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3 ocytes reduced alpha-smooth muscle actin expression in LX-2 cells treated with cholangiocyte-conditioned media.
5 These results were confirmed in photoreceptor-derived 661W cells treated with either H(2)O(2) or all-trans-retinal stres
6 ly profiled repair and metabolism in wild-type and Aag(-/-) cells treated with the alkylating agent methyl methanesulfona
7 All of these pathological events were rescued in acinar cells treated with a Piezo1 antagonist and in acinar cells fr
8 RISPR-Cas9 knockout screens in acute myeloid leukemia (AML) cells treated with various chemotherapies to map the drug-dep
9 s-triggered NF-kappaB, p38, and ERK pathways activation and cells treated with these pathway-specific inhibitors reduced
10 sed Nef-mediated down-regulation of MHC-I, but not CD4, and cells treated with CMA showed reduced formation of the Nef:MH
11 nvolved in actin core organization in podosomes, as well as cells treated with the inhibitors of the Arp2/3 complex, fail
14 IP followed by sequencing (ChIP-seq) in MCF-7 breast cancer cells treated with the proteasome inhibitor MG132, and we fur
15 Meanwhile, the rate of de novo lipid synthesis in cancer cells treated with 17beta-estradiol was increased by 42%.
16 from the plasma membrane to endosomes in pancreatic cancer cells treated with the AXL ligand growth arrest-specific 6 (G
25 eatment, these responder patients, as well as hematopoietic cells treated with FeCl(3) and Deferasirox, showed a specific
26 inase (MAPK) and endothelial NO synthase (eNOS) in EA.hy926 cells treated with conditioned medium from Corin-siRNA- or AN
27 IC), a single enzyme in de novo purine biosynthesis, and in cells treated with a small molecule inhibitor of ATIC homodim
28 s PTPRF-mediated activation of Wnt signaling was blocked in cells treated with clathrin endocytosis inhibitor.
29 arized division, peptidoglycan organization is different in cells treated with PBP2 and PBP3-specific inhibitors.
30 sing siRNA prevents degradation of c-Jun, ETV4, and ETV5 in cells treated with either LT or the MEK1/2 inhibitor, U0126.
32 We observed similar regulation of Rapgef3 expression in cells treated with a highly specific inhibitor of LRRK2 prote
33 f a direct role for pol IV in double strand break repair in cells treated with double strand break-inducing antibiotics.
34 gle agent cisplatin-treated cells, the opposite was true in cells treated with cisplatin/JH-RE-06.
37 recapitulated by simulating lipotoxicity in skeletal muscle cells treated with saturated FA, palmitate.
39 The phenotype and molecular characteristics of cells treated with LSD1 inhibitors were highly similar to cel
40 in in the nucleus, we estimated heterochromatin contents of cells treated with different drugs by quantifying the fluores
41 We analyzed matched time course RNAseq profiling of cells treated with single drugs and their combinations and fo
43 Uninfected and HIV-infected macrophages and T cells treated with trehalose exhibited increased markers of a
46 d caspase 3/7 activity in MDA-MB-231 cells in comparison to cells treated with DTX-loaded un-crosslinked MLNP (used as a
47 f cells treated with LSD1 inhibitors were highly similar to cells treated with UM171, an agent promoting expansion of HSC
49 tic protein MCL-1 as a driver of adaptive survival in tumor cells treated with oncogene targeted therapies, providing a r
50 n 2 (PBP2) are unable to initiate polarized division, while cells treated with inhibitors that prevent peptidoglycan cros