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1 KCdelta disrupts association of Src with the ErbB2 receptor.
2 d interfered with trastuzumab binding to the ERBB2 receptor.
3 because of constitutive dimerization of the ErbB2 receptor.
4 lities including heterodimerization with the ErbB2 receptor.
5 ess a synthetic ligand-inducible form of the ErbB2 receptor.
6 or proliferative signaling downstream of the ErbB2 receptor.
7 f expression of oestrogen, progesterone, and ERBB2 receptors.
9 at express a dominant-negative mutant of the ErbB2 receptor among oligodendrocytes, using an MBP prom
11 cFv induces downstream signaling through the ErbB2 receptor and H7 prevents transferrin binding to th
12 elated with decreased phosphorylation of the ErbB2 receptor and reduced activation of Src and MAPK/ER
13 ssion of activated (phosphorylated) EGFR and ERBB2 receptors and downstream signal intermediates were
17 ut not CCh, stimulated the formation of EGFR/ErbB2 receptor dimers and the recruitment of p85 to ErbB
18 uitment of the p85 subunit of PI3-K to ErbB3/ErbB2 receptor dimers, while the PI3-K inhibitor, wortma
20 se expected changes in neuregulin levels and ErbB2 receptor expression after PNS injury were disrupte
22 BB3 receptors are apparently segregated from ERBB2 receptors in their resting state, and both ligand-
23 dose of compound reduced phosphorylation of ErbB2 receptors in tumor-bearing mice, demonstrating tar
27 Downregulation of the overexpressed 185-kDa ErbB2 receptor is rapidly (2-6 hours) induced by the HSP
29 , the contrasting effects of PS341 and GA on ErbB2 receptor localization, polyubiquitination, and deg
30 e expression of the NH2 terminally truncated ErbB2 receptor (p95ErbB2) in breast cancer correlates wi
35 Protein levels of the full-length 185 kD ErbB2 receptor significantly decreased following NE trea
36 he two pathways in DCIS occurs regardless of ErbB2 receptor status and inhibition of Notch and ErbB1/
39 new method to assign oestrogen receptor and ERBB2-receptor status to breast carcinoma based on mRNA
41 pothesized to interact with and activate the ErbB2 receptors, suggesting an intramembrane-growth fact
43 rect bacterial ligation to and activation of ErbB2 receptor tyrosine kinase (RTK) signaling without E
45 nd metastasis, physically interacts with the ErbB2 receptor tyrosine kinase and augments receptor tyr
46 noma cell lines and associates with both the ErbB2 receptor tyrosine kinase and the LAR receptor tyro
53 uregulin-1beta (NRG-1beta), a ligand for the erbB2 receptor tyrosine kinase, we hypothesized that act
57 have shown that forced overexpression of the ErbB2-receptor tyrosine kinase (RTK) promotes androgen-i
59 gand-dependent activation of glial erbB4 and erbB2 receptors, without affecting erbB1 (EGF) receptor
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