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Sam68 contributes to intestinal inflammation in experimental and human colitis

Wendy A Goodman1, Shrikanth C Basavarajappa1, Angela R Liu1

  • 1Department of Pathology, School of Medicine, Case Western Reserve University and University Hospitals Cleveland Medical Center, 2103 Cornell Road, Room 6526, Wolstein Research Building, Cleveland, OH, 44106, USA.

Cellular and Molecular Life Sciences : CMLS
|October 25, 2021
PubMed
Summary

Deleting Sam68 protein protects against experimental colitis by reducing tumor necrosis factor (TNF)-associated inflammation. Sam68 is upregulated in ulcerative colitis (UC) patients, suggesting it as a therapeutic target.

Keywords:
InflammationInflammatory bowel diseaseKHDRBS1NF-kappaBTNF

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