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This study explores the role of SHIP1 deficiency in the development of eosinophilic pneumonia and Crohn’s-like ileitis in mice models. Conducted by researchers from SUNY Upstate Medical University and UCSF, the findings reveal significant stability of SHIP1 deficiency across individual samples, with no correlation to patient treatment histories or clinical outcomes. These insights contribute to the understanding of mucosal inflammation in inflammatory bowel disease (IBD). For further details, please check the poster presentation.
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SHIP1 deficiency in IBD Sandra Fernandes1, James C. Ryan2, William G. Kerr1 1SUNY-Upstate Medical University, Syracuse, NY 2UCSF/SFVA, San Francisco, CA Friday, December 13, 2013
DISCLOSURES • Nothing to disclose
SHIP1 and PI3K/Akt pathway Fernandes& al., 2013
SHIP-/- mice Germline SHIP1-deficiency cause fatal eosinophilic pneumonia and Crohn’s-like ileitis in mice For more on SHIP1 and mucosal inflammation in mouse model, please visit poster P-188 Kerr & al., GUT, 2011
Western Blotting SHIP1 : P1C1 + goat anti-mouse HRP, Actin : C-19 + donkey anti-goat HRP, Santa Cruz Biotechnologies
Protein degradation or translation inhibition? Modified from Grabbe & al. 2011 Ameres & Zamore, 2013
Take home message • SHIP1-deficiency is found in 10/47 samples (>20% of samples) • Both CD and UC • SHIP1-deficiency is stable over months • No correlation to treatments at time of sampling or to other clinical parameters • No reduction in SHIP1 mRNA levels • Translational or post-translational
Acknowledgments • William Kerr • James Ryan and his team at UCSF/SFVA • NeetuSrivastava • Raki Sudan • Bonnie Toms • Robert Brooks • Matt Gumbleton • Sonia Iyer • SudhaNeelam • Christie Youngs • Katie Miller • Scott Stegemann • Summer students • CCFA (Senior Research Award to WGK) • NIH • Paige Arnold Butterfly Run • Carol M. Baldwin Foundation