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. 1999 Aug;19(8):5548–5556. doi: 10.1128/mcb.19.8.5548

FIG. 2.

FIG. 2

FIG. 2

FIG. 2

FIG. 2

FIG. 2

FIG. 2

Functional knockout of CIF150 (hTAFII150) protein leads to cell cycle arrest in G2 or M and to reduced gene expression of cyclin B1. (A) Analyses of the cell cycle of HeLa cells 36 h after transfection with the CIF150 specific antisense oligomer B or oligomer Bx (reverse sequence). The different concentrations of the oligomers are indicated. (B) Cell cycle analyses of IMR90 cells after 36 h of oligomer treatment. (C) Total RNA, derived from HeLa cells treated with oligomer B or Bx, analyzed by quantitative RT-PCR (lanes 1 to 6, 100, 200, and 300 nM concentrations of oligomer B and Bx) and Northern blot analysis (lanes 7 to 10) with CIF150- and β-actin-specific primers or 32P-labeled cDNA probes. (D) HeLa cell extracts from different time points, after antisense oligomer (400 nM) treatment, analyzed by immunoblotting for the decrease of CIF150 protein. Control (C) nuclear extract (lane 1) and molecular size markers (M) (lane 2) were loaded. (E) Cyclin B1 protein expression decreases after CIF150 antisense treatment (100, 200, and 300 nM) of HeLa cells. (F) Differential PCR display identifies genes that are transcriptionally dependent on CIF150. A representative nondenaturing gel of differential display products is shown. Total RNA was prepared 24 h (lane 1 and 2) or 36 h (lane 3 and 4) after oligomer transfection. Arrows indicate cDNAs which are specifically upregulated or downregulated after antisense treatment.