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1 ation of the apical and basal surfaces of an acinus.
2 terizing the 3D morphometry of the pulmonary acinus.
3 er cells and apoptosis of inner cells of the acinus.
4 nsport of inhaled particles in the pulmonary acinus.
5 tional shaping of a solitary lumen within an acinus.
6 acinus and through the luminal space of the acinus.
7 on of Akt provokes the apoptotic cleavage of acinus.
8 capillaries (air blood barriers) within each acinus.
9 nd periductal cells expanding into the liver acinus.
12 ted screen, Cdk5 genetically interacted with Acinus (Acn), a primarily nuclear protein, which promote
13 lator is the Drosophila melanogaster protein Acinus (Acn), which is necessary for autophagy induction
14 ore EJC plus the accessory factors RnpS1 and Acinus aid in definition and efficient splicing of neigh
15 ers, showing an aberrant distribution in the acinus, an increase not explained by a reduction in hepa
16 we show that SRPK2 binds and phosphorylates acinus, an SR protein essential for RNA splicing, and re
18 hanism may adjust bile salt uptake along the acinus and protect periportal hepatocytes from harmful b
20 n of alpha6-integrin to the periphery of the acinus and thus facilitates the polarization of outer ac
21 sts that L(pro) contains a SAP (for SAF-A/B, Acinus, and PIAS) domain, a protein structure associated
23 ant R248W, R175H, and R273H disrupted normal acinus architectures with filled lumen and led to format
25 yclin A1 expression through escalating CtBP2/acinus complex formation, and gambogic amide might be us
32 tiation of mammary epithelial cell (MEC) for acinus formation by using the in vitro 3D culture system
33 igenicity in breast cancer cells and impeded acinus formation in immortalized normal mammary epitheli
35 pe p53 in MCF-10A cells was not required for acinus formation, but knockdown of endogenous wild-type
36 ed that KLF8 expression disrupted the normal acinus formation, which could be prevented by the MMP in
41 ensation during apoptosis by phosphorylating acinus in the nucleus, revealing a specific mechanism by
43 ture and morphometry of the intact pulmonary acinus is an essential step toward a more complete under
44 a 3D context form polarized, growth-arrested acinus-like colonies whereas the latter form disorganize
45 l mammospheres, which display a well-defined acinus-like structure with polarized expression of E-cad
47 xamination of day 7 vector controls revealed acinus-like structures characteristic of normal mammary
48 epithelial cells from benign prostate formed acinus-like structures that exhibited differentiated pro
49 which mammary epithelial cells form hollow, acinus-like structures, we previously demonstrated that
51 nsferase expression across the human hepatic acinus may be important in the manifestation of certain
54 We demonstrate that Akt phosphorylation of acinus on serine 422 and 573 results in its resistance t
57 ing OP or EP under conditions known to alter acinus organization, i.e. collagen crosslinking and/or E
63 ibose) polymerase protein and degradation of acinus protein with a significant increase in the expres
65 65, Luc7-like protein 3 (Luc7L3), SRSF11 and Acinus S', but not with the bona fide RS-domain of SRSF1
68 romatin immunoprecipitation assays show that Acinus-S' associates with RAREs within the promoters of
71 ndently of ligand, and the C-terminal end of Acinus-S' is sufficient for the repression of RAR-regula
74 c, enhances cyclin A1 transcription, whereas acinus S422A, an unphosphorylatable mutant, blocks the s
77 , promotes the interaction between CtBP2 and acinus through triggering acinus phosphorylation by Akt.
80 ine particles can easily reach the pulmonary acinus, where gas is exchanged, but they need to mix wit
81 nd occurred in periportal regions of hepatic acinus, whereas perivenous areas were weakly stained or
82 anscription corepressor CtBP2 directly binds acinus, which is regulated by nerve growth factor (NGF),
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