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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.
8 onoclonal antibody (Herceptin) that inhibits ErbB2 receptors.
9 anization, i.e. collagen crosslinking and/or ErbB2 receptor activation.
10 ly classified based on the expression of the ERBB2 receptor (also known as HER2) and hormone receptor
11 at express a dominant-negative mutant of the ErbB2 receptor among oligodendrocytes, using an MBP prom
12                                              ErbB2 receptor and AKT were robustly phosphorylated in m
13 cFv induces downstream signaling through the ErbB2 receptor and H7 prevents transferrin binding to th
14 elated with decreased phosphorylation of the ErbB2 receptor and reduced activation of Src and MAPK/ER
15 ssion of activated (phosphorylated) EGFR and ERBB2 receptors and downstream signal intermediates were
16               We first showed that levels of erbB2 receptor are significantly decreased in an animal
17          CP-724,714 is a potent inhibitor of erbB2 receptor autophosphorylation in intact cells and i
18 he expression of estrogen, progesterone, and ERBB2 receptors) breast cancer cells.
19 ut not CCh, stimulated the formation of EGFR/ErbB2 receptor dimers and the recruitment of p85 to ErbB
20 uitment of the p85 subunit of PI3-K to ErbB3/ErbB2 receptor dimers, while the PI3-K inhibitor, wortma
21 r matrix, whereas cells devoid of functional ErbB2 receptors do not.
22 se expected changes in neuregulin levels and ErbB2 receptor expression after PNS injury were disrupte
23 clinical features including variable ER, PR, ERBB2 receptor expression and two distinct pathogenic BR
24                   The subsequent increase in erbB2 receptor expression makes the glia more responsive
25 BB3 receptors are apparently segregated from ERBB2 receptors in their resting state, and both ligand-
26  dose of compound reduced phosphorylation of ErbB2 receptors in tumor-bearing mice, demonstrating tar
27         We hypothesized that blockade of the erbB2 receptor induces cardiomyocyte death through a mit
28                                          The ErbB2 receptor is a clinically validated cancer target w
29                                          The Erbb2 receptor is activated by UV irradiation, the prima
30  Downregulation of the overexpressed 185-kDa ErbB2 receptor is rapidly (2-6 hours) induced by the HSP
31     Herceptin, an inhibitory antibody to the erbB2 receptor, is a potent chemotherapeutic but causes
32 , the contrasting effects of PS341 and GA on ErbB2 receptor localization, polyubiquitination, and deg
33 e expression of the NH2 terminally truncated ErbB2 receptor (p95ErbB2) in breast cancer correlates wi
34                                  Herein, the ErbB2 receptor pathway is inhibited with the selective m
35 onditioned media and neuregulin-1 stimulated erbB2 receptor phosphorylation in type II cells.
36          In the absence of GGF signaling via erbB2 receptors, radial glial development is abnormal.
37                            Activation of the ErbB2 receptor signaling pathways can enhance various me
38     Protein levels of the full-length 185 kD ErbB2 receptor significantly decreased following NE trea
39 he two pathways in DCIS occurs regardless of ErbB2 receptor status and inhibition of Notch and ErbB1/
40 ibitors should be investigated regardless of ErbB2 receptor status.
41 PT/lapatinib or DAPT/gefitinib regardless of ErbB2 receptor status.
42 nd human epidermal growth factor receptor 2 (ERBB2) receptor status, and at least 1 documented line o
43  new method to assign oestrogen receptor and ERBB2-receptor status to breast carcinoma based on mRNA
44 dhesion kinase, which occurs downstream from erbB2 receptor stimulation.
45 pothesized to interact with and activate the ErbB2 receptors, suggesting an intramembrane-growth fact
46                                          The ErbB2 receptor tyrosine kinase (RTK) is expressed in bas
47 rect bacterial ligation to and activation of ErbB2 receptor tyrosine kinase (RTK) signaling without E
48                    In a mouse model of basal ErbB2 receptor tyrosine kinase 2 (ErbB2)-positive breast
49 nd metastasis, physically interacts with the ErbB2 receptor tyrosine kinase and augments receptor tyr
50 noma cell lines and associates with both the ErbB2 receptor tyrosine kinase and the LAR receptor tyro
51                        Overexpression of the ERBB2 receptor tyrosine kinase and the mitochondrial inn
52                             Deregulated Her2/ErbB2 receptor tyrosine kinase drives tumorigenesis and
53 (p.Asp769Tyr) in the catalytic domain of the ERBB2 receptor tyrosine kinase in a patient with schwann
54                                          The ErbB2 receptor tyrosine kinase is overexpressed in appro
55                                          The ErbB2 receptor tyrosine kinase plays a critical role in
56                                              ErbB2 receptor tyrosine kinase plays a role in neureguli
57                         We hypothesized that ErbB2 receptor tyrosine kinase, a regulator of cancer ce
58 uregulin-1beta (NRG-1beta), a ligand for the erbB2 receptor tyrosine kinase, we hypothesized that act
59 , brain lipid binding protein (BLBP) and the erbB2 receptor tyrosine kinase.
60 at the cell cortex, acting downstream of the ErbB2 receptor tyrosine kinase.
61  epidermal growth factor receptor (EGFR) and ErbB2 receptor tyrosine kinases (RTKs).
62 have shown that forced overexpression of the ErbB2-receptor tyrosine kinase (RTK) promotes androgen-i
63 decreased activation of the cardioprotective ERBB2 receptor, which can be modified by neuregulin.
64                            Inhibition of the ErbB2 receptor with Herceptin unexpectedly enhances nerv
65 gand-dependent activation of glial erbB4 and erbB2 receptors, without affecting erbB1 (EGF) receptor