Role of LITAF in LPS-induced lethality
MetadataShow full item record
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]
PLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact email@example.com.Thesis (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2007 (Dept. of Periodontology and Oral Biology).Includes bibliographical references: leaves 54-58.
RightsThis 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 firstname.lastname@example.org.