ライフサイエンスコーパス: corticotroph

1 20 cells, a mouse anterior pituitary-derived corticotroph.

2 this time must lie at a level other than the corticotroph.

3 ng cells before birth, with the exception of corticotrophs.

4 tch of identity from melanotrophs to ectopic corticotrophs.

5 cally targeted ACTH secretion from pituitary corticotrophs.

6 specifically those of the intermediate lobe corticotrophs.

7 it would not be able to act directly on the corticotrophs.

8 itory factor (LIF) in human fetal and murine corticotrophs.

9 ivity and/or responsiveness of the pituitary corticotrophs.

10 of AVP which then enhances CRH action on the corticotrophs.

11 taries showed that only lactotroph (PRL) and corticotroph (ACTH) hormone-producing cells and tumors e

12 LIF-activated STAT3 indirectly mediates LIF corticotroph action by inducing and potentiating CRH-ind

13 ng the in vivo role of STAT3 in LIF-mediated corticotroph action.

14 ents with hypercortisolemia due to pituitary corticotroph adenomas (Cushing disease).

15 ecapitulated early features pathognomonic of corticotroph adenomas, including corticotroph expansion

16 IL-6 receptors are present on pituitary corticotrophs and adrenocortical cells, consistent with

17 -induced ACTH output from anterior pituitary corticotrophs and may also involve increased hypothalami

18 Corticotrophs are excitable cells that receive input fro

19 Corticotrophs are excitable cells that receive input fro

20 No evidence was found that corticotrophs are glucokinase positive, and the identity

21 Although corticotrophs are known to be electrically excitable, io

22 els controlling the electrical properties of corticotrophs are poorly understood.

23 Although corticotrophs are spontaneously active and increase in e

24 Although corticotrophs are spontaneously active and increase in e

25 We now demonstrate in corticotroph AtT-20 cells that LIF-stimulated endogenous

26 ed in transiently transfected ACTH-secreting corticotroph AtT-20 cells.

27 eiotropic neuroimmune cytokine that promotes corticotroph cell differentiation and induces proopiomel

28 In a recent study in the pituitary corticotroph cell line AtT20, oxidative stress stimulate

29 in signaling when transiently expressed in a corticotroph cell line.

30 were expressed in the AtT-20 mouse pituitary corticotroph cell line.

31 rs, we preferentially targeted EGFR to mouse corticotroph cell nuclei, which resulted in higher Pomc

32 ssion, thus limiting its accumulation in the corticotroph cell.

33 ed the action of LIF on proliferating murine corticotroph cells (AtT20).

34 gulation by glucocorticoids in murine AtT-20 corticotroph cells and in several primary tissues.

35 Anterior pituitary corticotroph cells are a central component of the hypoth

36 Anterior pituitary corticotroph cells are a central component of the hypoth

37 ther these data suggest that in AtT20 D16:16 corticotroph cells BK channels are important targets for

38 to be a differentiation factor for pituitary corticotroph cells by preferential phenotypic switching

39 AtT20 D16:16 clonal mouse anterior pituitary corticotroph cells.

40 F-mediated neuroimmunoendocrine interface in corticotroph cells.

41 nduced cell cycle block occurring at G1/S in corticotroph cells.

42 that in surgically resected human and canine corticotroph cultured tumors, blocking EGFR suppressed e

43 ption in vitro, suggesting a role for LIF in corticotroph development.

44 We demonstrate that corticotrophs display highly heterogeneous spontaneous a

45 In mouse corticotroph EGFR transfectants, ACTH secretion was enha

46 nels with TRAM-34 resulted in an increase in corticotroph excitability and exaggerated CRH/AVP-stimul

47 ides a mechanism for differential control of corticotroph excitability in response to different stres

48 ides a mechanism for differential control of corticotroph excitability in response to different stres

49 The ability of corticotroph excitability to be differentially regulated

50 The ability of corticotroph excitability to be differentially regulated

51 gnomonic of corticotroph adenomas, including corticotroph expansion and partial glucocorticoid resist

52 ciclib; CYC202), which specifically reversed corticotroph expansion in live Tg:Pomc-Pttg embryos.

53 ses of these three markers of differentiated corticotroph function indicate LIF to be a differentiati

54 n kinase pathway did not affect LIF-mediated corticotroph function.

55 ipate in the ability of alcohol to stimulate corticotrophs' function.

56 Among the 5 cell types in AL, the numbers of corticotrophs, gonadotrophs, and somatotrophs were equal

57 he unequivocal identification of live murine corticotrophs in culture.

58 on pituitary proopiomelanocortin-expressing corticotrophs in the mouse.

59 receptor expression in human fetal pituitary corticotrophs in vivo and demonstrated LIF stimulation o

60 The anterior pituitary corticotroph is a major control point for the regulation

61 vasopressin (AVP) cause a depolarization of corticotrophs, leading to a sustained increase in action

62 These results demonstrate that corticotroph LIF action is receptor mediated and involve

63 the release of adrenocorticotrophin from the corticotroph-like cell line AtT20 as an in vitro model s

64 ings provide evidence that the regulation of corticotroph NF-kappaB activity by CRH is related to the

65 ocorticotropic hormone (ACTH) secretion from corticotroph or ectopic tumours have been identified.

66 Early development of corticotroph pathologies in Tg:Pomc-Pttg embryos facilit

67 These results demonstrate a mechanism for corticotroph plasticity with rapid "on" and "off" ACTH i

68 but the physiological relevance of the dual corticotroph regulation is not understood.

69 In contrast, corticotrophs, rostral-tip POU1F1-independent thyrotroph

70 xiting cell cycle at early stages, including corticotrophs, rostral-tip thyrotrophs, and gonadotrophs

71 om the stomach, it stimulates lactotroph and corticotroph secretion, increases appetite and adiposity

72 Pituitary corticotroph SOCS-3 is a novel intracellular regulator o

73 xpress TRH receptors, and in AtT20 pituitary corticotrophs, TRH receptor immunoreactivity was primari

74 cotroph tumors as well as in human and mouse corticotroph tumor cell lines.

75 bitor, attenuated Pomc expression, inhibited corticotroph tumor cell proliferation, and induced apopt

76 covitine suppresses ACTH expression, induces corticotroph tumor cell senescence and cell cycle exit b

77 Although PAM sf-CD is unstable in AtT-20 corticotroph tumor cells, it is readily detected in prim

78 uppressed ACTH secretion in human and murine corticotroph tumor cells.

79 tive CDK inhibitors could effectively target corticotroph tumor growth and hormone secretion.

80 In vivo, TR4 overexpression promotes murine corticotroph tumor growth as well as enhances ACTH and c

81 group C, member 2) is overexpressed in human corticotroph tumors as well as in human and mouse cortic

82 Development of murine corticotroph tumors, generated by subcutaneous injection

83 indings directly link TR4 to the etiology of corticotroph tumors, hormone secretion, and cell growth

84 expression was observed in canine and human corticotroph tumors, we preferentially targeted EGFR to

85 Seven of the eight corticotroph tumours analysed by immunohistochemistry st

86 in expression, are not a general feature of corticotroph tumours, even those with intermediate lobe

87 n of all pituitary cell lineages, except the corticotrophs, was affected, suggesting that a distinct,

88 es the release of corticotropin by pituitary corticotrophs, which results in low plasma corticotropin