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1 luteinizing hormone (LH) from the pituitary gonadotroph.
2 eased in size and contain reduced numbers of gonadotrophs.
3 al alphaT3-1 cells and primary rat pituitary gonadotrophs.
4 ake approximately 2 weeks to desensitize the gonadotrophs.
5 ized in the same cells of the pituitary, the gonadotrophs.
6 cretion was examined in female rat pituitary gonadotrophs.
7 ium (BK) channels on somatotrophs but not on gonadotrophs.
8 lls were treated with hypothalamic peptides, gonadotroph adenomas were the only group that released i
9 ptide pancreastatin can regulate CgB mRNA in gonadotroph adenomas, suggesting an autocrine effect of
10 gB and follicle-stimulating hormone mRNAs in gonadotroph adenomas, whereas CgA mRNA levels did not ch
13 creastatin and CgA were present diffusely in gonadotroph and null cell adenomas, but only a few prola
15 uitination of IP(3)R1 in alphaT3-1 pituitary gonadotrophs and found that IP(3)R1 ubiquitination is hi
17 ERK1/2) in normal and immortalized pituitary gonadotrophs and transfected cells expressing the GnRH r
18 ynthesized in the same cell (i.e., pituitary gonadotrophs) and several of the alpha subunit sequences
19 l types in AL, the numbers of corticotrophs, gonadotrophs, and somatotrophs were equally decreased in
20 egulation of Ca2+ signaling and secretion in gonadotrophs, and that these actions are mediated by P2
21 as a key regulator of Lhb expression in the gonadotroph by integrating homeostatic information with
23 n vitro in GH3 somato/lactotroph and LbetaT2 gonadotroph cell lines; knockdown of PACT expression wit
24 model the intracellular calcium dynamics of gonadotroph cells by adapting the model of Li and Rinzel
25 N-207 exerts highly selective effects on the gonadotroph cells containing LH-RH receptors and is less
28 TP induced an inward depolarizing current in gonadotrophs clamped at -90 mV, associated with an incre
29 a fast-activating BK conductance to spiking gonadotrophs converts the activity of these cells to bur
30 on, suggesting that it is not the absence of gonadotroph differentiation, but rather the deficient hy
31 s a therapeutic agent to eliminate pituitary gonadotrophs, eliminating the need for chronic GnRH anal
32 igh basal levels of hormone secretion, while gonadotrophs exhibit spontaneous spiking and have low ba
34 ior pituitary lactotrophs, somatotrophs, and gonadotrophs exhibited spontaneous and extracellular cal
37 VEGF-A isoforms culminates in alterations in gonadotroph function opposite to those of LTs, with up-r
38 sms through which LH-RH antagonists suppress gonadotroph functions and LH-RH receptor (LH-RH-R) produ
39 ormone (LHRH) antagonists suppress pituitary gonadotroph functions and LHRH-receptor (LHRH-R) express
40 Ca2+-dependent rise in [Ca2+]i in identified gonadotrophs in a Mg2+- and suramin-sensitive manner.
41 ty between bursting somatotrophs and spiking gonadotrophs is due to the presence of large conductance
42 f five clinically nonfunctioning adenomas, a gonadotroph luteinizing hormone/follicle-stimulating hor
43 s an elevation in BK current expression in a gonadotroph model system leads to the generation of plat
44 clinically nonfunctioning adenomas (NFAs) of gonadotroph origin; however, expression status of other
45 s in human, rat somatolactotroph, and murine gonadotroph pituitary tumor cells, and suppressed in vit
46 er the deficient hypothalamic stimulation of gonadotrophs, that underlies typical hypogonadotrophic h
47 from sharp spikes to plateau-like spikes in gonadotrophs triggered luteinizing hormone secretion.
48 nt and growth of murine somatolactotroph and gonadotroph tumors, generated by subcutaneous injection
50 lack of action potential-driven secretion in gonadotrophs was not due to the proportion of spontaneou
52 corticotrophs, rostral-tip thyrotrophs, and gonadotrophs, were generated, while hormone-producing ce
53 were roughly equipotent in rising [Ca2+]i in gonadotrophs, while ADP was effective only at submillimo
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