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1 ssor role in bladder cancer was revealed for KiSS-1.
2 lating MMP-9 synthesis are not the target of KiSS-1.
3 ucture, and refined chromosomal location for KiSS-1.
4 Invasion and motility were unaffected by KiSS-1.
6 ibed role in melanoma, our results show that KiSS-1 also functions as a metastasis suppressor gene in
7 ybridization histochemistry indicated robust KiSS-1 and GPR54 mRNA expression in the region of the ar
9 Sp1 are strong transcriptional regulators of KiSS-1 and that loss or decreased expression of AP-2alph
10 by AP-1, Sp1, and Ets transcription factors, KiSS-1 did not alter the binding of these factors to the
12 did not observe any significant differential KiSS-1 expression along cell cycle by sorting analysis.
13 for the loss of tumor metastasis suppressor KiSS-1 expression and thus increased cancer metastasis.
14 ll lines, HT-1080, stably transfected with a KiSS-1 expression construct, demonstrated substantially
20 ression of Sp1 and DRIP-130 not only rescues KiSS-1 expression, but also induces an inhibition of the
21 creased MMP-9 amounts was not antagonized by KiSS-1 expression, suggesting that MAPK pathways modulat
27 e undertook a study to determine whether the KiSS-1 gene, previously shown to suppress cancer spread
33 and we describe the expression of GPR54 and KiSS-1 in the hypothalamus during the peripubertal perio
35 e gene product of metastasis suppressor gene KiSS-1, is the endogenous ligand for the G-protein-coupl
41 an chromosome 6q16.3-q23, results in reduced KiSS-1 promoter activation in highly malignant melanoma
42 domain, AP-2B, together with Sp1, increased KiSS-1 promoter activity dramatically, suggesting that A
43 ements within the first 100-bp region of the KiSS-1 promoter and that targeted deletion of a single G
49 otein, our results imply a mechanism whereby KiSS-1 regulates events downstream of cell-matrix adhesi
51 suggest that DRIP-130 is a key regulator in KiSS-1 transactivation in normal tissue, and that the lo
52 lly, suggesting that AP-2alpha regulation of KiSS-1 transcription does not require direct binding to
56 racellular matrix components was unaffected, KiSS-1 transfectants spread on immobilized type-IV colla
60 ancer cell lines, lower transcript levels of KiSS-1 were observed in the invasive bladder carcinomas
61 d human melanoma metastasis suppressor gene, KiSS-1, which maps to chromosome 1q32-q41, could suppres
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