id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
work_ab5yqvyjbbaqpjryzbekdb7t7m	Wei Mo	CXCR4/CXCL12 Mediate Autocrine Cell- Cycle Progression in NF1-Associated Malignant Peripheral Nerve Sheath Tumors	2013.0	14	.pdf	application/pdf	8678	823	61	CXCR4, a G-protein-coupled receptor, as highly expressed in mouse models of NF1-deficient MPNSTs, of CXCR4 activity either by shRNA or pharmacological inhibition decreases MPNST cell growth in culture find enriched in Nf1-deficient cells and particularly in Nf1-deficient MPNSTs. Expression of CXCR4 and its ligand, CXCL12, mouse and human MPNST cells, tumor allografts, and spontaneous GEMMs. Moreover, analysis of human primary and cultured MPNST cells, as well as human tissue microarray analysis, reveals conserved pathway activation. sequences (so that it is not targeted by the shRNA) re-established CXCR4 protein levels and overcame the cell growth inhibition (Figures 2A and S2B). 104 or 105 MPNST-Tripz-CXCR4 cells were injected subcutaneously into nude mice, and one group received D1 protein level decrease in CXCR4-depleted MPNST cells and MPNST cells with exogenous CXCR4 expression (Figures 3E CXCR4-depleted MPNST cells (Figure 4A). mRNA and protein levels in CXCR4-WT-MPNST cells (Figures CXCL12 protein to cultured CXCR4-depleted MPNST cells.	./cache/work_ab5yqvyjbbaqpjryzbekdb7t7m.pdf	./txt/work_ab5yqvyjbbaqpjryzbekdb7t7m.txt