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. 2020 Apr 27;48(10):5710–5719. doi: 10.1093/nar/gkaa295

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© The Author(s) 2020. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 3. — HnRNP C promotes transcription of CELF2. (A) Quantification of CELF2 mRNA following inhibition of transcription by actinomycin D in wildtype Jurkat cells (WT) versus those expressing shRNA against hnRNP C (sh-hnRNP C) is shown. CELF2 levels were measured by RT-PCR and normalized to actin. (B) CELF2 mRNA expression, as measured by RT-PCR and normalized to actin, following PMA treatment of wildtype Jurkat cells (WT) versus those expressing shRNA against hnRNP C (sh-hnRNP C). Treatment of Jurkat cells with an inhibitor to NF-κB (NFκBi) was previously shown to block the transcriptional induction induced by PMA (9). For both panels A and B, values are from at least 3 biologically independent experiments. Error bars represent standard deviation. (C) A representative gel used for quantification in panel B.