{'fraction_non_alphanumeric': 0.027406417112299464, 'fraction_numerical': 0.01537433155080214, 'mean_word_length': 5.537117903930131, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Transcription factor MafB is a mediator of retinoic acid‐induced monocytic cell differentiation

All‐trans‐retinoic acid (RA), the major active metabolite of vitamin A, regulates monocytic cell cycle and differentiation. We asked whether MafB, a factor involved in development and hematopoiesis, is a mediator of RA‐induced differentiation in THP‐1 human monocytic cells. MafB mRNA and protein levels were up‐regulated by RA dose‐ and time‐dependently. RA and TNFα synergistically regulated MafB expression, mainly at the transcriptional level. MafB protein was highly phosphorylated. Blocking the ERK and p38 pathways reduced phospho‐MafB protein without changing mRNA levels. Next, MafB target genes were screened. SPOCK1, CCL2 and Blimp1 were identified as potential targets, due to the presence of Maf recognition elements in their putative promoter regions. These genes are related to cell communication and differentiation. By RT‐PCR analysis, the regulation of SPOCK1, Blimp1 and CCL2 mRNA levels were highly correlated with MafB mRNA. Decreased expression of SPOCK1, Blimp1 and CCL2 was observed when MafB phosphorylation was blocked. Chromatin immunoprecipitation assays showed increased MafB protein binding to the elements on the promoter regions of SPOCK1, Blimp1 and CCL2 in cells treated with RA and TNFα. We conclude that RA and TNFα‐induced MafB may play a role in monocytic cell differentiation through transcriptional regulation of SPOCK1, CCL2 and Blimp1. Support: NIH DK41479.