Role of LITAF in LPS-induced lethality
Date
2007
DOI
Authors
Halaweh, Anas
Version
OA Version
Citation
Abstract
Accurate discrimination between nomal and dysregulated inflammatory processes
requires a deeper understanding of the regulatory mechanisms abbeting gene
transcription of pro-inflarrmatory cytokines such as Tumor Necrosis Factor-α (TNF-α).
Our study was build upon recent results in which the novel transcription factor
Lipopolysaccharide-Induced TNF AIpha Factor (LITAF) was identified, CIoned, and
Partially characterized. Based on the main hypotheses that: 1) LITAF regulates TNF gene
expression in vivo and 2) it plays an important role in inflammatory disease, and to
further our understanding of the role of LITAF gene product, through its capacity to
regulate TNF activity, in the development of inflammatory diseases, including
Periodontitis, We have generated a LITAF knockout mouse model (LITAF-/-).
Polymerase chain reaction (PCR) for genotyping and Westem blot analysis were
Performed to confirm the deletion of LITAF in LITAF knockout mice. This model
Offered opportunities to further investigate LPS induced inflammatory disease at the in
vivolevel. [TRUNCATED]
Description
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Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2007 (Dept. of Periodontology and Oral Biology).
Includes bibliographical references: leaves 54-58.
Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2007 (Dept. of Periodontology and Oral Biology).
Includes bibliographical references: leaves 54-58.
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.