c-FLIP Maintains Tissue Homeostasis by Preventing Apoptosis and Programmed Necrosis

Xuehua Piao, Sachiko Komazawa-Sakon, Takashi Nishina, Masato Koike, Jiang-Hu Piao, Hanno Ehlken, Hidetake Kurihara, Mutsuko Hara, Nico Van Rooijen, Günther Schütz, Masaki Ohmuraya, Yasuo Uchiyama, Hideo Yagita, Ko Okumura, You-Wen He, Hiroyasu Nakano*

*To whom correspondence should be addressed. E-mail: hnakano{at}juntendo.ac.jp

This PDF file includes:

• Fig. S1. Histological analysis of the small intestine and colon.
• Fig. S2. c-Flip^F/F;Villin-Cre;Tnfr1^+/– mice do not develop colitis.
• Fig. S3. ConA-induced hepatitis is exacerbated in c-Flip^F/F;Alb-Cre mice.
• Fig. S4. Degradation of RIPK1 protein correlates with selective induction of apoptosis in the liver.
• Fig. S5. c-FLIP in hepatocytes, but not hematopoietic cells, plays a crucial role in the protection of hepatocytes from cell death.
• Fig. S6. Administration of clodronate liposomes and anti-ASGM1 antibody depletes Kupffer cells and NK cells, respectively.
• Fig. S7. Clodronate liposomes inhibit poly I:C–induced depletion of c-FLIP protein in the livers of c-Flip^F/F;Mx1-Cre mice through suppression of Ifnb1 expression.
• Table S1. Elimination of Tnfr1 partially rescues the perinatal lethality of c-Flip^F/F;Villin-Cre mice.
• Table S2. Genotyping of c-Flip^F/F;Alfp-Cre mice that were generated by crossing c-Flip^F/+;Alfp-Cre mice with c-Flip^F/F mice.
• Table S3. Elimination of Tnfr1 does not rescue the perinatal lethality of c-Flip^F/F;Alfp-Cre mice.

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© 2012 American Association for the Advancement of Science