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Of note, supraphysiological expression of transgenic factor VII or factor IX in mouse models has led to thromboembolic premature death in some previous reports.
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Genomic PCR analysis revealed integration of 4 transgenic factors in iPS cells (supporting information Figure S2).
Furthermore, data from RT-PCR analysis showed that transgenic 4 factors were completely silenced and endogenous pluripotency markers Oct4, Sox2, Rex1 as well as Nanog were successfully activated (Figure 3C).
In the rheumatoid factor transgenic mouse model, Marshak-Rothstein and colleagues have shown that TLR9 signaling via DNA from dying cells is a critical factor for activation of self-reactive B cells [29].
hTNFtg, human tumour necrosis factor transgenic; JNK, c-Jun N-terminal kinase.
Next, he discussed inducible human tumor necrosis factor transgenic (hTNFtg) mice.
Generation of heterozygous human tumor necrosis factor transgenic (hTNFtg) mice (strain Tg197) were described previously [ 14].
To investigate pathogenetic involvement of autoAb, tumour necrosis factor transgenic (TNFtg) mice were used as an animal model of RA.
Analyses were performed in human tumor necrosis factor transgenic (hTNFtg) mice, which suffer from chronic destructive arthritis, and wild-type mice.
For in vivo studies, FAP-deficient mice were crossed into the human tumor necrosis factor transgenic mice (hTNFtg), which develop a chronic inflammatory arthritis.
To elucidate the role of CD44 in arthritis, human tumour necrosis factor transgenic (hTNFtg) mice were crossed with CD44 knockout mice.
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