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1 m of Ab-mediated destruction of transplanted liver parenchymal cells.
2 ides whose concentration is regulated by the liver parenchymal cells.
3 aterial between the sinusoidal lumen and the liver parenchymal cells.
4 l for PPARalpha-regulated gene expression in liver parenchymal cells.
5 n to occur via a regulatory protein found in liver parenchymal cells.
6                                              Liver parenchymal cell allografts initiate both CD4-depe
7 nant hexokinase in pancreatic beta-cells and liver parenchymal cells and functions as a critical comp
8 ndogenous HGD promoter was localised to only liver parenchymal cells and kidney proximal tubules in a
9 present not only in immune cells but also in liver parenchymal cells and the complexity of the cell p
10                  These findings suggest that liver parenchymal cells are the dominant source of Type
11                       FGFR type 4 (FGFR4) in liver parenchymal cells binds only FGF-1, whereas FGFR1
12 ates in the regulation of innate immunity in liver parenchymal cells both in vitro and in vivo and to
13 nd that p62/SQSTM1, a protein upregulated in liver parenchymal cells but downregulated in HCC-associa
14 e hypothesis that acute damage of allogeneic liver parenchymal cells by the CD4-dependent pathway is
15          cKK-E12 was highly selective toward liver parenchymal cell in vivo, with orders of magnitude
16  miR-194, which is specifically expressed in liver parenchymal cells, in preventing liver cancer cell
17 t S. aureus and E. coli and its promotion of liver parenchymal cell infiltration, vascularization, an
18                         We studied mice with liver parenchymal cell (LPC)-specific disruption of the
19                         Mice lacking NEMO in liver parenchymal cells (LPC) spontaneously develop stea
20 ned conditional ablation of Jnk1 and Jnk2 in liver parenchymal cells (LPCs) (JNK1/2(LPC-KO) mice; KO,
21       While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous
22 etic inhibition of catalytic IKK activity in liver parenchymal cells (LPCs; IKKalpha/beta(LPC-KO) ) w
23  cells that form a barrier between blood and liver parenchymal cells, NS2(H126R) activates RNase L, w
24 , we report that targeted deletion of PBP in liver parenchymal cells (PBP(Liv-/-)) results in the abr
25 te that MyD88 in immune cells rather than in liver parenchymal cells plays an important role in infla
26          To do so, we created mice harboring liver parenchymal cell-specific deletion of HOIP (Hoip(D
27 lls located in the subendothelial space, and liver parenchymal cells, take on the roles of antigen-pr
28                           HOIP deficiency in liver parenchymal cells triggered tumorigenesis at 18 mo
29 re, we show that targeted deletion of PBP in liver parenchymal cells, using the Cre-loxP system, resu
30 aloglycoprotein-receptor (ASGP-R) located on liver parenchymal cells was originally identified and ch
31 ole of linear ubiquitination specifically in liver parenchymal cells, we investigated the physiologic
32  acid (0.5% w/w) for 2 wk, killed, and their liver parenchymal cells were isolated.
33 g water for 1 mo, were sacrificed, and their liver parenchymal cells were isolated.