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2 uced dermal microvascular endothelial cells (DMVEC) as detected by indirect immunofluorescence assay
3 uman dermal microvascular endothelial cells (DMVEC) in culture results in the conversion of cobblesto
4 uman dermal microvascular endothelial cells (DMVEC) to form colonies of proliferating latently infect
5 n of dermal microvascular endothelial cells (DMVEC) transforms the cells from a cobblestone-like mono
8 n of dermal microvascular endothelial cells (DMVECs) with KSHV recapitulates many of the features of
9 uman dermal microvascular endothelial cells (DMVECs) with KSHV than supernatants from BC-3 or BCP-1 P
10 b/db dermal microvascular endothelial cells (DMVECs), as well as remedied paracrine angiogenic functi
13 was strongly induced in latently infected E-DMVEC, whereas the expression levels of the IGF-IR remai
16 tion of spindle cell colonies and plaques in DMVEC cultures provides for the first time a quantitativ
18 th increased c-Kit expression, KHSV-infected DMVEC displayed enhanced proliferation in response to th
19 the early lytic cycle both in KSHV-infected DMVEC and in the body cavity-based lymphoma BCBL1 PEL ce
20 All spindle-shaped cells in KSHV-infected DMVEC cultures express the latency-associated nuclear pr
21 showed that transformation of KSHV-infected DMVEC was inhibited by small interfering RNA directed at
22 ulins 3 and 5 was decreased in KSHV-infected DMVEC, fibulins 1C/1D were increased, and fibulins 4, 6,
24 ls and of KSHV (JSC-1) persistently infected DMVEC cells displayed cytoplasmic vGCR protein expressio
26 tisense oligomers, we observed inhibition of DMVEC proliferation and foci formation using antisense m
30 spindle cell conversion phenotype in primary DMVEC cultures that is directly associated with latent s
32 man genes in infected compared to uninfected DMVEC cultures in both the presence and absence of TPA.
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