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The gene editing tool has become a foothold in vivo application for assimilation of molecular pathways. CRISPR is unique to the development of solving neurological diseases for several reasons. For example, CRISPR allows researchers to quickly generate animal and human cell models, allowing them to study how genes function in a nervous system.
CD163 (Cluster of Differentiation 163) is a protein that in humans is encoded by the CD163 gene. [5] CD163 is the high affinity scavenger receptor for the hemoglobin-haptoglobin complex [6] and in the absence of haptoglobin - with lower affinity - for hemoglobin alone. [7] It also is a marker of cells from the monocyte/macrophage lineage. [8]
THP-1 cells are used as a models to study the monocyte-macrophage differentiation process, [6] antigen presentation [7] [8] and as a model to examine some macrophage-related physiological processes, for example the macrophage cholesterol efflux. [9]
Genome editing, or genome engineering, or gene editing, is a type of genetic engineering in which DNA is inserted, deleted, modified or replaced in the genome of a living organism. Unlike early genetic engineering techniques that randomly insert genetic material into a host genome, genome editing targets the insertions to site-specific locations.
CRISPR gene editing is a revolutionary technology that allows for precise, targeted modifications to the DNA of living organisms. Developed from a natural defense mechanism found in bacteria, CRISPR-Cas9 is the most commonly used system.
While these two markers are sufficient to differentiate between neutrophils and monocytes, eosinophils have a similar CD15 expression to neutrophils. Therefore, CD16 is used as a further marker to identify neutrophils: mature neutrophils are CD16high, while eosinophils and monocytes are both CD16low.
The gene then needs to be mapped by comparing the inheritance of the phenotype with known genetic markers. Genes that are close together are likely to be inherited together. [12] Another option is reverse genetics. This approach involves targeting a specific gene with a mutation and then observing what phenotype develops. [12]
CCL2 is primarily secreted by monocytes, macrophages and dendritic cells. Platelet derived growth factor is a major inducer of CCL2 gene. CCR2 and CCR4 are two cell surface receptors that bind CCL2. [14] CCL2 exhibits a chemotactic activity for monocytes and basophils. However, it does not attract neutrophils or eosinophils.
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