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1 20 cells, a mouse anterior pituitary-derived corticotroph.
2 this time must lie at a level other than the corticotroph.
3 nd showed drastic reduction in the number of corticotrophs.
4 ng cells before birth, with the exception of corticotrophs.
5 tch of identity from melanotrophs to ectopic corticotrophs.
6 cally targeted ACTH secretion from pituitary corticotrophs.
7  specifically those of the intermediate lobe corticotrophs.
8  it would not be able to act directly on the corticotrophs.
9 itory factor (LIF) in human fetal and murine corticotrophs.
10 ivity and/or responsiveness of the pituitary corticotrophs.
11 of AVP which then enhances CRH action on the corticotrophs.
12 lectrical excitability of anterior pituitary corticotrophs.
13 to the tonic spiking behaviour of unstressed corticotrophs.
14 ted on by a single neurosurgeon including 28 corticotroph, 27 gonadotroph, 24 somatotroph, 17 lactotr
15 taries showed that only lactotroph (PRL) and corticotroph (ACTH) hormone-producing cells and tumors e
16  LIF-activated STAT3 indirectly mediates LIF corticotroph action by inducing and potentiating CRH-ind
17 ng the in vivo role of STAT3 in LIF-mediated corticotroph action.
18 icotropic hormone (ACTH)-secreting pituitary corticotroph adenoma leads to hypercortisolaemia with hi
19 al resection of the causal tissue, including corticotroph adenoma or ectopic tumour for ACTH-dependen
20 ents with hypercortisolemia due to pituitary corticotroph adenomas (Cushing disease).
21                     Potential new targets in corticotroph adenomas include the epidermal growth facto
22 eting dopamine and somatostatin receptors on corticotroph adenomas with cabergoline or pasireotide, o
23              The least likely to invade were corticotroph adenomas, at a rate of 32% intraoperatively
24 ecapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion
25      IL-6 receptors are present on pituitary corticotrophs and adrenocortical cells, consistent with
26 -induced ACTH output from anterior pituitary corticotrophs and may also involve increased hypothalami
27                                              Corticotrophs are excitable cells that receive input fro
28                                              Corticotrophs are excitable cells that receive input fro
29                   No evidence was found that corticotrophs are glucokinase positive, and the identity
30                                     Although corticotrophs are known to be electrically excitable, io
31 els controlling the electrical properties of corticotrophs are poorly understood.
32                                     Although corticotrophs are spontaneously active and increase in e
33                        We now demonstrate in corticotroph AtT-20 cells that LIF-stimulated endogenous
34 ed in transiently transfected ACTH-secreting corticotroph AtT-20 cells.
35                             Surprisingly, CS corticotrophs (but not unstressed) display CRH-induced b
36 eiotropic neuroimmune cytokine that promotes corticotroph cell differentiation and induces proopiomel
37           In a recent study in the pituitary corticotroph cell line AtT20, oxidative stress stimulate
38 in signaling when transiently expressed in a corticotroph cell line.
39 were expressed in the AtT-20 mouse pituitary corticotroph cell line.
40 rs, we preferentially targeted EGFR to mouse corticotroph cell nuclei, which resulted in higher Pomc
41 denoma/pituitary neuroendocrine tumor of the corticotroph cell type (TPIT lineage) in 10 of 15 and a
42 ssion, thus limiting its accumulation in the corticotroph cell.
43 ed the action of LIF on proliferating murine corticotroph cells (AtT20).
44 gulation by glucocorticoids in murine AtT-20 corticotroph cells and in several primary tissues.
45                           Anterior pituitary corticotroph cells are a central component of the hypoth
46 ther these data suggest that in AtT20 D16:16 corticotroph cells BK channels are important targets for
47 to be a differentiation factor for pituitary corticotroph cells by preferential phenotypic switching
48 AtT20 D16:16 clonal mouse anterior pituitary corticotroph cells.
49 F-mediated neuroimmunoendocrine interface in corticotroph cells.
50 nduced cell cycle block occurring at G1/S in corticotroph cells.
51 that in surgically resected human and canine corticotroph cultured tumors, blocking EGFR suppressed e
52 ption in vitro, suggesting a role for LIF in corticotroph development.
53                      CS (but not unstressed) corticotrophs display corticotrophin-releasing hormone-i
54                          We demonstrate that corticotrophs display highly heterogeneous spontaneous a
55                                     In mouse corticotroph EGFR transfectants, ACTH secretion was enha
56 nels with TRAM-34 resulted in an increase in corticotroph excitability and exaggerated CRH/AVP-stimul
57                                              Corticotroph excitability can be finely tuned by the sto
58 ides a mechanism for differential control of corticotroph excitability in response to different stres
59 esponse is dependent upon anterior pituitary corticotroph excitability in response to hypothalamic se
60                         A key determinant of corticotroph excitability is large conductance calcium-
61 ontext dependent allowing dynamic control of corticotroph excitability over a large range of time dom
62 tion with L-type calcium channels to control corticotroph excitability over diverse time domains and
63  we hypothesise that chronic stress promotes corticotroph excitability through a BK-dependent mechani
64  small number of BK channels can finely tune corticotroph excitability through stress-induced changes
65                               The ability of corticotroph excitability to be differentially regulated
66 gnomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resist
67 ciclib; CYC202), which specifically reversed corticotroph expansion in live Tg:Pomc-Pttg embryos.
68 lectrophysiological recordings from isolated corticotrophs from CS male mice display spontaneous elec
69                                              Corticotrophs from CS mice displayed significant increas
70 ses of these three markers of differentiated corticotroph function indicate LIF to be a differentiati
71 n kinase pathway did not affect LIF-mediated corticotroph function.
72 ipate in the ability of alcohol to stimulate corticotrophs' function.
73 Among the 5 cell types in AL, the numbers of corticotrophs, gonadotrophs, and somatotrophs were equal
74 he unequivocal identification of live murine corticotrophs in culture.
75  on pituitary proopiomelanocortin-expressing corticotrophs in the mouse.
76 receptor expression in human fetal pituitary corticotrophs in vivo and demonstrated LIF stimulation o
77                       The anterior pituitary corticotroph is a major control point for the regulation
78   The increased spontaneous bursting from CS corticotrophs is BK-dependent and mathematical modelling
79  vasopressin (AVP) cause a depolarization of corticotrophs, leading to a sustained increase in action
80               These results demonstrate that corticotroph LIF action is receptor mediated and involve
81 the release of adrenocorticotrophin from the corticotroph-like cell line AtT20 as an in vitro model s
82 ings provide evidence that the regulation of corticotroph NF-kappaB activity by CRH is related to the
83 isolated ACTHD, led to a strong reduction of corticotrophs number in pituitary organoids.
84 ocorticotropic hormone (ACTH) secretion from corticotroph or ectopic tumours have been identified.
85 tress (CS) is partly a function of increased corticotroph output.
86                         Early development of corticotroph pathologies in Tg:Pomc-Pttg embryos facilit
87    These results demonstrate a mechanism for corticotroph plasticity with rapid "on" and "off" ACTH i
88  but the physiological relevance of the dual corticotroph regulation is not understood.
89                                 In contrast, corticotrophs, rostral-tip POU1F1-independent thyrotroph
90 xiting cell cycle at early stages, including corticotrophs, rostral-tip thyrotrophs, and gonadotrophs
91 om the stomach, it stimulates lactotroph and corticotroph secretion, increases appetite and adiposity
92                                    Pituitary corticotroph SOCS-3 is a novel intracellular regulator o
93 e precursors development (TBX19, POU1F1) and corticotrophs terminal differentiation (PCSK1, POMC), an
94 ch as the stress-hormone-secreting pituitary corticotrophs that are switched from spiking to bursting
95 xpress TRH receptors, and in AtT20 pituitary corticotrophs, TRH receptor immunoreactivity was primari
96 cotroph tumors as well as in human and mouse corticotroph tumor cell lines.
97 bitor, attenuated Pomc expression, inhibited corticotroph tumor cell proliferation, and induced apopt
98 covitine suppresses ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit b
99     Although PAM sf-CD is unstable in AtT-20 corticotroph tumor cells, it is readily detected in prim
100 uppressed ACTH secretion in human and murine corticotroph tumor cells.
101 tive CDK inhibitors could effectively target corticotroph tumor growth and hormone secretion.
102  In vivo, TR4 overexpression promotes murine corticotroph tumor growth as well as enhances ACTH and c
103 group C, member 2) is overexpressed in human corticotroph tumors as well as in human and mouse cortic
104                        Development of murine corticotroph tumors, generated by subcutaneous injection
105 indings directly link TR4 to the etiology of corticotroph tumors, hormone secretion, and cell growth
106  expression was observed in canine and human corticotroph tumors, we preferentially targeted EGFR to
107                           Seven of the eight corticotroph tumours analysed by immunohistochemistry st
108  in expression, are not a general feature of corticotroph tumours, even those with intermediate lobe
109 ccurate localization of small PitNETs of the corticotroph type in patients with de novo CD.
110 itary neuroendocrine tumors (PitNETs) of the corticotroph type lead to Cushing disease (CD), a condit
111 n of all pituitary cell lineages, except the corticotrophs, was affected, suggesting that a distinct,
112 es the release of corticotropin by pituitary corticotrophs, which results in low plasma corticotropin

 
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