The lipopolysaccharide (LPS)-induced increase in serum amyloid A (SAA) expression is independent of the NF-κB pathway.

The addition of LPS significantly increases the expression level of SAA1/3 (A), an effect that is not inhibited by the NF-κB inhibitor, BAY11-7082 (B). The SAA expression level was normalized to that of ß-actin (ACTB) and is presented...

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Bibliographic Details
Main Author:	Masaki Wakai (12261915) (author)
Other Authors:	Ryohei Hayashi (3663382) (author), Yoshitaka Ueno (3663376) (author), Kana Onishi (8901368) (author), Takeshi Takasago (12261918) (author), Takuro Uchida (756174) (author), Hidehiko Takigawa (12261921) (author), Ryo Yuge (6383417) (author), Yuji Urabe (134994) (author), Shiro Oka (4329796) (author), Yasuhiko Kitadai (3343847) (author), Shinji Tanaka (172295) (author)
Published:	2022
Subjects:	Biochemistry Medicine Cell Biology Molecular Biology Immunology Developmental Biology Cancer Biological Sciences not elsewhere classified Chemical Sciences not elsewhere classified nf -&# 954 another inflammatory biomarker uc remains unclear uc mouse models promote saa1 expression induces saa expression saa1 expression robust biomarker family expression ulcerative colitis study demonstrates significantly expressed serum amyloid results suggested reactive protein promoting mechanism previously described pathway may nuclear factor intestinal tract colorectal inflammation clinical remission asa ). aminosalicylic acid
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The lipopolysaccharide (LPS)-induced increase in serum amyloid A (SAA) expression is independent of the NF-κB pathway.

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