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1                                              Sertoli cells (SCs) regulate testicular fate in the diff
2                                              Sertoli cells are considered the "supporting cells" of t
3                                              Sertoli cells facilitate the generation of several biolo
4                                              Sertoli cells produce GDNF and other growth factors and
5                                              Sertoli cells, also known as 'mother' or 'nurse' cells,
6                                              Sertoli cells, can function as non-professional toleroge
7                    Analysis of SC-SF-1(-/-) (Sertoli cell specific Nr5a1 knockout) testes demonstrate
8                      It has been viewed as a Sertoli-cell driven process, but growing evidence sugges
9               Sin3A-deleted testes exhibit a Sertoli-cell only phenotype, consistent with the absolut
10 ratubular germ cell neoplasia was found in a Sertoli cell adenoma.
11 ule severely reduced Sox9 transcription in a Sertoli cell line.
12                   These observations mimic a Sertoli cell-only syndrome in humans and may have transl
13 tate prior to transdifferentiating towards a Sertoli cell fate.
14 nfirming a requirement for PPARD in accurate Sertoli cell function.
15  led to a dis-organization of F-actin across Sertoli cell cytosol, causing truncation of actin microf
16 estis barrier (BTB), formed between adjacent Sertoli cells, undergoes extensive remodeling to facilit
17           Four days after BC administration, Sertoli cells are preferentially depleted, and can be re
18 mary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and NOD2 crosstalk converged in
19             Ex vivo, ibuprofen also affected Sertoli cell by suppressing AMH production and mRNA expr
20  of potential feminizing genes, DMRT1 allows Sertoli cells to participate in RA signaling, which is e
21                                     Although Sertoli cells are a driving force in the de novo formati
22 lC-2 in retinal pigment epithelial cells and Sertoli cells, respectively, whereas leukodystrophy was
23 he same stage in developing chondrocytes and Sertoli cells and determined SOX9 target genes in these
24  changes, including paratesticular cysts and Sertoli cell adenomas.
25 including testicular atrophy, reduced LC and Sertoli cell (SC) number, decreased circulating testoste
26 , we observed progressive germ cell loss and Sertoli cell only tubules in Lkb1(cko) testes from mice
27 is-to-ovary genetic reprogramming occurs and Sertoli cells transdifferentiate into granulosa-like cel
28  germ cell (Dazl), proliferating (PCNA), and Sertoli cell populations, and quantitated levels of apop
29 s in protein distribution at the Sertoli and Sertoli-germ-cell cell interface and by phosphorylation
30 ted spermatogonia, primary spermatocytes and Sertoli cells in the testis, resulting in cell death and
31 tercellular spaces between spermatogenic and Sertoli cells as well as the spermatid deformities.
32 cell-cell adhesion between spermatogenic and Sertoli cells through its interaction with NECL4 on Sert
33 o the pachytene stage, as spermatogonial and Sertoli cells were unaffected in knockout mice.
34 c failure that presents clinically in men as Sertoli-cell only (SCO) pathology of the testis.
35  in both BA19 and CB; other pathways such as Sertoli cell signaling and fatty acid oxidation were spe
36 tor cells acquire SOX9 expression and become Sertoli cells that form testis cords, whereas the remain
37   Although these changes are usually benign, Sertoli adenomas can sometimes harbor premalignant lesio
38 e peptides in facilitating crosstalk between Sertoli and germ cells to support spermatogenesis and th
39  is supported by intricate crosstalk between Sertoli cells and germ cells including spermatogonia, sp
40 ages revealed a normal BTB structure between Sertoli cells in the BT-IgSF-KO mice, we conclude that i
41                A deficiency of RDH10 in both Sertoli and germ cells in juvenile mice results in a blo
42 ehyde dehydrogenases (RALDH) present in both Sertoli cells (SCs) and germ cells (GCs).
43 quired for the lineage specification of both Sertoli and granulosa cells by repressing Sf1 expression
44         Furthermore, differentiation of both Sertoli and granulosa cells was blocked when Wt1 was del
45 ignificantly reduced Leydig cell numbers but Sertoli cell specific AR ablation had no effect.
46 gocytic clearance of apoptotic germ cells by Sertoli cells is essential for spermatogenesis, little o
47 gocytic clearance of apoptotic germ cells by Sertoli cells is vital for germ cell development and dif
48 ficient clearance of apoptotic germ cells by Sertoli cells using LAP.Although phagocytic clearance of
49  of the seminiferous epithelium delimited by Sertoli cells and peritubular myoid (PM) cells.
50 s3, CRB3) is a polarity protein expressed by Sertoli and germ cells at the basal compartment in the s
51 t testis, Rai14 was found to be expressed by Sertoli and germ cells, structurally associated with act
52 helium of the seminiferous tubule, formed by Sertoli cells, thus leading to impaired spermatogenesis.
53 cycle (i) RALDH-dependent synthesis of RA by Sertoli cells (SC), the supporting cells of the germ cel
54 nal characteristics of large-cell calcifying Sertoli cell tumors of the testes (LCCSCTs).
55  conserved among mammals and that we called 'Sertoli Cell Signature' (SCS).
56 ated N-glycans that participate in germ cell-Sertoli cell adhesion.
57 ons indicate that BSG may act as a germ cell-Sertoli cell attachment molecule.
58 e spermatocyte stage, BSG-mediated germ cell-Sertoli cell interactions appear to be necessary for int
59                            Supporting cells (Sertoli and granulosa) and steroidogenic cells (Leydig a
60 s exert deleterious effects on Leydig cells, Sertoli cells, and germ cells via very different mechani
61                                 In contrast, Sertoli cell-only tubules were detected in parallel xeno
62 vel transcription factors likely controlling Sertoli cell differentiation.
63                       Using primary cultured Sertoli cells as an in vitro model that mimics the BTB i
64 rd elongation and expansion due to decreased Sertoli cell proliferation.
65 ce, and these were associated with decreased Sertoli cell number in Ppard(+/+) mice.
66  74%) and low-signal-intensity, well-defined Sertoli cell adenomas (26 of 46 testes, 56%).
67                   These changes destabilized Sertoli cell blood-testis barrier (BTB) integrity.
68 cal role in mammalian gonads is to determine Sertoli cells, we correlated this genomic signature with
69 esis and are at increased risk of developing Sertoli cell tumors.
70                         These differentiated Sertoli cells remained mitotically active when cultured
71 dysgenesis (Leydig cell aggregation, ectopic Sertoli cells, malformed seminiferous cords) is not evid
72 ocal aggregation of Leydig cells and ectopic Sertoli cells (SC).
73 t in re-aggregated testis, including ectopic Sertoli cells and intratubular Leydig cells (ITLCs).
74 re, and cooperated with endogenous embryonic Sertoli and primordial germ cells in the generation of t
75 lar-like structures, and expressed embryonic Sertoli-specific markers.
76 onstrate the generation of induced embryonic Sertoli-like cells (ieSCs) by ectopic expression of five
77 codes a core NMD factor, in murine embryonic Sertoli cells (SCs) leads to severe testicular atrophy a
78 line resulted in up-regulation of endogenous Sertoli cell transcripts and Wt1 (Arg495Gly/Arg495Gly) X
79 erm cells inside tubules lined by epithelial Sertoli cells.
80 al-time polymerase chain reaction to examine Sertoli and germ cell markers on rat testes and human fe
81  substance (MIS), which is produced by fetal Sertoli cells shortly after commitment of the bipotentia
82 y during development, is essential for fetal Sertoli cell survival and controls the cell cycle of Ser
83  to a genomic bar code of the fate of foetal Sertoli cells.
84 lone can compensate for the loss of SOX9 for Sertoli cell differentiation during female-to-male sex r
85 iotic transitions are coordinated by RA from Sertoli (somatic) cells.
86      Primary and immortalized GAR22beta(-/-) Sertoli cells moved faster than wild-type cells.
87                   In this study we generated Sertoli cell-specific Nr5a1 KO mice (SC-SF-1(-/-)) at E1
88 , receptors, and integrins required for germ-Sertoli cell adhesion and dynamic junctional restructuri
89                                        Human Sertoli cells obtained from men at ages 15, 23, 36 and 4
90                           PFOS induces human Sertoli cell injury which can be rescued by overexpressi
91                  Herein, we maintained human Sertoli cells in a mitotically active state in vitro, th
92 rovide evidence that ZIKV infection of human Sertoli cells, which are an important component of the s
93 an in vitro infection model of primary human Sertoli cells.
94 f P-glycoprotein by RNAi was found to impede Sertoli cell BTB function, making the tight junction (TJ
95 r knockdown by RNAi was also found to impede Sertoli cell-cell GJ communication, disrupting protein d
96             A knockdown (KD) of plastin 3 in Sertoli cells by RNA interference using an in vitro mode
97     Transgenic mice expressing miR-471-5p in Sertoli cells show increased germ cell apoptosis and com
98 helial cells and germ cells, while absent in Sertoli cells or BTB site.
99  we found that Notch signaling was active in Sertoli cells at various fetal, neonatal, and adult stag
100 emonstrate that Notch signaling is active in Sertoli cells throughout development and that proper reg
101 importance, a knockdown of laminin alpha2 in Sertoli cells was shown to induce the Sertoli cell tight
102  was sparsely expressed in germ cells and in Sertoli cells.
103 of proliferating cellular nuclear antigen in Sertoli cells were observed in Ppard(+/+) mice as compar
104 xt investigated if overexpression of Cx43 in Sertoli cells could rescue the PFOS-induced cell injury.
105            Indeed, overexpression of Cx43 in Sertoli cells with an established TJ-barrier blocked the
106 der than 10 weeks, accompanied by defects in Sertoli cell polarity and testicular junctional complexe
107                                   Defects in Sertoli cells often lead to infertility, but replacement
108 testes and found that an RDH10 deficiency in Sertoli cells, but not in germ cells, results in a mild
109  in which Zbtb20 was specifically deleted in Sertoli cells.
110 naling components have long been detected in Sertoli and germ cells in the developing and mature test
111               In testis, RA acts directly in Sertoli, Leydig and pre-meiotic germ cells.
112 ve regulatory sites around genes enriched in Sertoli and pregranulosa cells; however, active enhancer
113 led several potential modifiers expressed in Sertoli cells at the time of testis determination in mic
114 e found that WT1 and KDR are co-expressed in Sertoli cells of the testes and somatic cells of embryon
115 promoter and thus inhibits its expression in Sertoli cells.
116 in the re-organization of actin filaments in Sertoli cells during the epithelial cycle, participating
117 perturbed organization of actin filaments in Sertoli cells, disruption of the blood-testis barrier an
118 ta on inflammasome expression or function in Sertoli cells.
119                    The absence of BT-IgSF in Sertoli cells in both global and conditional mouse mutan
120 uggles to generate a productive infection in Sertoli cells, limiting its dissemination in the host.
121 uration, and formation of tight junctions in Sertoli cells, thus confirming a requirement for PPARD i
122 concomitant activation of CTNNB1 and KRAS in Sertoli cells also caused testicular granulosa cell tumo
123 lls in the testes, but at very low levels in Sertoli cells.
124 permatogenesis, its specific localization in Sertoli cells makes Zbtb20 a useful marker for the ident
125       Here, we found that it is localized in Sertoli cells at the blood-testis barrier (BTB) and at t
126    Arid4a and Arid4b are expressed mainly in Sertoli cells of testes, which implies that their roles
127  filaments and alpha-tubulin microtubules in Sertoli and McCoy cells.
128 tions in the organization of microtubules in Sertoli cells and a loss of barrier integrity despite a
129 ing actin microfilaments and microtubules in Sertoli cells so that they failed to support cell adhesi
130 e, intracellular domain of NOTCH1 (NICD1) in Sertoli cells.
131 arity of targets in chondrocytes, but not in Sertoli cells.
132 orphology and the position of the nucleus in Sertoli cells were normal, however, in the nesprin-3-kno
133 tive effects on cytoskeletal organization in Sertoli cell epithelium and pertinent Sertoli cell funct
134 s would be modulated through this pathway in Sertoli cells.
135 gh this transepithelial transport pathway in Sertoli cells.
136 gh this transepithelial transport pathway in Sertoli cells.
137 in, or the use of a synthetic F5 peptide, in Sertoli cells with an established functional blood-testi
138 elial ovarian tumors (29%), predominantly in Sertoli-Leydig cell tumors (26 of 43, or 60%), including
139                   This was most prominent in Sertoli cells of the testis, in which nesprin-3 is requi
140                      A knockdown of Rai14 in Sertoli cells cultured in vitro by RNAi was found to per
141 SHR ablation also caused small reductions in Sertoli cell numbers up to day 20 with more marked effec
142 drive expression of a transgenic reporter in Sertoli cells.
143 ate that Ins2 is a direct target of Rhox5 in Sertoli cells, and we show that this regulation is physi
144               CRB3 knockdown (KD) by RNAi in Sertoli cells with an established tight junction (TJ)-pe
145 of testes, which implies that their roles in Sertoli cell function are to support spermatogenesis and
146 k180, LC3, Atg12, Becn1, Rab5 and Rubicon in Sertoli cells.
147 ere, we demonstrate that deletion of Shp2 in Sertoli cells results in infertility in mice.
148 e mechanisms controlled by LKB1 signaling in Sertoli cell functions and testicular biology have not b
149 physiological function of NOTCH signaling in Sertoli cells has not been demonstrated.
150          Androgen receptor (AR) signaling in Sertoli cells is known to be important for germ-cell pro
151          We conclude that NOTCH signaling in Sertoli cells is required for proper regulation of the t
152 that proper regulation of Notch signaling in Sertoli cells is required for the maintenance of gonocyt
153 constitutively activating NOTCH signaling in Sertoli cells leads to premature differentiation of all
154 e the cells that activate NOTCH signaling in Sertoli cells through their expression of the NOTCH liga
155 ), a crucial mediator of NOTCH signaling, in Sertoli cells using Amh-cre.
156  Here we show that after ablation of Sox9 in Sertoli cells of adult, fertile Sox8(-/-) mice, testis-t
157                    Roles for testosterone in Sertoli cell maturation, antimicrobial peptide secretion
158 c deletion of transcription factor Zbtb20 in Sertoli cells has no apparent influence on spermatogenes
159 stis barrier (BTB), PFOS was found to induce Sertoli cell injury by perturbing actin cytoskeleton thr
160                     PFOS was found to induce Sertoli cell injury through disruptive effects on actin
161 de was able to block the NC1 peptide-induced Sertoli cell tight junction-permeability barrier disrupt
162                  Interestingly, PFOS-induced Sertoli cell injury associated with a down-regulation of
163 rected], was found to block the PFOS-induced Sertoli cell injury by rescuing the PFOS-induced F-actin
164                                 PFOS induces Sertoli cell injury using testicular cells isolated from
165 eptide regulates testis function by inducing Sertoli cell blood-testis barrier (BTB) remodeling and i
166 ding highlighted the ability of Ct to infect Sertoli cells, although with a unique growth profile and
167 tions in the cytoskeletal fibres of infected Sertoli cells.
168 osa cells can reprogram granulosa cells into Sertoli cells.
169 mmed juvenile and adult granulosa cells into Sertoli-like cells, triggering formation of structures r
170                    Transdifferentiation into Sertoli-like cells and osteoblasts was attributed in par
171 not exclusive, source of RA in the testes is Sertoli cells.
172 leads to malfunction of the somatic (Leydig, Sertoli) cells and consequent downstream TDS disorders.
173 gnaling protein that is required to maintain Sertoli cell function and could serve as a novel target
174 ion of bipotential precursor cells into male Sertoli cells or female granulosa cells.
175 sexual cell-fate reprogramming in which male Sertoli cells transdifferentiate into their female equiv
176                                 In ARKO mice Sertoli cell numbers were reduced at all ages from birth
177  of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD
178  NOD1 and NOD2 expression in human and mouse Sertoli cells.
179 s of the DMRT1 transcription factor in mouse Sertoli cells, even in adults, activates Foxl2 and repro
180  Changes in PGD2 secretion in juvenile mouse Sertoli cells (SC5 cells) were measured using an ELISA.
181 staglandin D2 (PGD2) inhibition in SC5 mouse Sertoli cells, evidence of binding at the COX-2 active s
182                         We found that mutant Sertoli cells were morphologically normal before and aft
183                  Germ cell-specific, but not Sertoli cell-specific Nhe8 disruption recapitulated the
184 tion of this approach, we identified a novel Sertoli cell enhancer upstream of Wt1, and used it to dr
185  correctly depict the presence or absence of Sertoli cell adenomas in 19 of 23 testes (83%).
186 erstitial progenitors, through the action of Sertoli cell-derived Hedgehog signals, become positive f
187 me, are regulated inside a niche composed of Sertoli cells, and other testis cell types.
188 cell survival and controls the cell cycle of Sertoli cells during differentiation.
189 cells, with likely secondary degeneration of Sertoli cells, including the blood-testis barrier, which
190 s, SOX9 is required for the determination of Sertoli cells that orchestrate testis morphogenesis.
191  also molecularly defined the development of Sertoli, Leydig and peritubular myoid cells during the p
192 fects are correlated with a dysregulation of Sertoli-expressed genes that are required for germ cell
193 permatogenesis by modulating the function of Sertoli cells during early testis development.
194 20 a useful marker for the identification of Sertoli cells in seminiferous tubules.
195 anisms governing the functional integrity of Sertoli cells have remained largely unexplored.
196 oring junction) function along the length of Sertoli cell in the testis.
197                           Due to the loss of Sertoli and germ cells, the testis weights of SC-SF-1(-/
198 tion and MNG induction appears to be loss of Sertoli cell-germ cell membrane adhesion, probably due t
199  I of meiosis but does inhibit maturation of Sertoli cells, which continue to express the immaturity
200           Herein, using an in vitro model of Sertoli cell blood-testis barrier (BTB), PFOS was found
201  was localized specifically in the nuclei of Sertoli cells in seminiferous tubules.
202 ation of plectin to the nuclear perimeter of Sertoli cells, the resulting link between the nuclear en
203  BTB in the rat testis and the phenotypes of Sertoli cell-conditional Cx43 knockout mice share many o
204 nockout mice (SCSKO), a normal population of Sertoli cells was observed, but the blood-testis barrier
205 d in 37% of patients despite a prevalence of Sertoli cell-only pattern on preoperative biopsy.
206 ysis revealed that the expression program of Sertoli cells is altered upon inactivation of Sin3A in g
207 atory pathways involved in the regulation of Sertoli cell function and male fertility.
208 e for Akap9 in the coordinated regulation of Sertoli cells in the testis.
209 tion was effectively blocked by treatment of Sertoli cell epithelium with a p-Akt1/2 activator SC79,
210 lity to reproduce is completely dependent on Sertoli cells.
211 strate PFOS exerts its disruptive effects on Sertoli cell function downstream through Akt1/2.
212 y to support NC1 peptide-mediated effects on Sertoli cell function in the testis using the rat as an
213  cells through its interaction with NECL4 on Sertoli cells.
214 ed by H3K27ac were enriched proximal to only Sertoli-enriched genes.
215 ating step for 1 month were transferred onto Sertoli feeder cells, they differentiated into functiona
216 t with NSun2 in spermatogonial stem cells or Sertoli cells.
217 equired for the survival of trophectoderm or Sertoli cells.
218  (GODZ; also known as DHHC3) and its paralog Sertoli cell gene with a zinc finger domain-beta (SERZ-b
219 ion in Sertoli cell epithelium and pertinent Sertoli cell functions.
220 ired phagocytosis by specialized phagocytes: Sertoli cells and the retinal pigmented epithelium (RPE)
221                    Interestingly, phenotypic Sertoli cell dysfunction in the Arid4a(-/-)Arid4b(+/-) m
222                             Neonatal porcine Sertoli cells (NPSC) are immune privileged cells showing
223 s regulating Cyp26b1 expression in postnatal Sertoli cells, the main components of the stem cell nich
224  provide evidence, based on an embryonic pre-Sertoli cell line, that this domain functions at a thres
225 ending are unaffected in a rat embryonic pre-Sertoli cell line, the variants exhibited selective defe
226 pe A, Int, B spermatogonia as well as in pre-Sertoli cells and Leydig cells but was undetectable in s
227 s is initiated when expression of Sry in pre-Sertoli cells directs the gonad toward a male-specific f
228 tiated by upregulation of Sox9 by SRY in pre-Sertoli cells.
229 n impaired the cell junctions of the primary Sertoli cells and failed to support the clonal formation
230 y restores the cell junctions of the primary Sertoli cells and the clonal formation of SSCs.
231 ession of structural proteins and protecting Sertoli cells from early apoptosis.
232        We found that in primary pre-pubertal Sertoli cells and in adult Sertoli line, TLR4\NOD1 and N
233                    Furthermore, pre-pubertal Sertoli cells exhibit two distinct transcriptional state
234              We find that androgen regulates Sertoli cell phagocytosis by controlling expression of m
235 -testis barrier (BTB) involved in regulating Sertoli cell adhesion via its effects on the occludin-zo
236 n reducing occupancy of DNA sites regulating Sertoli-cell differentiation [the testis-specific SRY-bo
237 en in adults, activates Foxl2 and reprograms Sertoli cells into granulosa cells.
238 ntified several misregulated genes in SCARKO Sertoli cells, many of which have been previously implic
239 nal formation of SSCs co-cultured with SCSKO Sertoli cells.
240                                      Several Sertoli cell-expressed genes, such as Gdnf and Cyp26b1,
241 s strands of tight junctions between somatic Sertoli cells that restricts solutes from crossing the p
242                                Its key step, Sertoli cell differentiation in the embryonic gonadal ri
243 sites during sex determination, we subjected Sertoli cells from mouse fetal testes to DNaseI-seq and
244 a without direct contact with the supporting Sertoli cells, we show that haploid spermatids express t
245 recursor cells differentiate into testicular Sertoli cells or ovarian granulosa cells.
246 er ovarian pre-granulosa cells or testicular Sertoli cells.
247                               In the testis, Sertoli cells are the key niche cells directing the popu
248          This study is proof of concept that Sertoli cells, upon specific stimulation, could particip
249                   Here the authors show that Sertoli cells employ LC3-associated phagocytosis (LAP) b
250                                By E15.5, the Sertoli cell and germ cell population declined in SC-SF-
251 androgen receptor (AR) knockout mice and the Sertoli cell-specific RB knockout mice.
252 rmatid (apical ES) interface, as well as the Sertoli cell-cell (basal ES) interface at the blood-test
253 d via changes in protein distribution at the Sertoli and Sertoli-germ-cell cell interface and by phos
254 ed by changes in F-actin organization at the Sertoli cell BTB in vitro and in vivo, associated with a
255 ns at the tight junction and basal ES at the Sertoli cell BTB.
256  turn led to protein mis-localization at the Sertoli cell BTB.
257 uced the rate of actin polymerization at the Sertoli cell BTB.
258                      This includes ES at the Sertoli cell-elongating/elongated spermatid interface, w
259 pecific, actin-rich adherens junction at the Sertoli cell-spermatid interface) to coordinate cellular
260 testes, most notably at the apical ES at the Sertoli-spermatid interface, and expressed stage-specifi
261  posits that MGCA are sequestered behind the Sertoli cell barrier in seminiferous tubules.
262 by the blood-testis barrier, also called the Sertoli cell (SC) barrier (SCB).
263 rmer promoting and the latter disrupting the Sertoli cell tight junction-permeability barrier functio
264 ecise organization of binding motifs for the Sertoli cell reprogramming factors SOX9, GATA4 and DMRT1
265 rier, recapitulated the defects found in the Sertoli cell-specific androgen receptor (AR) knockout mi
266 ses and single-cell RNAseq (scRNAseq) in the Sertoli-cell androgen receptor knockout (SCARKO) mutant
267 ressed sFRP1 using lentiviral vectors in the Sertoli-germ cell coculture system.
268 ha2 in Sertoli cells was shown to induce the Sertoli cell tight junction permeability barrier disrupt
269  of bundles of actin microfilaments near the Sertoli cell plasma membrane.
270  transcription factor for maintenance of the Sertoli cell phenotype.
271 hich we believe may lead to apoptosis of the Sertoli cell population, inferring the possibility that
272 e (FSH) acts through receptors (FSHR) on the Sertoli cell to stimulate spermatogenesis while androgen
273 quitously (ARKO mice) or specifically on the Sertoli cells (SCARKO mice).
274  testis growth through receptors (AR) on the Sertoli cells, Leydig cells and peritubular myoid cells.
275  form localized immune complexes outside the Sertoli cell barrier.
276 ed in vitro by RNAi was found to perturb the Sertoli cell tight junction-permeability function in vit
277 n of rictor by RNAi was found to perturb the Sertoli cell TJ-barrier function in vitro and the BTB in
278                           PFOS perturbed the Sertoli cell tight junction (TJ)-permeability barrier, c
279  a transient loss of plastin 3 perturbed the Sertoli cell tight junction-permeability barrier, mediat
280 which is known as apical ES and possibly the Sertoli-Sertoli cell interface, known as basal ES, at th
281 t overexpression of Cx43 indeed resealed the Sertoli cell tight junction-permeability barrier based o
282              Throughout spermatogenesis, the Sertoli cell blood-testis barrier (BTB) is strictly regu
283 icrofilament, thereby failing to support the Sertoli cell morphology and adhesion protein complexes (
284                    Although we show that the Sertoli cells of the testis secrete insulin protein, thi
285            In light of new evidence that the Sertoli cells of the testis secrete insulin, it is curre
286 on than androgen action mediated through the Sertoli cells although androgen action through other cel
287 ndent on FSH and androgen action through the Sertoli cells.
288  the actions of FSH and androgen through the Sertoli cells.
289 ecruitment of actin-related protein 3 to the Sertoli cell-cell interface, where it became more tightl
290                      ES is restricted to the Sertoli-spermatid (apical ES) interface, as well as the
291        Large cysts of germ cells transit the Sertoli cell tight junctions (SCTJs) without compromisin
292                                        These Sertoli-like cells facilitated neuronal differentiation
293 l-cell adhesions of developing germ cells to Sertoli nurse cells, with likely secondary degeneration
294 introduction of HSD17B3 via gene-delivery to Sertoli cells in adulthood partially rescues the adult p
295 e caused, at least partly, by disruptions to Sertoli cell function and increased germ cell apoptosis,
296 germ cell membrane adhesion, probably due to Sertoli cell microfilament redistribution.
297  intrinsic and extrinsic genes responsive to Sertoli-cell androgen signaling that promotes cellular s
298 s, there is evidence of pregranulosa cell-to-Sertoli cell transdifferentiation near birth, following
299                       The use of an in vitro Sertoli cell barrier to describe how ZIKV or inflammator
300  interactions of other testicular cells with Sertoli cells and to test novel antivirals for clearing

 
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