Our data indicate that p38α and JNK2 are dispensable in NO induced cell death, but Jnk1 null cells are markedly protected from NO-induced cell death.
Indeed, Jnk1−/− MEFs were markedly protected against NO-induced cell death compared with Jnk2−/− MEFs and wild type MEFs (Figure 6D).
Importantly, Fischer 344 rats that survived pulmonary infection with subsp. novicida were markedly protected against subsequent pulmonary challenge with subsp. tularensis, suggesting that subsp. novicida may be a useful platform for the development of vaccines against subsp. tularensis.
Previous studies have revealed that mice deficient in CHOP or in the PRR's SRA, CD36, TLR4, or TLR2, are markedly protected from macrophage apoptosis by this two-hit pathway [9], [24], [27], [46].
We show that after a single dose of CCl4, animals pretreated with the broad-spectrum MMP- and TACE-inhibitor Marimastat, as well as animals deficient in both TNF-α receptors (p55 and p75) were markedly protected, as demonstrated by attenuated necroinflammatory injury on histology and 5-fold lower serum ALT levels, compared to their wild type controls.
MMP-8 deficient mice are markedly protected against TNF-α induced lethal hepatitis [ 22].
Chickens in all immunized groups were markedly protected against FT (p < 0.05) (Table 1).
YAP siRNA-treated cells irradiated similarly were markedly protected from UV-induced cell death, showing only 18% apoptosis.
Therefore, caspase-7-deficient mice were resistant to LPS-induced lymphocyte apoptosis and were markedly protected from LPS-induced lethality independently of the excessive production of serum cytokines.
In a mouse lethal septic shock model, Xu and coworkers [ 54] observed that animals deficient in ICAM-1 were markedly protected against death.
