Skip to main content
. 2019 Oct 3;4(19):e128713. doi: 10.1172/jci.insight.128713

Figure 4. HBZ regulates the expression of the osteoclastogenic factor RANKL through c-Fos.

Figure 4

(A) Gene expression data obtained from Gene Expression Omnibus at the NCBI (GSE33615). RNA from PBMCs of 26 patients with acute ATL vs. 21 normal uninfected HTLV-1–negative, healthy donors, normalized to actin shown as log fold over average TNFSF11 (RANKL) gene expression in normal subjects. (B) Quantitative PCR (qPCR) detection of RANKL transcription in Jurkat cells compared with HBZ-expressing Jurkat cells. (C) qPCR detection of RANKL transcription in Kit-225 cells expressing WT HBZ and 2 HBZ mutants; HBZ (SM1) encodes WT HBZ protein but carries silent mutations that disrupt HBZ RNA sequence and secondary structure; HBZ (ΔHBZ) expressed WT HBZ RNA but does not express HBZ protein. (D) qPCR detection of FOS transcription in Jurkat cells compared with HBZ-expressing Jurkat cells. (E) qPCR detection of FOS transcription in Kit-225 cells expressing WT HBZ and 2 HBZ mutants: SM1 and ΔHBZ. (F) qPCR detection of RANKL (G) and HBZ transcription in HBZ-expressing Jurkat cells (Jurkat-HBZ) in the presence and absence of FOS. Data is representative of 2–3 biological replicates. Error bars in this figure represent ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 (2-tailed distribution, homoscedastic student’s t test for 2 groups or 1-way ANOVA for multiple comparison).