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Transcription factors and inflammatory gene regulation: strategic approaches

Transcription factors and inflammatory gene regulation: strategic approaches
Transcription factors and inflammatory gene regulation: strategic approaches
In chronic inflammatory diseases, the expression of multiple genes, including those for cytokines, chemokines, adhesion molecules, receptors, and inflammatory enzymes, is often upregulated. The problem for many academic or industrial scientists is to elucidate the mechanisms behind this upregulation to further the understanding of inflammation or to explore possible means of therapeutic intervention. Common research problems faced by investigators would be to analyze the regulation of a novel gene in response to various inflammatory stimuli or alternatively to investigate the mechanisms of induction of an established gene in response to novel stimuli. Whereas the induction of many inflammatory genes is thought to occur, at least partly, at the level of increased transcription, it is important to address the possible role of posttranscriptional, translational, or even posttranslational control. For example, release or synthesis of the protein of interest from suitably stimulated cells could be examined in the presence or absence of transcriptional inhibitors, such as actinomycin D, or translational inhibitors, such as cycloheximide. Thus, a dependence on de novo transcription and/or translation may be demonstrated. Therefore, whether the protein of interest is simply released from preformed cellular stores or is synthesized from preformed mRNA can be elucidated. Northern blot analysis, reverse transcription polymerase chain reaction (RT-PCR), or ribonuclease protection assays can be used to examine steady-state mRNA levels, which if elevated gives rise to a presumption of transcriptional control
978-0-89603-923-0
295-313
Springer
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee
Newton, Robert
4a2c2a99-b7ad-4373-8840-96fbb5b5313e
Staples, Karl J.
e0e9d80f-0aed-435f-bd75-0c8818491fee

(2001) Transcription factors and inflammatory gene regulation: strategic approaches. In, Human Airway Inflammation. (Methods in Molecular Medicine, , (doi:10.1385/1-59259-151-5:295), 56) New York, US. Springer, pp. 295-313. (doi:10.1385/1-59259-151-5:295).

Record type: Book Section

Abstract

In chronic inflammatory diseases, the expression of multiple genes, including those for cytokines, chemokines, adhesion molecules, receptors, and inflammatory enzymes, is often upregulated. The problem for many academic or industrial scientists is to elucidate the mechanisms behind this upregulation to further the understanding of inflammation or to explore possible means of therapeutic intervention. Common research problems faced by investigators would be to analyze the regulation of a novel gene in response to various inflammatory stimuli or alternatively to investigate the mechanisms of induction of an established gene in response to novel stimuli. Whereas the induction of many inflammatory genes is thought to occur, at least partly, at the level of increased transcription, it is important to address the possible role of posttranscriptional, translational, or even posttranslational control. For example, release or synthesis of the protein of interest from suitably stimulated cells could be examined in the presence or absence of transcriptional inhibitors, such as actinomycin D, or translational inhibitors, such as cycloheximide. Thus, a dependence on de novo transcription and/or translation may be demonstrated. Therefore, whether the protein of interest is simply released from preformed cellular stores or is synthesized from preformed mRNA can be elucidated. Northern blot analysis, reverse transcription polymerase chain reaction (RT-PCR), or ribonuclease protection assays can be used to examine steady-state mRNA levels, which if elevated gives rise to a presumption of transcriptional control

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Published date: 2001
Organisations: Faculty of Medicine

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Local EPrints ID: 374529
URI: http://eprints.soton.ac.uk/id/eprint/374529
ISBN: 978-0-89603-923-0
PURE UUID: 99f4a45a-7902-4332-b901-68f243c0bb7f
ORCID for Karl J. Staples: ORCID iD orcid.org/0000-0003-3844-6457

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Date deposited: 19 Feb 2015 09:39
Last modified: 06 Jun 2018 12:39

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Author: Robert Newton
Author: Karl J. Staples ORCID iD

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