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1  G(s) and G(q) compete for activation by the TSH receptor.
2 ated a series of LHR mutants and chimeric LH-TSH receptors.
3 ies against the thyroid-stimulating hormone (TSH) receptor.
4  along with the thyroid-stimulating hormone (TSH) receptor and adenylyl cyclase isotypes differing wi
5 lso occur in the extracellular domain of the TSH receptor, and support a model in which the extracell
6 icularly thyroid peroxidase and thyrotropin (TSH) receptor] and of high affinity monoclonal antibodie
7 AM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-media
8 firmed the increased affinity of stimulating TSH receptor antibodies for the shed A subunit rather th
9 ermined by clinical assessment, detection of TSH-receptor antibodies and, if necessary, radionuclide
10 ccording to the currently most reliable anti-TSH receptor antibody-ELISA used to diagnose Graves dise
11 1, 2013, from a thyroid-stimulating hormone (TSH)-receptor antibody (TRAb) test register in south Wal
12 roxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD.
13  and activation to the hTSH chimera, whereas TSH receptor binding and activation were abolished.
14 ment of the seat-belt was more important for TSH receptor binding and signal transduction than the Cy
15  hCG chimera that bound to and activated the TSH receptor but not the CG/lutropin (LH) receptor.
16 ractionation chromatography, activated human TSH receptors, but not LH and FSH receptors, and showed
17 se of human FSH/thyroid-stimulating hormone (TSH) receptor chimeras suggested a novel mechanism for r
18 ch shares equal identity to the FSH, LH, and TSH receptors from mammals.
19  TSH/cAMP-induced negative regulation of the TSH receptor gene in thyrocytes, suppression of MHC clas
20                     Direct sequencing of the TSH receptor gene revealed a mutation in one allele resu
21 vating somatic mutations in the thyrotropin (TSH) receptor have been identified as a cause of hyperfu
22                      To examine thyrotropin (TSH) receptor homophilic interactions we fused the human
23 r homophilic interactions we fused the human TSH receptor (hTSHR) carboxyl terminus to green fluoresc
24 d FSH receptors, and showed high affinity to TSH receptors in a radioligand receptor assay.
25 -70, a TSH-receptor antagonist, suggesting a TSH receptor-mediated action.
26 the fetal pars tuberalis (PT) and consequent TSH receptor-mediated effects on tanycytes lining the 3(
27                                  Fluorescent TSH receptors on the plasma membrane were functional as
28             The thyroid-stimulating hormone (TSH) receptor signals via G(s) to produce cAMP and via G
29 n in the anterior pituitary known to express TSH receptors suggested a paracrine mechanism.
30  of the physiological roles of extra-thyroid TSH receptor systems and the structural-functional basis
31 viously reported that the human thyrotropin (TSH) receptor tagged with green fluorescent protein (TSH
32 54-alpha(s) was co-expressed with either the TSH receptor that activates both alpha(s) and alpha(q) o
33 ssociated with mutations in the thyrotropin (TSH) receptor, the cause of thyroid agenesis is unknown.
34 internalization in thyroid cells, endogenous TSH receptors traffic retrogradely to the trans-Golgi ne
35                             The gene for the TSH receptor (TSH-R) was expressed in intestinal T cells
36 ghput screening to identify a small-molecule TSH receptor (TSHR) agonist that was modified to produce
37 been associated with activating mutations in TSH receptor (TSHR) and G(s)alpha encoding genes.
38 eam of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TSH/TSHR-me
39                                              TSH receptor (TSHR) engagement stimulates the production
40 teoclastic bone resorption, mediated via the TSH receptor (TSHR) found on osteoblast and osteoclast p
41 stem, the expression and distribution of the TSH receptor (TSHr) has been studied by immunoprecipitat
42 ch requires TSH binding to both sites of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 pr
43 g affinity (negative cooperativity) requires TSH receptor (TSHR) homodimerization, the latter involvi
44  tested whether persistent cAMP signaling by TSH receptor (TSHR) is dependent on internalization.
45          Mutations in the genes encoding the TSH receptor (TSHR) or the Gs protein alpha subunit (GNA
46 ed cAMP production involving coupling of the TSH receptor (TSHR) to Gs at low TSH doses and to G(i/o)
47 responsive BM cells defined by expression of TSH receptor (TSHR) using flow cytometry were selectivel
48          Thyrotropin (TSH) activation of the TSH receptor (TSHR), a 7-transmembrane-spanning receptor
49                       (GPCR)The receptor for TSH receptor (TSHR), a G protein coupled receptor (GPCR)
50 the constitutively active ligand-independent TSH receptor (TSHR).
51                                 Thyrotropin (TSH) receptor (TSHR) A and B subunits are formed by intr
52 o gain insight into the thyrotropin hormone (TSH) receptor (TSHR) cleavage, we sought to convert the
53                             The thyrotropin (TSH) receptor (TSHR) is a member of the heterotrimeric G
54                             The thyrotropin (TSH) receptor (TSHR) signals via G proteins of all four
55 ent bind to the thyroid stimulating hormone (TSH) receptor (TSHR) with high affinity, inhibit labelle
56 athogenic autoantibodies to the thyrotropin (TSH) receptor (TSHR), can be treated but not cured.
57 y acting on the thyroid-stimulating hormone (TSH) receptor (TSHR), TSH negatively regulates osteoclas
58 he thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to acutely and persistent
59                                        TSHR (TSH receptors) were confirmed in cardiomyocytes, and exp