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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 along with the thyroid-stimulating hormone (TSH) receptor and adenylyl cyclase isotypes differing wi
4 lso occur in the extracellular domain of the TSH receptor, and support a model in which the extracell
5 icularly thyroid peroxidase and thyrotropin (TSH) receptor] and of high affinity monoclonal antibodie
6 AM, and porin could be abolished by K1-70, a TSH-receptor antagonist, suggesting a TSH receptor-media
7 firmed the increased affinity of stimulating TSH receptor antibodies for the shed A subunit rather th
8 ccording to the currently most reliable anti-TSH receptor antibody-ELISA used to diagnose Graves dise
10 ment of the seat-belt was more important for TSH receptor binding and signal transduction than the Cy
12 ractionation chromatography, activated human TSH receptors, but not LH and FSH receptors, and showed
13 se of human FSH/thyroid-stimulating hormone (TSH) receptor chimeras suggested a novel mechanism for r
15 TSH/cAMP-induced negative regulation of the TSH receptor gene in thyrocytes, suppression of MHC clas
17 vating somatic mutations in the thyrotropin (TSH) receptor have been identified as a cause of hyperfu
19 r homophilic interactions we fused the human TSH receptor (hTSHR) carboxyl terminus to green fluoresc
25 of the physiological roles of extra-thyroid TSH receptor systems and the structural-functional basis
26 viously reported that the human thyrotropin (TSH) receptor tagged with green fluorescent protein (TSH
27 54-alpha(s) was co-expressed with either the TSH receptor that activates both alpha(s) and alpha(q) o
28 ssociated with mutations in the thyrotropin (TSH) receptor, the cause of thyroid agenesis is unknown.
29 internalization in thyroid cells, endogenous TSH receptors traffic retrogradely to the trans-Golgi ne
31 ghput screening to identify a small-molecule TSH receptor (TSHR) agonist that was modified to produce
32 eam of thyroid-stimulating hormone (TSH) and TSH receptor (TSHR) and is indispensable for TSH/TSHR-me
34 teoclastic bone resorption, mediated via the TSH receptor (TSHR) found on osteoblast and osteoclast p
35 stem, the expression and distribution of the TSH receptor (TSHr) has been studied by immunoprecipitat
36 ch requires TSH binding to both sites of the TSH receptor (TSHR) homodimer, and TSH-stimulated IP1 pr
37 g affinity (negative cooperativity) requires TSH receptor (TSHR) homodimerization, the latter involvi
40 responsive BM cells defined by expression of TSH receptor (TSHR) using flow cytometry were selectivel
44 o gain insight into the thyrotropin hormone (TSH) receptor (TSHR) cleavage, we sought to convert the
46 ent bind to the thyroid stimulating hormone (TSH) receptor (TSHR) with high affinity, inhibit labelle
48 y acting on the thyroid-stimulating hormone (TSH) receptor (TSHR), TSH negatively regulates osteoclas
49 he thyrotropin [thyroid-stimulating hormone (TSH)] receptor (TSHR) is known to acutely and persistent
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