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1 hibiting growth hormone release in pituitary somatotrophs.
2 , including via a direct effect on pituitary somatotrophs.
3 triggered secretion only in lactotrophs and somatotrophs.
4 mixed pituitary cells and in highly purified somatotrophs.
5 (ET) receptors were studied in rat pituitary somatotrophs.
6 annels in mixed pituitary cells and purified somatotrophs.
7 ncluding 28 corticotroph, 27 gonadotroph, 24 somatotroph, 17 lactotroph, 5 null-cell and 6 plurihormo
9 2 and SSTR5 are involved in GH regulation in somatotroph adenoma cells, whereas SSTR5 exclusively reg
10 a somatostatin receptor ligand that targets somatotroph adenoma GH secretion in patients with acrome
17 ed DNA damage, aneuploidy, and senescence in somatotroph adenomas, we studied links between cAMP sign
21 summary, GHRH-R is specifically expressed in somatotrophs and GH-producing adenomas, suggesting that
24 lar to this receptor's actions in the normal somatotrophs and may be involved in the growth of GH-sec
25 e proliferation and maintenance of pituitary somatotrophs and other cell types of the anterior pituit
26 iginating from late-born precursors, such as somatotrophs and POU1F1-dependent thyrotrophs, were seve
27 ence in electrical activity between bursting somatotrophs and spiking gonadotrophs is due to the pres
29 although rat anterior pituitary lactotrophs, somatotrophs, and gonadotrophs exhibited spontaneous and
30 p185(c-neu) protein expression in GH3 lacto-somatotroph but not in adrenocorticotropic hormone-secre
32 e (GH) gene expression in anterior pituitary somatotrophs by binding to the GHRH receptor, a G-protei
34 nous GH mRNA, GH content, pituitary size and somatotroph cell number were also reduced significantly
36 ecretion inhibitor (TSI) targeting pituitary somatotroph cells to suppress growth hormone (GH) secret
39 mote calcium influx, whereas lactotrophs and somatotrophs fired plateau-bursting action potentials th
40 pathways have been implicated in regulating somatotroph function, the physiological relevance of thi
43 th heregulin, the ErbB3 ligand, in rat lacto-somatotroph (GH4C1) tumor cells specifically induced pro
47 n essential role in the specification of the somatotroph, lactotroph and thyrotroph lineages and in t
48 scription factor required for development of somatotroph, lactotroph, and thyrotroph cell lineages an
49 NA and protein were detected in GH3 and MMQ (somatotroph-lactotroph lineages) and TtT/GF cells, and e
51 < 0.05), excluding dysfunction of pituitary somatotrophs or GHRH neurons as a cause for the absent G
53 cifically targeting GH secretion rather than somatotroph proliferation may be an advantage in the med
54 that BK channel activation in rat pituitary somatotrophs prolongs membrane depolarization, leading t
55 ET(A) receptors to the G(i)/G(o) pathway in somatotrophs provides an effective mechanism to change t
56 stigate the role of CBP as a target of IGF-1 somatotroph regulation using the MtT/S somatotroph cell
67 exocytosis and endocytosis in rat pituitary somatotrophs using patch-clamp capacitance, FM1-43 fluor
68 numbers of corticotrophs, gonadotrophs, and somatotrophs were equally decreased in Pact(-/-) mice wi
69 The RET receptor, uniquely co-expressed in somatotrophs with PIT1, induces apoptosis when unligande