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1 er activity of genes encoding kisspeptin and neurokinin B.
2 B > senktide > substance P = neurokinin A > neurokinin B.
3 s to concentrations of neurokinin A (10 nM), neurokinin B (0.1 microM), substance P (1 microM), neuro
5 NA and have elucidated the putative sites of neurokinin B action in the rat central nervous system.
6 te nucleus (ARC) that co-express kisspeptin, neurokinin B and dynorphin (KNDy cells) are essential fo
7 he Tac2 gene, which encodes the neuropeptide neurokinin B and its corresponding receptor neurokinin 3
8 ative feedback interactions mediated through neurokinin-B and dynorphin signaling respectively are co
10 at release the neurotransmitters kisspeptin, neurokinin B, and dynorphin (KNDy neurons), and produce
11 the hypothalamus that coexpress kisspeptin, neurokinin B, and dynorphin (termed KNDy cells) which fo
12 eus, known as KNDy neurons for co-expressing neurokinin B, and dynorphin, drive pulsatile GnRH releas
14 es for their natural ligands substance P and neurokinin B but also exhibited surprisingly high affini
15 arked alterations in hypothalamic kisspeptin/neurokinin B/dynorphin (KNDy) neurons, we hypothesized t
16 are also effects at the ARH to disrupt Kiss1/neurokinin B/dynorphin neuronal function through inhibit
18 trophy of neurons expressing substance P and neurokinin B gene transcripts in the infundibular (arcua
19 ing at the NK-3 receptor homolog was [MePhe7]neurokinin B > senktide > substance P = neurokinin A > n
20 hich includes substance P, neurokinin A, and neurokinin B, have three distinct receptors: NK-1, NK-2,
22 h similar rank orders of potency of [MePhe7] neurokinin B = neurokinin B = senktide > NKA = substance
25 ses kisspeptin into the median eminence, and neurokinin B (NKB) and dynorphin onto neighboring Kiss1(
27 Patients with loss-of-function mutation in neurokinin B (NKB) and its receptor show hypogonadotropi
28 Human genetic studies have revealed that neurokinin B (NKB) and its receptor, neurokinin-3 recept
29 determine whether preprodynorphin (Dyn) and neurokinin B (NKB) are coexpressed in Kiss1 neurons in t
30 f neurons expressing the substance P (SP) or neurokinin B (NKB) genes in the human hypothalamus and b
36 derable evidence suggests that dynorphin and neurokinin B (NKB) neurons in the hypothalamic arcuate n
38 ction mutations in the genes encoding either neurokinin B (NKB) or its receptor, NK3 (NK3R), result i
40 procal plots of identical slope when [MePhe7]neurokinin B (NKB) was used as the other competition par
41 ior of Kiss1(ARH) neurons, expressing Kiss1, neurokinin B (NKB), and dynorphin (Dyn), varies througho
42 tergic 'KNDy' neurons co-express kisspeptin, neurokinin B (NKB), and dynorphin and exhibit a highly s
44 ng substance P (SP), neurokinin A (NKA), and neurokinin B (NKB), that are encoded by the tac1 (SP and
45 conservation and physiological functions of neurokinin B (NKB), we identified tachykinin (tac) and t
47 called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR3) result in pubertal failure
48 mine D2 receptor (DRD2), hot flashes and the neurokinin B receptor (TACR3), cigarette smoking and rec
53 promising advances in basic research of the neurokinin B/Tac2 pathway in both animals and humans, cl
54 in receptor (KISS1R, formerly called GPR54), neurokinin B (TAC3), and the neurokinin B receptor (TACR
56 ncluding substance P (SP), neurokinin A, and neurokinin B, which are recognized for their roles in th
57 s include substance P (SP), neurokinin A and neurokinin B, which interact with three G-protein-couple