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1 plete inhibition of Mphi-mediated tumor cell cytostasis.
2 t growth, and resistance to TGF-beta-induced cytostasis.
3 -induced inhibition of protein synthesis and cytostasis.
4 mor cells to heat-stable enterotoxin-induced cytostasis.
5 and is directly involved in the induction of cytostasis.
6  cyclic nucleotide accumulation required for cytostasis.
7  IGF-I-induced Akt phosphorylation to induce cytostasis.
8  Ser-490 are implicated in the regulation of cytostasis.
9 ing a role for gamma-PAK in the induction of cytostasis.
10  overexpression in those cells and increased cytostasis.
11 8 h of chemotherapy, before the induction of cytostasis.
12 hile the majority of cells undergo a form of cytostasis.
13 rnative mechanisms for antiestrogen-mediated cytostasis.
14 ration by NO donors was not due to metabolic cytostasis.
15 ffective therapy, which induced Rb-dependent cytostasis.
16              PD 153035 caused dose-dependent cytostasis (200 nmol/L to 1 micromol/L) and apoptosis (>
17 3 phenotype was expressed and in Thy4 during cytostasis, a mp53 phenotype was manifested, as determin
18 d play an important role in cytotoxicity and cytostasis against many pathogenic microorganisms.
19           What determines the choice between cytostasis and apoptosis is not clear.
20 that SphK2 may influence the balance between cytostasis and apoptosis of human cancer cells.
21 of protein kinase activity but do not induce cytostasis and are not bound to the ER.
22 DETA-NONOate played an important role in the cytostasis and arrest of these tumor cells in the G(1) p
23 to rapamycin by decreasing rapamycin-induced cytostasis and autophagy.
24  tyrosine kinase inhibitor PD 153035 induces cytostasis and caspase-dependent apoptosis in EGFR ligan
25  impaired (1 micromol/L, 4-24 h), leading to cytostasis and cell cycle arrest within 24 h by decrease
26 n tomography ([18F]FLT-PET) to measure early cytostasis and cytotoxicity induced by cisplatin treatme
27 in parallel with phenotypic data on cellular cytostasis and cytotoxicity.
28 enotypes controlled by these states, such as cytostasis and death.
29                              This NO-induced cytostasis and decrease in cyclin D1 was reversible for
30 nduce proliferation while high levels induce cytostasis and inhibition of protein synthesis.
31 itivity to phorbol myristate acetate-induced cytostasis and megakaryocytic differentiation, suggestin
32  therapy using miRNAs as agents that mediate cytostasis and promote muscle differentiation.
33 metry-based assay that is not biased against cytostasis and reduced cell number.
34 at CDK4/6 inhibition is a potent mediator of cytostasis and that RB loss can be readily compensated f
35 of action, including induction of apoptosis, cytostasis, and antiangiogenesis.
36 d EMT and invasion, restore TGFbeta-mediated cytostasis, and inhibit three-dimensional organoid growt
37 itor of HSP90, acting via several processes (cytostasis, apoptosis, invasion, and angiogenesis) to in
38                        CCT018159 caused cell cytostasis associated with a G(1) arrest and induced apo
39 l line is simply an index of cytotoxicity or cytostasis, but the patterns of 60 such GI50 values enco
40                             A-357300 induces cytostasis by cell cycle arrest at the G(1) phase select
41                 A model for the induction of cytostasis by gamma-PAK through targeting of gamma-PAK t
42 stable enterotoxins induce colon cancer cell cytostasis by targeting guanylyl cyclase C (GCC) signali
43                    Antiestrogens induce both cytostasis (cell cycle arrest) and apoptosis, but the re
44 ions seen in confluent replicon cells, i.e., cytostasis combined with a sharp decrease in replicon co
45                     Neither cytotoxicity nor cytostasis correlated with expression of p21Waf1/Cip1 Th
46 work confers resistance to TGF-beta-mediated cytostasis during the development of the telencephalic n
47 cells, moreover, bypassed TGF-beta1-mediated cytostasis evident in control short hairpin RNA-expressi
48          Our results suggest that NO-induced cytostasis in breast cancer cells was due to PKR activat
49 WAF1 (p21) is important for TGFbeta-mediated cytostasis in epithelial cells but not in hematopoietic
50 lonogenic survival and induced apoptosis and cytostasis in formed tumor colonies.
51  is not mediated by apoptosis but results in cytostasis in four cell lines tested.
52 d variable apoptosis (>10 micromol/L) but no cytostasis in ligand-independent cell lines.
53 -NONOate, a nitric oxide (NO) donor, induced cytostasis in the human breast cancer cells MDA-MB-231,
54 P1 also inhibits gene expression and induces cytostasis in transfected cells when it is expressed at
55 adapt quickly to CDK4/6 inhibition and evade cytostasis, in part, via noncanonical cyclin D1-CDK2-med
56 laxis and bradyphylaxis restores cancer cell cytostasis induced by heat-stable enterotoxins.
57 iated apoptotic block undergo a drug-induced cytostasis involving the accumulation of p53, p16(INK4a)
58 iated by natural killer cells in vitro or to cytostasis mediated by macrophages than control transduc
59                           TGF-beta-dependent cytostasis occurred in normal and cancer cells through p
60 because many new agents are thought to cause cytostasis rather than cytotoxicity.
61 ury and converted the reversible, NO-induced cytostasis response of cells to an apoptotic response.
62 agents, early clinical data demonstrate only cytostasis when used as monotherapy.

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