ABSTRACT
Blinatumomab, as a novel bispecific antibody targeting CD19 and CD3, can induce T lymphocytes to precisely target CD19 positive B lymphocytes to apoptosis. At present, it is the only bispecific antibody approved for the treatment of hematological malignancies in China. Blinatumomab is effective in the treatment of newly diagnosed, relapsed/refractory, minimal residual disease positive patients with B-cell acute lymphoblastic leukemia (B-ALL) . It can improve the survival of the patients and is well tolerated. The further study of blinatumomab can provide theoretical basis and new ideas for induction therapy, salvage therapy and subsequent hematopoietic stem cell transplantation in patients with B-ALL.
ABSTRACT
Objective To investigate the effect of sterol regulating element binding protein (SREBP1c) and its ac-tive form (SREBP1cm) on human protein kinase R-like endoplasmic reticulum kinase (PERK).Methods Re-porter victors of PERK promoter and its truncations were constructed with pGL 3-basic and co-transfected with internal reference pRL-SV40 into cell and luciferase activity was detected .pcDNA3.1 ( -)-SREBP1c or pcDNA3.1 ( -)-SREBP1cm was co-transfected with PERK promoter transcriptional activity core regions and the detection of dual -lu-ciferase reporter gene was used to analyze the regulation of SREBP 1c/1cm on PERK promoter transcriptional activity . The expression level of PERK mRNA and protein were detected by RT-PCR and Western blot .Results PERK pro-moter and truncations were successfully constructed into pGL 3-basic, and PERK promoter core area of transcription-al activity had determined;Dual-luciferase report gene showed that SREBP 1c inhibited PERK promoter transcrip-tional activity and SREBP1cm promoted PERK promoter transcriptional activity .RT-PCR and Western blot showed that SREBP1c decreased PERK mRNA and protein expression , but SREBP1cm increased PERK mRNA and protein expression, which was consistent with the detection of dual-luciferase report gene .Conclusions SREBP1c and SREBP1cm have a opposite regulation effect on PERK promoter transcriptional activity and its expression .