ライフサイエンスコーパス: gonadotroph

1 luteinizing hormone (LH) from the pituitary gonadotroph.

2 ium (BK) channels on somatotrophs but not on gonadotrophs.

3 eased in size and contain reduced numbers of gonadotrophs.

4 al alphaT3-1 cells and primary rat pituitary gonadotrophs.

5 ake approximately 2 weeks to desensitize the gonadotrophs.

6 ized in the same cells of the pituitary, the gonadotrophs.

7 cretion was examined in female rat pituitary gonadotrophs.

8 e neurosurgeon including 28 corticotroph, 27 gonadotroph, 24 somatotroph, 17 lactotroph, 5 null-cell

9 lls were treated with hypothalamic peptides, gonadotroph adenomas were the only group that released i

10 ptide pancreastatin can regulate CgB mRNA in gonadotroph adenomas, suggesting an autocrine effect of

11 gB and follicle-stimulating hormone mRNAs in gonadotroph adenomas, whereas CgA mRNA levels did not ch

12 centrations (10(-13) mol/L) of TGF-beta 1 in gonadotroph adenomas.

13 The results suggest that in gonadotrophs an oscillatory Ca2+ signal is sensed by the

14 creastatin and CgA were present diffusely in gonadotroph and null cell adenomas, but only a few prola

15 The highest levels were present in gonadotroph and null cell adenomas.

16 uitination of IP(3)R1 in alphaT3-1 pituitary gonadotrophs and found that IP(3)R1 ubiquitination is hi

17 ACTH cells increased 2.2-fold, whereas gonadotrophs and thyrotrophs were unchanged.

18 ERK1/2) in normal and immortalized pituitary gonadotrophs and transfected cells expressing the GnRH r

19 ynthesized in the same cell (i.e., pituitary gonadotrophs) and several of the alpha subunit sequences

20 l types in AL, the numbers of corticotrophs, gonadotrophs, and somatotrophs were equally decreased in

21 egulation of Ca2+ signaling and secretion in gonadotrophs, and that these actions are mediated by P2

22 stnatally and up to puberty, while embryonic gonadotrophs are maintained.

23 Gonadotrophs are the essential pituitary endocrine cells

24 The division of gonadotrophs based on separate origins has implications

25 as a key regulator of Lhb expression in the gonadotroph by integrating homeostatic information with

26 We show that in the LbetaT2 gonadotroph cell line, overexpression of CBP augmented t

27 n vitro in GH3 somato/lactotroph and LbetaT2 gonadotroph cell lines; knockdown of PACT expression wit

28 , followed by plurihormonal tumors (40%) and gonadotroph cell tumors (33%), both with intraoperative

29 model the intracellular calcium dynamics of gonadotroph cells by adapting the model of Li and Rinzel

30 N-207 exerts highly selective effects on the gonadotroph cells containing LH-RH receptors and is less

31 The binding of GnRH to gonadotroph cells in the pituitary stimulates inositol 1

32 A selective damage to the pituitary gonadotroph cells was found at 1 week after a single i.v

33 TP induced an inward depolarizing current in gonadotrophs clamped at -90 mV, associated with an incre

34 a fast-activating BK conductance to spiking gonadotrophs converts the activity of these cells to bur

35 We further demonstrate that postnatal gonadotroph differentiation happens independently of gon

36 on, suggesting that it is not the absence of gonadotroph differentiation, but rather the deficient hy

37 s a therapeutic agent to eliminate pituitary gonadotrophs, eliminating the need for chronic GnRH anal

38 igh basal levels of hormone secretion, while gonadotrophs exhibit spontaneous spiking and have low ba

39 Gonadotrophs exhibited calcium signals during prolonged

40 ior pituitary lactotrophs, somatotrophs, and gonadotrophs exhibited spontaneous and extracellular cal

41 Conversely, pituitary gonadotrophs express relatively few BK channels and fire

42 Gonadotrophs first appear in the embryonic pituitary, al

43 simultaneously in single anterior pituitary gonadotrophs from ovariectomized female rats.

44 VEGF-A isoforms culminates in alterations in gonadotroph function opposite to those of LTs, with up-r

45 sms through which LH-RH antagonists suppress gonadotroph functions and LH-RH receptor (LH-RH-R) produ

46 ormone (LHRH) antagonists suppress pituitary gonadotroph functions and LHRH-receptor (LHRH-R) express

47 Ca2+-dependent rise in [Ca2+]i in identified gonadotrophs in a Mg2+- and suramin-sensitive manner.

48 ty between bursting somatotrophs and spiking gonadotrophs is due to the presence of large conductance

49 f five clinically nonfunctioning adenomas, a gonadotroph luteinizing hormone/follicle-stimulating hor

50 While gonadotrophs may display heterogeneity in their response

51 s an elevation in BK current expression in a gonadotroph model system leads to the generation of plat

52 clinically nonfunctioning adenomas (NFAs) of gonadotroph origin; however, expression status of other

53 rine adult gonadotroph population, with most gonadotrophs originating from postnatal pituitary stem c

54 s in human, rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vit

55 unsuspected dual origin of the murine adult gonadotroph population, with most gonadotrophs originati

56 ajor factors accounting for weakening of the gonadotroph secretory function during continuous GnRH tr

57 er the deficient hypothalamic stimulation of gonadotrophs, that underlies typical hypogonadotrophic h

58 tected in all secretory cell types, Asic2 in gonadotrophs, thyrotrophs, and somatotrophs, and Asic4 i

59 from sharp spikes to plateau-like spikes in gonadotrophs triggered luteinizing hormone secretion.

60 nt and growth of murine somatolactotroph and gonadotroph tumors, generated by subcutaneous injection

61 Spontaneous activity in gonadotrophs was characterized by high amplitude, sharp

62 lack of action potential-driven secretion in gonadotrophs was not due to the proportion of spontaneou

63 Using in-vivo and ex-vivo calcium imaging of gonadotrophs, we show that GnRH predominantly activates

64 ession to progesterone in PNA mice and their gonadotrophs were also less sensitive to GnRH.

65 otrophs, and, interestingly, lactotrophs and gonadotrophs were less affected.

66 corticotrophs, rostral-tip thyrotrophs, and gonadotrophs, were generated, while hormone-producing ce

67 were roughly equipotent in rising [Ca2+]i in gonadotrophs, while ADP was effective only at submillimo