ライフサイエンスコーパス: somatotroph

1 triggered secretion only in lactotrophs and somatotrophs.

2 mixed pituitary cells and in highly purified somatotrophs.

3 (ET) receptors were studied in rat pituitary somatotrophs.

4 annels in mixed pituitary cells and purified somatotrophs.

5 hibiting growth hormone release in pituitary somatotrophs.

6 , including via a direct effect on pituitary somatotrophs.

7 These results indicate that in somatotrophs a cyclic nucleotide-controlled plasma membr

8 2 and SSTR5 are involved in GH regulation in somatotroph adenoma cells, whereas SSTR5 exclusively reg

9 STAT3 and GH expression were concordant in a somatotroph adenoma tissue array.

10 In primary human somatotroph adenoma-derived cell cultures, STAT3 suppres

11 Pituitary somatotroph adenomas result in dysregulated growth hormo

12 a potential therapeutic target for pituitary somatotroph adenomas.

13 x 1 (POU1F1) as well as severe disruption of somatotroph and thyrotroph differentiation.

14 summary, GHRH-R is specifically expressed in somatotrophs and GH-producing adenomas, suggesting that

15 Rat somatotrophs and lactotrophs exhibit spontaneous burstin

16 rization comparable with signals observed in somatotrophs and lactotrophs.

17 lar to this receptor's actions in the normal somatotrophs and may be involved in the growth of GH-sec

18 e proliferation and maintenance of pituitary somatotrophs and other cell types of the anterior pituit

19 iginating from late-born precursors, such as somatotrophs and POU1F1-dependent thyrotrophs, were seve

20 ence in electrical activity between bursting somatotrophs and spiking gonadotrophs is due to the pres

21 although rat anterior pituitary lactotrophs, somatotrophs, and gonadotrophs exhibited spontaneous and

22 p185(c-neu) protein expression in GH3 lacto-somatotroph but not in adrenocorticotropic hormone-secre

23 large conductance potassium (BK) channels on somatotrophs but not on gonadotrophs.

24 e (GH) gene expression in anterior pituitary somatotrophs by binding to the GHRH receptor, a G-protei

25 IGF-1 somatotroph regulation using the MtT/S somatotroph cell line.

26 nous GH mRNA, GH content, pituitary size and somatotroph cell number were also reduced significantly

27 GHRH-R was specifically localized in somatotroph cells in the normal pituitary.

28 ecretion inhibitor (TSI) targeting pituitary somatotroph cells to suppress growth hormone (GH) secret

29 by promoting the proliferation of pituitary somatotroph cells.

30 mote calcium influx, whereas lactotrophs and somatotrophs fired plateau-bursting action potentials th

31 pathways have been implicated in regulating somatotroph function, the physiological relevance of thi

32 Here we show that rat pituitary somatotrophs generate spontaneous [Ca(2+)](i) oscillatio

33 Blocking BK channels in bursting lacto-somatotroph GH4C1 cells changes their firing activity to

34 th heregulin, the ErbB3 ligand, in rat lacto-somatotroph (GH4C1) tumor cells specifically induced pro

35 Our results suggest that pituitary somatotrophs have the ability to undergo continuous exoc

36 cally reduces the numbers of lactotrophs and somatotrophs in the pituitary.

37 n essential role in the specification of the somatotroph, lactotroph and thyrotroph lineages and in t

38 scription factor required for development of somatotroph, lactotroph, and thyrotroph cell lineages an

39 NA and protein were detected in GH3 and MMQ (somatotroph-lactotroph lineages) and TtT/GF cells, and e

40 L gene expression, and reversed EGF-mediated somatotroph-lactotroph phenotype switching.

41 < 0.05), excluding dysfunction of pituitary somatotrophs or GHRH neurons as a cause for the absent G

42 that BK channel activation in rat pituitary somatotrophs prolongs membrane depolarization, leading t

43 ET(A) receptors to the G(i)/G(o) pathway in somatotrophs provides an effective mechanism to change t

44 stigate the role of CBP as a target of IGF-1 somatotroph regulation using the MtT/S somatotroph cell

45 ic mice expressing the intact hGH locus in a somatotroph-specific manner were generated.

46 In somatotrophs treated with pertussis toxin overnight, the

47 provide evidence that STAT3 directly induces somatotroph tumor cell GH.

48 sitive feedback loop between STAT3 and GH in somatotroph tumor cells.

49 In addition, S3I-201 attenuated somatotroph tumor growth and GH secretion in a rat xenog

50 owth and PRL secretion in experimental lacto-somatotroph tumors.

51 exocytosis and endocytosis in rat pituitary somatotrophs using patch-clamp capacitance, FM1-43 fluor

52 numbers of corticotrophs, gonadotrophs, and somatotrophs were equally decreased in Pact(-/-) mice wi