Page 13 - M. Immunology

Regulation Of JAK/STAT Signaling With Cell-Permeable SOCS3
Suppresses Acute Inflammatory Disorders

Shinyoung Park, Sukyeong Jeong, Jaehyeon Kim, Chohyun Kim, Mikyung Kim, Youngsil Choi And Daewoong Jo
Metabolic Disease Team, Cellivery R&D Institute, Cellivery Therapeutics, Inc., Seoul 03929, Korea.

BACKGROUND AIM
Suppressor of cytokine signaling 3 (SOCS3) functions as a negative-feedback regulator An advanced macromolecule transduction domain
of JAK/STAT signaling to suppresses JAK kinase activity and promote degradation of (aMTD) and a solubilization domain were utilized to
the activated cytokine receptor complex. Since transcription factors including STAT3 develop improved cell-permeable (iCP-) SOCS3 as
have play a major role in transmitting inflammatory cytokine signals to the nucleus, protein based biotherapeutic anti-inflammation agent
SOCS3 is a key physiological regulator of cytokine-mediated STAT3 signaling. for IBD and hepatitis was examined. .
METHODS
We developed a cell-permeable SOCS3 protein with enhanced solubility, namely improved cell-permeable (iCP)-SOCS3, utilizing a sequence-
optimized advanced macromolecule transduction domain (aMTD) to deliver proteins into mammalian cells and tissues.

RESULTS

CONCLUSION REFERENCES Contact information

These results suggest iCP-SOCS3 targets Chung et al. (2020) Science Advances, 6: eaba 1193 Minyong Jung
in the pathogenesis of IBD and hepatitis Lim et al. (2013) Clinical Cancer Research, 19: 680-690 New Drug & Business Development
so that it may provide therapeutic effect on Lim et al. (2013) Biometerials, 34: 6261-6271 Cellivery Therapeutics, Inc.
acute inflammatory disorder by negatively
regulating JAK/STAT signaling. Lim et al. (2012) Molecular Therapy, 20: 1540-1549 jungmy@cellivery.com
Jo et al. (2005) Nature Medicine, 11: 892-898 +82-2-3151-8900