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1 ostral anterior pituitary gland (location of corticotropes).
2  anterior pituitary cells highly enriched in corticotropes.
3 nce of the resting membrane potential of rat corticotropes.
4  Ba(2+)-treated (77 +/- 15 spikes (5 min)-1) corticotropes.
5 ogranin processing in AtT-20 mouse pituitary corticotropes.
6 t on somatotrope cells that directly contact corticotropes.
7 works governing the initial specification of corticotropes, a major component of this axis, are not f
8 ise to gonadotrope, thyrotrope, somatotrope, corticotrope and lactotrope cells in the anterior lobe a
9    Dll3 is expressed only in the presumptive corticotrope and melanotrope cells.
10 hat Notch signaling is sufficient to prevent corticotrope and melanotrope differentiation, resulting
11  adrenocorticotropin (ACTH) of pars distalis corticotropes and alpha-melanocyte-stimulating hormone (
12 cascade inhibits the differentiation of both corticotropes and melanotropes and results in the suppre
13 sary to repress premature differentiation of corticotropes and to promote proliferation of pituitary
14 pes, thyrotropes, somatotropes, lactotropes, corticotropes, and melanotropes-appear to be determined,
15 tive compartment, where it remains until the corticotropes are stimulated with corticotropin releasin
16 ssion system was used to construct an AtT-20 corticotrope cell line capable of inducible PAM-1 expres
17   These findings reveal FGF1 produced by the corticotrope cell network as an essential paracrine sign
18 te to the severe reduction in differentiated corticotrope cells and lower expression of the corticotr
19     We show that blocking differentiation of corticotrope cells leads to pituitary hypoplasia with a
20 xpressed in the anterior pituitary or AtT-20 corticotrope cells.
21 ch signaling must be suppressed in order for corticotrope differentiation to proceed and whether Notc
22 increased numbers of lactotropes and loss of corticotropes in the anterior pars distalis (APD), incre
23 ocorticotropic hormone (ACTH) secretion from corticotropes, inhibited IK(IR) by 25% and depolarized t
24 he activation of CRFR1 on anterior pituitary corticotropes, leading to the release of glucocorticoids
25 and survival, delineates the melanotrope and corticotrope lineage boundary, contributing to establish
26 n of the late (Pit1) lineage into the early (corticotrope) lineage.
27 ll specification, and an increased number of corticotropes, melanotropes, and gonadotropes in the pit
28 omelanocortin (POMC) gene, the anterior lobe corticotropes, producing adrenocorticotropin, and the in
29 her Notch signaling is sufficient to promote corticotrope proliferation, we examined the effects of p
30                         Gene knockout of the corticotrope-restricted transcription factor Tpit result
31 transcriptomic analyses identified FGF1 as a corticotrope-specific Tpit dosage-dependent target gene
32 ing, cell survival, and normal expression of corticotrope-specific transcription factors, which are n
33               Double mutants exhibit delayed corticotrope specification and complete failure of all o
34                 Following internalization in corticotropes, SSTR2 moves to a juxtanuclear syntaxin-6-
35 RH-binding protein (CRH-BP) is secreted from corticotropes, the pituitary CRH target cells, suggestin
36 rticotrope cells and lower expression of the corticotrope transcription factors, TPIT and NEUROD1.
37                                              Corticotrope tumor cell lines expressing integral membra
38                            When expressed in corticotrope tumor cells and primary anterior pituitary
39 homeostasis in neuroendocrine cells, we used corticotrope tumor cells in which AP-1 function was dimi
40            Overexpression of membrane PAM in corticotrope tumor cells reorganizes the actin cytoskele
41                                              Corticotrope tumor cells stably expressing P-CIP10 and P
42  was localized to the Golgi region of AtT-20 corticotrope tumor cells, and expression of integral mem
43                                        As in corticotrope tumor cells, expression of PAM or Myc-TMD/C
44 nules by stably expressing rat DBM in AtT-20 corticotrope tumor cells, which contain regulated granul
45 ant of PAM-1) was stably expressed in AtT-20 corticotrope tumor cells.
46 3A) was expressed in HEK293 cells and AtT-20 corticotrope tumor cells.