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Updated: Aug 24, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
Published on: September 1, 2019
SLC22A4 and RUNX1: identification of RA susceptible genes
Ryo Yamada1, Shinya Tokuhiro, Xiotian Chang
1Laboratory for Rheumatic Diseases, SNP Research Center, Institute of Physical and Chemical Research, 1-7-22 Suehiro-cho, Tsurumi-ku, 230-0045, Yokohama, Kanagawa, Japan. ryamada@src.riken.go.jp
Abstract:
Recently we reported that SLC22A4 and RUNX1 are associated with rheumatoid arthritis (RA). SLC22A4 is an organic cation transporter with unknown physiological function, and RUNX1 is a hematological transcriptional regulator that has been shown to be responsible for acute myelogenic leukemia. It is suggested that the association of RUNX1 with RA is due to its regulation of expression of SLC22A4. Because the physiological function of SLC22A4 is still unclear, further investigation is needed into how SLC22A4 affects RA susceptibility. Although the association of RUNX1 with RA was identified as a regulatory factor of SLC22A4, it is possible that RUNX1 is a key molecule in autoimmunity, as it has been reported to be associated with systemic lupus erythematosus and psoriasis, two other autoimmune diseases.
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