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HT Experiment :

Experiment Id  GSE236979 Name  Effect of Nogo deficiency on the insulin signaling pathway
Experiment Type  RNA-Seq Study Type  WT vs. Mutant
Source  GEO Curation Date  2024-10-18
description  The elevation of Nogo-B expression in T2DM mice and Nogo-B knockdown alleviated diabetic symptoms in db/db mice prompted us to further investigate the involvement of Nogo-B in the insulin signaling pathway and T2DM. The three isoforms of Nogo are derived from various RNA splicing events, so deleting Nogo-B exons 2-4 results in the deficiency of other Nogo members, resulting in Nogo knockout (Nogo-/-) mice. As the liver is the key organ in the systemic response to insulin and controls glucose and lipid metabolism, we conducted RNA-seq of livers isolated from 8-week-old Nogo-/- mice and WT littermates. We conducted RNA-seq of livers isolated from normal chow fed 8-week-old Nogo-/- mice (NC) and WT littermates (CC). Each group is set up in three parallels.
  • variables:
  • genotype,
  • bulk RNA-seq

1 Publications

Trail: HTExperiment

6 Samples

Trail: HTExperiment