Could somone explain exactly what this means below? NOT HW just trying to get a better understanding on what this experiment is about.  To produce mice that are deficient for RAC1 in macrophages, female C57BL/6 mice homozygously expressing the floxed Rac1 gene (Rac1fl/fl) [6] were crossbred with male mice homozygously expressing Cre under the monocyte-specific lysozyme M promoter (LC) [12]. Mice were genotyped for Rac1 deficiency as previously described

Biochemistry
6th Edition
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Reginald H. Garrett, Charles M. Grisham
Chapter32: The Reception And Transmission Of Extracellular Information
Section: Chapter Questions
Problem 21P
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Link: Lack of RAC1 in macrophages protects against atherosclerosis - PMC (nih.gov)

Could somone explain exactly what this means below? NOT HW just trying to get a better understanding on what this experiment is about. 

To produce mice that are deficient for RAC1 in macrophages, female C57BL/6 mice homozygously expressing the floxed Rac1 gene (Rac1fl/fl) [6] were crossbred with male mice homozygously expressing Cre under the monocyte-specific lysozyme M promoter (LC) [12]. Mice were genotyped for Rac1 deficiency as previously described 

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Link: Lack of RAC1 in macrophages protects against atherosclerosis - PMC (nih.gov)

Could you explain the relationship between plaque, macrophages, RAC1, SM22 and smooth muslce cells? Would like to understand this topic below a bit better and the effects these things have on each other.

After discovering that advanced plaques had a greater macrophage RAC1 expression than intermediate plaques, immunofluorescence was used to stain human intermediate (type III) and advanced (type VI) atherosclerotic plaques. The anti-Mac-2 (Cedarlane) antibody was used to identify macrophages, while the RAC1 (Sigma-Aldrich) and SM22 (Abcam) antibodies were used to identify smooth muscle cells.  

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