Gene expression based on intracellular NF-kappa B activity activation effect gene in NF-kappa B overactivated cells and application

Abstract

The invention discloses a NF-kappa B specifically activated gene expression vector and application thereof. A gene expression technique is implemented by the NF-kappa B specifically activated gene expression vector. The gene expression vector contains two elements, i.e., a regulatory gene-expressed promoter sequence and a promoter downstream effect gene coding sequence, wherein the promoter sequence consist of a section of NF-kappa B response sequence and a minimal promoter sequence. After the gene expression vector is introduced into NF-kappa B overactivated cells, an effect gene on the vector is expressed under the activation of a sequence-specific transcription factor NF-kappa B, and the effect gene generates influence on cell physiology, such as cell growth inhibition, apoptosis and death. The gene expression technique provided by the invention can be used for treating diseases related to NF-kappa B overactivation, such as inflammation and cancers. The gene expression vector constructed by the invention can be used in the preparation of gene therapy reagents and drugs for treating diseases related to NF-kappa B overactivation.

Description

Technical field [0001] The invention relates to a gene expression technology and application in a NF-κB over-activated cell based on NF-κB activity activation effect gene in a cell, and belongs to the field of medical biotechnology. Background technique [0002] NF-κB is a transcription factor found in B lymphocytes, named for its involvement in the transcriptional regulation of immunoglobulin κ light chain. It was later discovered that NF-κB is a eukaryotic transcription factor widely distributed in various cells, and an important regulator of innate immunity, inflammation, cell survival, proliferation, and apoptosis. The NF-κB family has five members: RelA (p65), RelB, c-Rel, p50 / p105 (NF-κB1) and p52 / p100 (NF-κB2), all of which contain a highly conserved Rel homology region at the N-terminus (RHD), responsible for binding to DNA, dimerization, nuclear localization, and binding to NF-κB inhibitory proteins (such as IκB). RelA / p50 is the most common NF-κB target gene regulator...

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Problems solved by technology

However, unfortunately, the specificity of these chemical drugs is low, and they produce serious side effects while inhibiting the activity of NF-κB

[0007] At present, the research and development of NF-κB inhibitor drugs mainly focus on the treatment of diseases related to NF-κB overactivation by inhibiting the activity of NF-κB in cells. However, due to the diversity of NF-κB activation pathways in cells, Complexity, it is difficult to completely inhibit NF-κB activity by shutting down a pathway; in addition, cutting off a pathway may cause interference with other physiological processes responsible for the pathway, resulting in side effects

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