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We validated Nampt's involvement in arthritis using a CIA mouse model7,8 in wild-type and Nampt heterozygous knockdown DBA/1J mice, and we investigated further the pathways underlying Nampt's mechanism in arthritis through loss-of-function and gain-of-function studies experiments in mouse bone marrow-derived macrophages (BMM) and RNA sequencing (RNA-seq) of CIA mouse tissue.
Further, the pathways affected are diverse and tissue specific.
We explored further the pathways and cell types involved in this exacerbation of noncardiogenic pulmonary edema and lung inflammation.
To study further the pathways involved in the action of thrombin-induced HO-1 expression, transient transfection was performed by using the human HO-1 promoter-luciferase construct.
Therefore, isolation of additional mammary epithelial cell culture systems that respond to TGF-β with a conspicuous EMT is required in order to elucidate further the pathways that underlie this process.
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Further, the pathway via psychological distress was explored.
To investigate further the pathway of SAPK activation during ischaemia, we assayed the kinases thought to lie upstream of p38 and JNK.
To further elucidate the pathways mediating drug-induced differentiation we also investigated DNA methylation.
Therefore, to further elucidate the pathways through which NET4/Tmem53 affects the cell cycle, its knockdown was attempted.
To further characterize the pathways affected in the mutant mice and to determine how the physiological response was changed, we used Gene Ontology analysis and pathway mapping.
To further characterize the pathways in C. difficile, we also analyzed the variation in these pathways by overlaying LPI index for each gene.
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CEO of Professional Science Editing for Scientists @ prosciediting.com