p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment-Reference-Cited by-同舟云学术

p52 Overexpression Increases Epithelial Apoptosis, Enhances Lung Injury, and Reduces Survival after Lipopolysaccharide Treatment

Published:2016-01-15 Issue:4 Volume:196 Page:1891-1899
ISSN:0022-1767
Container-title:The Journal of Immunology
language:en
Short-container-title:J.I.

Author:

Saxon Jamie A.,Cheng Dong-Sheng,Han Wei,Polosukhin Vasiliy V.,McLoed Allyson G.,Richmond Bradley W.^ORCID,Gleaves Linda A.,Tanjore Harikrishna,Sherrill Taylor P.,Barham Whitney,Yull Fiona E.^ORCID,Blackwell Timothy S.

Publisher

The American Association of Immunologists

Subject

Immunology,Immunology and Allergy

Reference32 articles.

1. Nuclear Factor (NF)-κB2 (p100/p52) Is Required for Normal Splenic Microarchitecture and B Cell–mediated Immune Responses

2. Mice Deficient in Nuclear Factor (NF)-κB/p52 Present with Defects in Humoral Responses, Germinal Center Reactions, and Splenic Microarchitecture

3. Multiorgan inflammation and hematopoietic abnormalities in mice with a targeted disruption of RelB, a member of the NF-κB/Rel family

4. The Lymphotoxin-β Receptor Induces Different Patterns of Gene Expression via Two NF-κB Pathways

5. Essential Role of RelB in Germinal Center and Marginal Zone Formation and Proper Expression of Homing Chemokines

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