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1           We conclude that in RN46A neuronal cells, hypoxia activates an autocrine-paracrine antiapop
2 e domain 2 (PHD2) plays an important role in cell hypoxia adaptation by regulating the stability of H
3                                         beta-cell hypoxia and apoptosis were evaluated by immunohisto
4 ing of the blood vasculature, causing cancer cell hypoxia and death in distant avascular regions.
5 vessel density together with increased tumor cell hypoxia and death.
6                           In NDRG3-deficient cells, hypoxia- and lactate-induced inhibition of ER-to-
7 sulted in a dose-dependent reduction of beta-cell hypoxia, but beta-cell apoptosis was only reduced b
8                                        In CB cells, hypoxia caused inhibition of TASK-like channels,
9                 In primary human endothelial cells, hypoxia, desferrioxamine, or infection with Ad2/H
10                            In pVHL-deficient cells, hypoxia did not decrease the Na-K-ATPase activity
11 s (DiOC7 staining), and an increase in tumor cell hypoxia (EF5 staining).
12                             In the remaining cells, hypoxia either did not elicit any change or produ
13                    Here, we show that in HCC cells, hypoxia elevates expression of Cav1, which then a
14 re that in the human breast carcinoma BT-549 cells hypoxia enhanced expression of the transcription f
15 hat induces secretion of HMGB1 by epithelial cells, hypoxia establishes a microenvironment that favor
16              In MIA PaCa-2 pancreatic cancer cells, hypoxia increased p65-NFkappaB DNA binding and NF
17       In this paper, we show that, in cancer cells, hypoxia increased the levels and activity of the
18                                    In Muller cells, hypoxia increased the phosphorylation of cPLA(2)
19             In current-clamped CA1 pyramidal cells hypoxia induced a rapid, near-complete depolarizat
20                            In Hep3B or HepG2 cells hypoxia induces neither expression of PCBP nor for
21 an primary retinal microvascular endothelial cells, hypoxia induces the expression of ADORA2A by acti
22 , we show that metabolic stress induces beta-cell hypoxia inducible factor 2alpha (HIF-2alpha), which
23                        Loss of smooth muscle cell hypoxia inducible factor-1alpha underlies increased
24 ficiently to stabilize intestinal epithelial cell hypoxia-inducible factor (HIF).
25      Also, in normal fibroblasts and retinal cells, hypoxia inhibited the mTOR pathway and suppressed
26              In mouse lung and mammary tumor cells, hypoxia led to increases in cell adhesion, clotti
27                       In intervertebral disc cells, hypoxia promotes expression of Notch signaling pr
28 ted this mechanism in a cultured endothelial cell hypoxia-reoxygenation model, in a rat model of hemo
29 yocardial I/R injury and H9c2 cardiomyoblast cells hypoxia/reoxygenation (H/R) was used to assess whe
30 In cultured human umbilical vein endothelial cells, hypoxia/reoxygenation stimulated apoptosis.
31                                     In human cells, hypoxia restores steady-state levels of Fe-S clus
32       Here, we show that in nucleus pulposus cells, hypoxia robustly induces PHD3 expression and, to
33                               In most normal cells, hypoxia stabilizes hypoxia-inducible transcriptio
34                              In colon cancer cells, hypoxia stimulated multiple K-ras effector pathwa
35 of treatment were needed before severe tumor cell hypoxia was detected in K1735 tumors.
36 m therapeutic angiogenesis inhibition, tumor cell hypoxia was evaluated as a marker of ischemia using
37     In primary glioma-derived CD133 negative cells, hypoxia was able to induce neurospheres and hESC
38 ng the molecular mechanisms induced by tumor cell hypoxia with a special emphasis on therapeutic resi