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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.
31 ratubular germ cell neoplasia was found in a Sertoli cell adenoma.
32  74%) and low-signal-intensity, well-defined Sertoli cell adenomas (26 of 46 testes, 56%).
33  correctly depict the presence or absence of Sertoli cell adenomas in 19 of 23 testes (83%).
34  changes, including paratesticular cysts and Sertoli cell adenomas.
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
37 ated N-glycans that participate in germ cell-Sertoli cell adhesion.
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
43        We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and N
44 pe A, Int, B spermatogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in s
45  of the seminiferous epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.
46 y restores the cell junctions of the primary Sertoli cells and the clonal formation of SSCs.
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
53                                     Although Sertoli cells are a driving force in the de novo formati
54                                              Sertoli cells are considered the "supporting cells" of t
55                               In the testis, Sertoli cells are the key niche cells directing the popu
56                       Using primary cultured Sertoli cells as an in vitro model that mimics the BTB i
57 tercellular spaces between spermatogenic and Sertoli cells as well as the spermatid deformities.
58       Here, we found that it is localized in Sertoli cells at the blood-testis barrier (BTB) and at t
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
61 ons indicate that BSG may act as a germ cell-Sertoli cell attachment molecule.
62 an testes, the blood-testis barrier (BTB) or Sertoli cell barrier created by specialized junctions be
63  posits that MGCA are sequestered behind the Sertoli cell barrier in seminiferous tubules.
64                       The use of an in vitro Sertoli cell barrier to describe how ZIKV or inflammator
65                         These effects at the Sertoli cell barrier were mediated, in part, by epiderma
66 L-1alpha (100 pg/ml) was shown to "open" the Sertoli cell barrier when its integrity was assessed by
67  form localized immune complexes outside the Sertoli cell barrier.
68                   These changes destabilized Sertoli cell blood-testis barrier (BTB) integrity.
69              Throughout spermatogenesis, the Sertoli cell blood-testis barrier (BTB) is strictly regu
70           Herein, using an in vitro model of Sertoli cell blood-testis barrier (BTB), PFOS was found
71 n upregulation of beta-catenin expression in Sertoli cells both in vitro and in vivo.
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
74  turn led to protein mis-localization at the Sertoli cell BTB.
75 uced the rate of actin polymerization at the Sertoli cell BTB.
76 ns at the tight junction and basal ES at the Sertoli cell BTB.
77 testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild
78             Ex vivo, ibuprofen also affected Sertoli cell by suppressing AMH production and mRNA expr
79             A knockdown (KD) of plastin 3 in Sertoli cells by RNA interference using an in vitro mode
80              However, a knockdown of Cx43 in Sertoli cells by RNAi significantly reduced the kinetics
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
83                                              Sertoli cells, can function as non-professional toleroge
84               As Wt1 conditional knockout in Sertoli cells causes similar phenotypes to our stabilize
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
89 oli cell identity and misregulation of inter-Sertoli cell contacts.
90 xt investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell injury.
91 binase-expressing mice and in testis using a Sertoli cell Cre recombinase-expressing mouse.
92                      A knockdown of Rai14 in Sertoli cells cultured in vitro by RNAi was found to per
93                                      Primary Sertoli cells cultured in vitro were shown to establish
94                                Using primary Sertoli cells cultured in vitro with an established tigh
95                                     By using Sertoli cells cultured in vitro with an established TJ p
96 ific siRNA duplexes was performed in primary Sertoli cell cultures with an established TJ permeabilit
97                                      Primary Sertoli cell cultures with established functional BTB, b
98                                           In Sertoli cell cultures with established permeability barr
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
101                                Its key step, Sertoli cell differentiation in the embryonic gonadal ri
102  beta-catenin in fetal testes did not affect Sertoli cell differentiation, testis morphogenesis or ma
103 vel transcription factors likely controlling Sertoli cell differentiation.
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
108                      It has been viewed as a Sertoli-cell driven process, but growing evidence sugges
109 permatogenesis by modulating the function of Sertoli cells during early testis development.
110 ith the formation of tight junctions between Sertoli cells during postnatal development.
111               However, its potential role in Sertoli cells during testis formation has not been exami
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
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 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
121                                      Several Sertoli cell-expressed genes, such as Gdnf and Cyp26b1,
122                     Our study indicates that Sertoli cell expression of beta-catenin is dispensable f
123 tate prior to transdifferentiating towards a Sertoli cell fate.
124 re the basal membranes of adjacent polarized Sertoli cells form a niche for the proliferating spermat
125 ession of structural proteins and protecting Sertoli cells from early apoptosis.
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,
130 atory pathways involved in the regulation of Sertoli cell function and male fertility.
131 of testes, which implies that their roles in Sertoli cell function are to support spermatogenesis and
132 strate PFOS exerts its disruptive effects on Sertoli cell function downstream through Akt1/2.
133 nfirming a requirement for PPARD in accurate Sertoli cell function.
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
138 physiological function of NOTCH signaling in Sertoli cells has not been demonstrated.
139 anisms governing the functional integrity of Sertoli cells have remained largely unexplored.
140 beta-Catenin stabilization caused changes in Sertoli cell identity and misregulation of inter-Sertoli
141 oring junction) function along the length of Sertoli cell in the testis.
142                  Herein, we maintained human Sertoli cells in a mitotically active state in vitro, th
143                    The absence of BT-IgSF in Sertoli cells in both global and conditional mouse mutan
144 20 a useful marker for the identification of Sertoli cells in seminiferous tubules.
145  was localized specifically in the nuclei of Sertoli cells in seminiferous tubules.
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
150 e for Akap9 in the coordinated regulation of Sertoli cells in the testis.
151 cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which
152                  Interestingly, PFOS-induced Sertoli cell injury associated with a down-regulation of
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
155                     PFOS was found to induce Sertoli cell injury through disruptive effects on actin
156                                 PFOS induces Sertoli cell injury using testicular cells isolated from
157                           PFOS induces human Sertoli cell injury which can be rescued by overexpressi
158 e spermatocyte stage, BSG-mediated germ cell-Sertoli cell interactions appear to be necessary for int
159 e steady-state protein levels at the Sertoli-Sertoli cell interface at the BTB.
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
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 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
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 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
180 ule severely reduced Sox9 transcription in a Sertoli cell line.
181 sed to endosomes, and knock-down of Sdmg1 in Sertoli cell lines causes mis-localisation of the secret
182 lement that inhibits Pp transcription in non-Sertoli cell lines.
183 gocytic clearance of apoptotic germ cells by Sertoli cells lining the seminiferous epithelium.
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
187 ELMO1, respectively) were also important for Sertoli-cell-mediated engulfment.
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
190 germ cell membrane adhesion, probably due to Sertoli cell microfilament redistribution.
191 icrofilament, thereby failing to support the Sertoli cell morphology and adhesion protein complexes (
192      Primary and immortalized GAR22beta(-/-) Sertoli cells moved faster than wild-type cells.
193 ier created by specialized junctions between Sertoli cells near the basement membrane confers an immu
194                             Neonatal porcine Sertoli cells (NPSC) are immune privileged cells showing
195 ce, and these were associated with decreased Sertoli cell number in Ppard(+/+) mice.
196 SHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effec
197                                 In ARKO mice Sertoli cell numbers were reduced at all ages from birth
198                                        Human Sertoli cells obtained from men at ages 15, 23, 36 and 4
199  Here we show that after ablation of Sox9 in Sertoli cells of adult, fertile Sox8(-/-) mice, testis-t
200                    Sdmg1 is expressed in the Sertoli cells of embryonic testes from 12.5 dpc, and in
201    Arid4a and Arid4b are expressed mainly in Sertoli cells of testes, which implies that their roles
202         KitL localization is affected in the Sertoli cells of the KitL(L263A/L263A) testis and testis
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
205                    Although we show that the Sertoli cells of the testis secrete insulin protein, thi
206            In light of new evidence that the Sertoli cells of the testis secrete insulin, it is curre
207                   This was most prominent in Sertoli cells of the testis, in which nesprin-3 is requi
208  in the granulosa cells of the ovary and the Sertoli cells of the testis.
209 , we observed progressive germ cell loss and Sertoli cell only tubules in Lkb1(cko) testes from mice
210 c failure that presents clinically in men as Sertoli-cell only (SCO) pathology of the testis.
211               Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolut
212 d in 37% of patients despite a prevalence of Sertoli cell-only pattern on preoperative biopsy.
213                                 In contrast, Sertoli cell-only tubules were detected in parallel xeno
214 helial cells and germ cells, while absent in Sertoli cells or BTB site.
215 ion of bipotential precursor cells into male Sertoli cells or female granulosa cells.
216 recursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells.
217              We find that androgen regulates Sertoli cell phagocytosis by controlling expression of m
218  transcription factor for maintenance of the Sertoli cell phenotype.
219  of bundles of actin microfilaments near the Sertoli cell plasma membrane.
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
223                                              Sertoli cells produce GDNF and other growth factors and
224 alpha) since germ cells are known to control Sertoli cell production of this cytokine, and if yes, ho
225 rd elongation and expansion due to decreased Sertoli cell proliferation.
226                         These differentiated Sertoli cells remained mitotically active when cultured
227 ecise organization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1
228 ere, we demonstrate that deletion of Shp2 in Sertoli cells results in infertility in mice.
229 by the blood-testis barrier, also called the Sertoli cell (SC) barrier (SCB).
230 cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), the supporting cells of the germ cel
231 ocal aggregation of Leydig cells and ectopic Sertoli cells (SC).
232  Changes in PGD2 secretion in juvenile mouse Sertoli cells (SC5 cells) were measured using an ELISA.
233 quitously (ARKO mice) or specifically on the Sertoli cells (SCARKO mice).
234                       Androgen signaling via Sertoli cells (SCs) is essential for complete spermatoge
235 codes a core NMD factor, in murine embryonic Sertoli cells (SCs) leads to severe testicular atrophy a
236                                              Sertoli cells (SCs) regulate testicular fate in the diff
237                                           In Sertoli cells, Sdmg1 is localised to endosomes, and knoc
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
240  conserved among mammals and that we called 'Sertoli Cell Signature' (SCS).
241 ing actin microfilaments and microtubules in Sertoli cells so that they failed to support cell adhesi
242 ignificantly reduced Leydig cell numbers but Sertoli cell specific AR ablation had no effect.
243 rier, recapitulated the defects found in the Sertoli cell-specific androgen receptor (AR) knockout mi
244                                          Its Sertoli cell-specific expression is achieved, in part, t
245                  Germ cell-specific, but not Sertoli cell-specific Nhe8 disruption recapitulated the
246 androgen receptor (AR) knockout mice and the Sertoli cell-specific RB knockout mice.
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
254                                              Sertoli cells, the epithelial cell type within testis co
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
259                           PFOS perturbed the Sertoli cell tight junction (TJ)-permeability barrier, c
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
266        Large cysts of germ cells transit the Sertoli cell tight junctions (SCTJs) without compromisin
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
274 1 is required in fetal germ cells but not in Sertoli cells to prevent teratoma formation.
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
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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