sox9 by SRY in pre-Sertoli cells.
11 not exclusive, source of RA in the testes is Sertoli cells.
12 an in vitro infection model of primary human Sertoli cells.
13 equired for the survival of trophectoderm or Sertoli cells.
14 ndent on FSH and androgen action through the Sertoli cells.
15  the actions of FSH and androgen through the Sertoli cells.
16 osa cells can reprogram granulosa cells into Sertoli cells.
17  cells through its interaction with NECL4 on Sertoli cells.
18 rget genes can differ between germ cells and Sertoli cells.
19 ia also disrupts cyclical gene expression in Sertoli cells.
20 mrt1 is selectively mutated in germ cells or Sertoli cells.
21 y increases the adhesion of CHO cells to TM4 Sertoli cells.
22 major TGF-beta protein that acts directly on Sertoli cells.
23 arity of targets in chondrocytes, but not in Sertoli cells.
24 ired in both germ cells and their supporting Sertoli cells.
25 tions in the cytoskeletal fibres of infected Sertoli cells.
26 promoter and thus inhibits its expression in Sertoli cells.
27 er ovarian pre-granulosa cells or testicular Sertoli cells.
28 drive expression of a transgenic reporter in Sertoli cells.
29 gh this transepithelial transport pathway in Sertoli cells.
30 lls in the testes, but at very low levels in Sertoli cells.
31  to a genomic bar code of the fate of foetal Sertoli cells.
32 gh this transepithelial transport pathway in Sertoli cells.
33 k180, LC3, Atg12, Becn1, Rab5 and Rubicon in Sertoli cells.
34  was sparsely expressed in germ cells and in Sertoli cells.
35 ratubular germ cell neoplasia was found in a Sertoli cell adenoma.
36  74%) and low-signal-intensity, well-defined Sertoli cell adenomas (26 of 46 testes, 56%).
37  correctly depict the presence or absence of Sertoli cell adenomas in 19 of 23 testes (83%).
38  changes, including paratesticular cysts and Sertoli cell adenomas.
39 , receptors, and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuri
40 -testis barrier (BTB) involved in regulating Sertoli cell adhesion via its effects on the occludin-zo
41 ated N-glycans that participate in germ cell-Sertoli cell adhesion.
42 concomitant activation of CTNNB1 and KRAS in Sertoli cells also caused testicular granulosa cell tumo
43                                              Sertoli cells, also known as 'mother' or 'nurse' cells,
44 on than androgen action mediated through the Sertoli cells although androgen action through other cel
45 ding highlighted the ability of Ct to infect Sertoli cells, although with a unique growth profile and
46                                By E15.5, the Sertoli cell and germ cell population declined in SC-SF-
47 tions in the organization of microtubules in Sertoli cells and a loss of barrier integrity despite a
48 he same stage in developing chondrocytes and Sertoli cells and determined SOX9 target genes in these
49 n impaired the cell junctions of the primary Sertoli cells and failed to support the clonal formation
50  is supported by intricate crosstalk between Sertoli cells and germ cells including spermatogonia, sp
51        We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and N
52 t in re-aggregated testis, including ectopic Sertoli cells and intratubular Leydig cells (ITLCs).
53 pe A, Int, B spermatogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in s
54  of the seminiferous epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.
55 y restores the cell junctions of the primary Sertoli cells and the clonal formation of SSCs.
56 ired phagocytosis by specialized phagocytes: Sertoli cells and the retinal pigmented epithelium (RPE)
57  interactions of other testicular cells with Sertoli cells and to test novel antivirals for clearing
58 leads to malfunction of the somatic (Leydig, Sertoli) cells and consequent downstream TDS disorders.
59 s exert deleterious effects on Leydig cells, Sertoli cells, and germ cells via very different mechani
60 me, are regulated inside a niche composed of Sertoli cells, and other testis cell types.
61 ate that Ins2 is a direct target of Rhox5 in Sertoli cells, and we show that this regulation is physi
62 ses and single-cell RNAseq (scRNAseq) in the Sertoli-cell androgen receptor knockout (SCARKO) mutant
63  intrinsic and extrinsic genes responsive to Sertoli-cell androgen signaling that promotes cellular s
64                                     Although Sertoli cells are a driving force in the de novo formati
65                                              Sertoli cells are considered the "supporting cells" of t
66           Four days after BC administration, Sertoli cells are preferentially depleted, and can be re
67                               In the testis, Sertoli cells are the key niche cells directing the popu
68                       Using primary cultured Sertoli cells as an in vitro model that mimics the BTB i
69 tercellular spaces between spermatogenic and Sertoli cells as well as the spermatid deformities.
70       Here, we found that it is localized in Sertoli cells at the blood-testis barrier (BTB) and at t
71 led several potential modifiers expressed in Sertoli cells at the time of testis determination in mic
72  we found that Notch signaling was active in Sertoli cells at various fetal, neonatal, and adult stag
73 ons indicate that BSG may act as a germ cell-Sertoli cell attachment molecule.
74 an testes, the blood-testis barrier (BTB) or Sertoli cell barrier created by specialized junctions be
75  posits that MGCA are sequestered behind the Sertoli cell barrier in seminiferous tubules.
76                       The use of an in vitro Sertoli cell barrier to describe how ZIKV or inflammator
77                         These effects at the Sertoli cell barrier were mediated, in part, by epiderma
78 L-1alpha (100 pg/ml) was shown to "open" the Sertoli cell barrier when its integrity was assessed by
79  form localized immune complexes outside the Sertoli cell barrier.
80                   These changes destabilized Sertoli cell blood-testis barrier (BTB) integrity.
81              Throughout spermatogenesis, the Sertoli cell blood-testis barrier (BTB) is strictly regu
82 eptide regulates testis function by inducing Sertoli cell blood-testis barrier (BTB) remodeling and i
83           Herein, using an in vitro model of Sertoli cell blood-testis barrier (BTB), PFOS was found
84 f P-glycoprotein by RNAi was found to impede Sertoli cell BTB function, making the tight junction (TJ
85 ed by changes in F-actin organization at the Sertoli cell BTB in vitro and in vivo, associated with a
86  turn led to protein mis-localization at the Sertoli cell BTB.
87 uced the rate of actin polymerization at the Sertoli cell BTB.
88 ns at the tight junction and basal ES at the Sertoli cell BTB.
89 testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild
90             Ex vivo, ibuprofen also affected Sertoli cell by suppressing AMH production and mRNA expr
91             A knockdown (KD) of plastin 3 in Sertoli cells by RNA interference using an in vitro mode
92              However, a knockdown of Cx43 in Sertoli cells by RNAi significantly reduced the kinetics
93 s development is solely under the control of Sertoli cells, by uncovering an active and essential rol
94                                              Sertoli cells, can function as non-professional toleroge
95 rmatid (apical ES) interface, as well as the Sertoli cell-cell (basal ES) interface at the blood-test
96 r knockdown by RNAi was also found to impede Sertoli cell-cell GJ communication, disrupting protein d
97 ecruitment of actin-related protein 3 to the Sertoli cell-cell interface, where it became more tightl
98  BTB in the rat testis and the phenotypes of Sertoli cell-conditional Cx43 knockout mice share many o
99 xt investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell injury.
100                      A knockdown of Rai14 in Sertoli cells cultured in vitro by RNAi was found to per
101                                     By using Sertoli cells cultured in vitro with an established TJ p
102  led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation of actin microf
103 erstitial progenitors, through the action of Sertoli cell-derived Hedgehog signals, become positive f
104 lone can compensate for the loss of SOX9 for Sertoli cell differentiation during female-to-male sex r
105                                Its key step, Sertoli cell differentiation in the embryonic gonadal ri
106 vel transcription factors likely controlling Sertoli cell differentiation.
107 n reducing occupancy of DNA sites regulating Sertoli-cell differentiation [the testis-specific SRY-bo
108 s is initiated when expression of Sry in pre-Sertoli cells directs the gonad toward a male-specific f
109 perturbed organization of actin filaments in Sertoli cells, disruption of the blood-testis barrier an
110                      It has been viewed as a Sertoli-cell driven process, but growing evidence sugges
111 cell survival and controls the cell cycle of Sertoli cells during differentiation.
112 permatogenesis by modulating the function of Sertoli cells during early testis development.
113 in the re-organization of actin filaments in Sertoli cells during the epithelial cycle, participating
114                    Interestingly, phenotypic Sertoli cell dysfunction in the Arid4a(-/-)Arid4b(+/-) m
115                      This includes ES at the Sertoli cell-elongating/elongated spermatid interface, w
116                   Here the authors show that Sertoli cells employ LC3-associated phagocytosis (LAP) b
117 tion of this approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to dr
118 tive effects on cytoskeletal organization in Sertoli cell epithelium and pertinent Sertoli cell funct
119 ressing its dominant-negative mutant T17N in Sertoli cell epithelium was shown to block the TGF-beta3
120 tion was effectively blocked by treatment of Sertoli cell epithelium with a p-Akt1/2 activator SC79,
121 s of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and repro
122 staglandin D2 (PGD2) inhibition in SC5 mouse Sertoli cells, evidence of binding at the COX-2 active s
123                    Furthermore, pre-pubertal Sertoli cells exhibit two distinct transcriptional state
124                                      Several Sertoli cell-expressed genes, such as Gdnf and Cyp26b1,
125                                              Sertoli cells facilitate the generation of several biolo
126 tate prior to transdifferentiating towards a Sertoli cell fate.
127 re the basal membranes of adjacent polarized Sertoli cells form a niche for the proliferating spermat
128 ession of structural proteins and protecting Sertoli cells from early apoptosis.
129 sites during sex determination, we subjected Sertoli cells from mouse fetal testes to DNaseI-seq and
130 gnaling protein that is required to maintain Sertoli cell function and could serve as a novel target
131 e caused, at least partly, by disruptions to Sertoli cell function and increased germ cell apoptosis,
132 atory pathways involved in the regulation of Sertoli cell function and male fertility.
133 of testes, which implies that their roles in Sertoli cell function are to support spermatogenesis and
134 strate PFOS exerts its disruptive effects on Sertoli cell function downstream through Akt1/2.
135 y to support NC1 peptide-mediated effects on Sertoli cell function in the testis using the rat as an
136 nfirming a requirement for PPARD in accurate Sertoli cell function.
137 e mechanisms controlled by LKB1 signaling in Sertoli cell functions and testicular biology have not b
138 ion in Sertoli cell epithelium and pertinent Sertoli cell functions.
139  (GODZ; also known as DHHC3) and its paralog Sertoli cell gene with a zinc finger domain-beta (SERZ-b
140 tion and MNG induction appears to be loss of Sertoli cell-germ cell membrane adhesion, probably due t
141 c deletion of transcription factor Zbtb20 in Sertoli cells has no apparent influence on spermatogenes
142 physiological function of NOTCH signaling in Sertoli cells has not been demonstrated.
143 anisms governing the functional integrity of Sertoli cells have remained largely unexplored.
144 oring junction) function along the length of Sertoli cell in the testis.
145                  Herein, we maintained human Sertoli cells in a mitotically active state in vitro, th
146 introduction of HSD17B3 via gene-delivery to Sertoli cells in adulthood partially rescues the adult p
147                    The absence of BT-IgSF in Sertoli cells in both global and conditional mouse mutan
148 20 a useful marker for the identification of Sertoli cells in seminiferous tubules.
149  was localized specifically in the nuclei of Sertoli cells in seminiferous tubules.
150 ages revealed a normal BTB structure between Sertoli cells in the BT-IgSF-KO mice, we conclude that i
151 ed by specialized junctions between adjacent Sertoli cells in the seminiferous epithelium near the ba
152 ted spermatogonia, primary spermatocytes and Sertoli cells in the testis, resulting in cell death and
153 e for Akap9 in the coordinated regulation of Sertoli cells in the testis.
154 cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which
155                  Interestingly, PFOS-induced Sertoli cell injury associated with a down-regulation of
156 stis barrier (BTB), PFOS was found to induce Sertoli cell injury by perturbing actin cytoskeleton thr
157 rected], was found to block the PFOS-induced Sertoli cell injury by rescuing the PFOS-induced F-actin
158                     PFOS was found to induce Sertoli cell injury through disruptive effects on actin
159                                 PFOS induces Sertoli cell injury using testicular cells isolated from
160                           PFOS induces human Sertoli cell injury which can be rescued by overexpressi
161 e spermatocyte stage, BSG-mediated germ cell-Sertoli cell interactions appear to be necessary for int
162  known as apical ES and possibly the Sertoli-Sertoli cell interface, known as basal ES, at the blood-
163 ion of TJ-associated proteins at the Sertoli-Sertoli cell interface.
164 en in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells.
165 ysis revealed that the expression program of Sertoli cells is altered upon inactivation of Sin3A in g
166 gocytic clearance of apoptotic germ cells by Sertoli cells is essential for spermatogenesis, little o
167          Androgen receptor (AR) signaling in Sertoli cells is known to be important for germ-cell pro
168          We conclude that NOTCH signaling in Sertoli cells is required for proper regulation of the t
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 constitutively activating NOTCH signaling in Sertoli cells leads to premature differentiation of all
173  central component of TGF-beta signaling, in Sertoli cells led to testis cord dysgenesis and prolifer
174  testis growth through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.
175 uggles to generate a productive infection in Sertoli cells, limiting its dissemination in the host.
176  provide evidence, based on an embryonic pre-Sertoli cell line, that this domain functions at a thres
177 ending are unaffected in a rat embryonic pre-Sertoli cell line, the variants exhibited selective defe
178  of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD
179 ule severely reduced Sox9 transcription in a Sertoli cell line.
180 gocytic clearance of apoptotic germ cells by Sertoli cells lining the seminiferous epithelium.
181 permatogenesis, its specific localization in Sertoli cells makes Zbtb20 a useful marker for the ident
182 dysgenesis (Leydig cell aggregation, ectopic Sertoli cells, malformed seminiferous cords) is not evid
183 ntified several misregulated genes in SCARKO Sertoli cells, many of which have been previously implic
184                    Roles for testosterone in Sertoli cell maturation, antimicrobial peptide secretion
185 ELMO1, respectively) were also important for Sertoli-cell-mediated engulfment.
186 uncover a selective requirement for ELMO1 in Sertoli-cell-mediated removal of apoptotic germ cells an
187 germ cell membrane adhesion, probably due to Sertoli cell microfilament redistribution.
188 icrofilament, thereby failing to support the Sertoli cell morphology and adhesion protein complexes (
189      Primary and immortalized GAR22beta(-/-) Sertoli cells moved faster than wild-type cells.
190 ier created by specialized junctions between Sertoli cells near the basement membrane confers an immu
191                             Neonatal porcine Sertoli cells (NPSC) are immune privileged cells showing
192 ce, and these were associated with decreased Sertoli cell number in Ppard(+/+) mice.
193 SHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effec
194                                 In ARKO mice Sertoli cell numbers were reduced at all ages from birth
195                                        Human Sertoli cells obtained from men at ages 15, 23, 36 and 4
196  Here we show that after ablation of Sox9 in Sertoli cells of adult, fertile Sox8(-/-) mice, testis-t
197    Arid4a and Arid4b are expressed mainly in Sertoli cells of testes, which implies that their roles
198 e found that WT1 and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryon
199 astly, the BEST1 promoter was also active in Sertoli cells of the testis in transgenic mice where SOX
200                    Although we show that the Sertoli cells of the testis secrete insulin protein, thi
201            In light of new evidence that the Sertoli cells of the testis secrete insulin, it is curre
202                   This was most prominent in Sertoli cells of the testis, in which nesprin-3 is requi
203  in the granulosa cells of the ovary and the Sertoli cells of the testis.
204                                   Defects in Sertoli cells often lead to infertility, but replacement
205 , we observed progressive germ cell loss and Sertoli cell only tubules in Lkb1(cko) testes from mice
206 c failure that presents clinically in men as Sertoli-cell only (SCO) pathology of the testis.
207               Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolut
208 d in 37% of patients despite a prevalence of Sertoli cell-only pattern on preoperative biopsy.
209                   These observations mimic a Sertoli cell-only syndrome in humans and may have transl
210                                 In contrast, Sertoli cell-only tubules were detected in parallel xeno
211 helial cells and germ cells, while absent in Sertoli cells or BTB site.
212 ion of bipotential precursor cells into male Sertoli cells or female granulosa cells.
213 recursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells.
214              We find that androgen regulates Sertoli cell phagocytosis by controlling expression of m
215  transcription factor for maintenance of the Sertoli cell phenotype.
216  of bundles of actin microfilaments near the Sertoli cell plasma membrane.
217 der than 10 weeks, accompanied by defects in Sertoli cell polarity and testicular junctional complexe
218 hich we believe may lead to apoptosis of the Sertoli cell population, inferring the possibility that
219  germ cell (Dazl), proliferating (PCNA), and Sertoli cell populations, and quantitated levels of apop
220                                              Sertoli cells produce GDNF and other growth factors and
221 alpha) since germ cells are known to control Sertoli cell production of this cytokine, and if yes, ho
222 rd elongation and expansion due to decreased Sertoli cell proliferation.
223                         These differentiated Sertoli cells remained mitotically active when cultured
224 ecise organization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1
225 lC-2 in retinal pigment epithelial cells and Sertoli cells, respectively, whereas leukodystrophy was
226 ere, we demonstrate that deletion of Shp2 in Sertoli cells results in infertility in mice.
227 by the blood-testis barrier, also called the Sertoli cell (SC) barrier (SCB).
228 including testicular atrophy, reduced LC and Sertoli cell (SC) number, decreased circulating testoste
229 cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), the supporting cells of the germ cel
230 ocal aggregation of Leydig cells and ectopic Sertoli cells (SC).
231  Changes in PGD2 secretion in juvenile mouse Sertoli cells (SC5 cells) were measured using an ELISA.
232 quitously (ARKO mice) or specifically on the Sertoli cells (SCARKO mice).
233 ehyde dehydrogenases (RALDH) present in both Sertoli cells (SCs) and germ cells (GCs).
234 codes a core NMD factor, in murine embryonic Sertoli cells (SCs) leads to severe testicular atrophy a
235                                              Sertoli cells (SCs) regulate testicular fate in the diff
236  substance (MIS), which is produced by fetal Sertoli cells shortly after commitment of the bipotentia
237     Transgenic mice expressing miR-471-5p in Sertoli cells show increased germ cell apoptosis and com
238  in both BA19 and CB; other pathways such as Sertoli cell signaling and fatty acid oxidation were spe
239  conserved among mammals and that we called 'Sertoli Cell Signature' (SCS).
240 ing actin microfilaments and microtubules in Sertoli cells so that they failed to support cell adhesi
241 ignificantly reduced Leydig cell numbers but Sertoli cell specific AR ablation had no effect.
242                    Analysis of SC-SF-1(-/-) (Sertoli cell specific Nr5a1 knockout) testes demonstrate
243 rier, recapitulated the defects found in the Sertoli cell-specific androgen receptor (AR) knockout mi
244                  Germ cell-specific, but not Sertoli cell-specific Nhe8 disruption recapitulated the
245                   In this study we generated Sertoli cell-specific Nr5a1 KO mice (SC-SF-1(-/-)) at E1
246 androgen receptor (AR) knockout mice and the Sertoli cell-specific RB knockout mice.
247 pecific, actin-rich adherens junction at the Sertoli cell-spermatid interface) to coordinate cellular
248 y during development, is essential for fetal Sertoli cell survival and controls the cell cycle of Ser
249 tor cells acquire SOX9 expression and become Sertoli cells that form testis cords, whereas the remain
250 s, SOX9 is required for the determination of Sertoli cells that orchestrate testis morphogenesis.
251 s strands of tight junctions between somatic Sertoli cells that restricts solutes from crossing the p
252                                              Sertoli cells, the epithelial cell type within testis co
253 s regulating Cyp26b1 expression in postnatal Sertoli cells, the main components of the stem cell nich
254 ation of plectin to the nuclear perimeter of Sertoli cells, the resulting link between the nuclear en
255 cell-cell adhesion between spermatogenic and Sertoli cells through its interaction with NECL4 on Sert
256 e the cells that activate NOTCH signaling in Sertoli cells through their expression of the NOTCH liga
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
259 helium of the seminiferous tubule, formed by Sertoli cells, thus leading to impaired spermatogenesis.
260                           PFOS perturbed the Sertoli cell tight junction (TJ)-permeability barrier, c
261 The removal of calcium by EGTA perturbed the Sertoli cell tight junction barrier, but calcium repleti
262 ha2 in Sertoli cells was shown to induce the Sertoli cell tight junction permeability barrier disrupt
263 t overexpression of Cx43 indeed resealed the Sertoli cell tight junction-permeability barrier based o
264 de was able to block the NC1 peptide-induced Sertoli cell tight junction-permeability barrier disrupt
265 rmer promoting and the latter disrupting the Sertoli cell tight junction-permeability barrier functio
266  a transient loss of plastin 3 perturbed the Sertoli cell tight junction-permeability barrier, mediat
267 ed in vitro by RNAi was found to perturb the Sertoli cell tight junction-permeability function in vit
268        Large cysts of germ cells transit the Sertoli cell tight junctions (SCTJs) without compromisin
269 nsequently, this prevented the disruption of Sertoli cell TJ permeability barrier and redistribution
270 ntation in the epithelium, and a "tightened" Sertoli cell TJ permeability barrier, supporting the rol
271 n of rictor by RNAi was found to perturb the Sertoli cell TJ-barrier function in vitro and the BTB in
272 e (FSH) acts through receptors (FSHR) on the Sertoli cell to stimulate spermatogenesis while androgen
273  of potential feminizing genes, DMRT1 allows Sertoli cells to participate in RA signaling, which is e
274 e fetal Leydig cells that acts directly upon Sertoli cells to promote their proliferation during late
275 line resulted in up-regulation of endogenous Sertoli cell transcripts and Wt1 (Arg495Gly/Arg495Gly) X
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
279                     Further investigation of Sertoli cells treated with IL-1alpha revealed striking c
280 nal characteristics of large-cell calcifying Sertoli cell tumors of the testes (LCCSCTs).
281 esis and are at increased risk of developing Sertoli cell tumors.
282 as juvenile granulosa-cell, Leydig-cell, and Sertoli-cell tumours).
283 estis barrier (BTB), formed between adjacent Sertoli cells, undergoes extensive remodeling to facilit
284          This study is proof of concept that Sertoli cells, upon specific stimulation, could particip
285 ), a crucial mediator of NOTCH signaling, in Sertoli cells using Amh-cre.
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
291                                         When Sertoli cells were isolated from Sprague-Dawley rats and
292                         We found that mutant Sertoli cells were morphologically normal before and aft
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
295 o the pachytene stage, as spermatogonial and Sertoli cells were unaffected in knockout mice.
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
299               CRB3 knockdown (KD) by RNAi in Sertoli cells with an established tight junction (TJ)-pe
300            Indeed, overexpression of Cx43 in Sertoli cells with an established TJ-barrier blocked the

 
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