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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.
5              Genes affected by WNT5A include KISS-1, a metastasis suppressor, and CD44, involved in t
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
8 rous tissue results in rescued expression of KiSS-1 and reduced metastatic phenotype.
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
11                                        Thus, KiSS-1 diminishes MMP-9 expression by effecting reduced
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
15                Here we show that the loss of KiSS-1 expression in highly metastatic breast cancer cel
16 human chromosome 6q16.3-q23 is essential for KiSS-1 expression in normal tissues.
17             Furthermore, we demonstrate that KiSS-1 expression is regulated by Sp1 elements within th
18                                              KiSS-1 expression ratios provided prognostic information
19                          Patients with lower KiSS-1 expression showed a direct correlation with overa
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
22 RIP-130-modulated transcriptional control of KiSS-1 expression.
23 xpression of this collagenase was reduced by KiSS-1 expression.
24                            The expression of KiSS-1 gene and peptide and the distribution of metastin
25                                              KiSS-1 gene and peptide expression was higher in the hyp
26                           The product of the KiSS-1 gene is absent or expressed at low level in metas
27 e undertook a study to determine whether the KiSS-1 gene, previously shown to suppress cancer spread
28                                              KiSS-1 has been shown to function as a tumor metastasis
29      Loss of the metastasis suppressor gene, KiSS-1 has been strongly correlated to the progression o
30           The identification and sequence of KiSS-1 (HGMW-approved symbol, KISS1), a human malignant
31                 We observed complete loss of KiSS-1 in all invasive tumors under study as compared to
32 y activate the transcriptional regulation of KiSS-1 in breast cancer cells.
33  and we describe the expression of GPR54 and KiSS-1 in the hypothalamus during the peripubertal perio
34                  The mechanism through which KiSS-1 is lost during metastasis, however, is still not
35 e gene product of metastasis suppressor gene KiSS-1, is the endogenous ligand for the G-protein-coupl
36 noma cells, similar to the overexpression of KiSS-1 metastasis suppressor gene in those cells.
37                                              KiSS-1 mRNA levels detected by real-time PCR increased w
38 es positive for MMP-9 mRNA were deficient in KiSS-1 mRNA.
39                            The expression of KiSS-1 or KiSS1, like other tumor suppressor, is commonl
40               A polypeptide derived from the KiSS-1 product, designated kisspeptin-10 (Kp-10), activa
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
44                                 Although the KiSS-1 promoter contains multiple AP-2alpha binding elem
45 y metastatic breast cell lines did not alter KiSS-1 promoter-driven luciferase gene activity.
46 ption does not require direct binding to the KiSS-1 promoter.
47      Based on the predicted structure of the KiSS-1 protein, our results imply a mechanism whereby Ki
48                                Expression of KiSS-1 reduced metastatic potential by 95% compared to c
49 otein, our results imply a mechanism whereby KiSS-1 regulates events downstream of cell-matrix adhesi
50                      Metastin, also known as KiSS-1, the cognate ligand for the metastin receptor GPR
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
53 p1-binding sites of the promoter to activate KiSS-1 transcription.
54                    The expression pattern of KiSS-1 transcripts was analyzed using in situ hybridizat
55      Parental, vector-only transfectants and KiSS-1 transfectant clones were injected into the mammar
56 racellular matrix components was unaffected, KiSS-1 transfectants spread on immobilized type-IV colla
57 d IkappaBalpha levels in the cytosols of the KiSS-1 transfectants.
58                            The expression of KiSS-1 was found to be significantly associated with his
59                          Lower expression of KiSS-1 was revealed in cells derived from the most advan
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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