STAT5-Luc Reporter Cell Line-Ba/F3

CALR exon 9 frameshift mutations, found in essential thrombocythemia (ET) and primary myelofibrosis patients, trigger STAT protein activation in the presence of Myeloproliferative Leukemia Virus (MPL), leading to ET development in vivo. Researchers utilized the STAT5-Luc Reporter Cell Line to investigate the impact of Calreticulin (CALR) exon 9 frameshift mutations on signal transducer and activator of transcription (STAT) protein activation. CALR mutations, common in essential thrombocythemia (ET) and primary myelofibrosis, induce ET in vivo by activating STAT proteins in the presence of Myeloproliferative Leukemia Virus (MPL). By generating mice with a Calr frameshift mutation using CRISPR/Cas9, researchers demonstrated that loss of the KDEL motif and positively charged amino acids in the mutated C-terminus led to mild disease manifestations. In vitro experiments revealed weakened binding between the murine CALR mutant and MPL, resulting in reduced STAT5 activation and milder disease severity. This highlights the role of STAT5 activation in ET development.

Figure 1. STAT5 transcriptional activity was measured using a luciferase assay by researchers. 293T cells were transiently transfected with STAT5-LUC and the CALR WT, CALR del52 mutant, Calr WT, or Calr del19 mutant in the presence of the human thrombopoietin receptor (MPL) or murine Mpl. Weak activation of MPL-STAT5 signaling by the murine CALR del19 mutant was observed compared to WT CALR. (Shide K, et al., 2019)

By utilizing Creative Biogene's STAT5-Luc Reporter Cell Line-Ba/F3, researchers can efficiently investigate the impact of CALR exon 9 mutations on the STAT5 signaling pathway. This cell line harbors a luciferase reporter gene, enabling real-time monitoring of STAT5 activation. Researchers can simulate CALR mutations in this cell line and observe their effects on the STAT5 signaling pathway. This approach accelerates experimental processes, reduces the need for experimental animals, and enhances the accuracy and reliability of data, facilitating a deeper understanding of the relationship between CALR mutations and disease development.