ArticlePhysiological reports2014
Obesity-dependent dysregulation of glucose homeostasis in kinase suppressor of ras 2-/- mice.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Endothelial KSR2 regulated by genetic variation protects against atherosclerosis through AMPKα1 stabilization.Theranostics · 2026Article
- Obese-diabetic femaleJBMR plus · 2025Article
- Identification ofGenes · 2024Article
- Contrasting effects ofeLife · 2022Article
- SIRT1-NOX4 signaling axis regulates cancer cachexia.The Journal of experimental medicine · 2020Article
- Article
- KSR as a therapeutic target for Ras-dependent cancers.Expert opinion on therapeutic targets · 2017Review
- Kinase Suppressor of Ras 2 (KSR2) expression in the brain regulates energy balance and glucose homeostasis.Molecular metabolism · 2017Article
- Coordinating ERK signaling via the molecular scaffold Kinase Suppressor of Ras.F1000Research · 2017Review
- Cell non-autonomous regulation of hepatic IGF-1 and neonatal growth by Kinase Suppressor of Ras 2 (KSR2).Scientific reports · 2016Article
- Genome-wide association study identifies African-ancestry specific variants for metabolic syndrome.Molecular genetics and metabolism · 2015Article
- Ultrastructural study of spermatogenesis in KSR2 deficient mice.Transgenic research · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Disruption of KSR2 in humans and mice decreases metabolic rate and induces obesity, coincident with dysregulation of glucose homeostasis. Relative to wild-type mice, ksr2(-/-) mice are small prior to weaning with normal glucose tolerance at 6 weeks of age, but demonstrate excess adiposity by 9 weeks and glucose intolerance by 12-14 weeks. Defects in AICAR tolerance, a measure of whole-body AMPK activation, are detectable only when ksr2(-/-) mice are obese. Food restriction prevents the obesity of adult ksr2(-/-) mice and normalizes glucose and AICAR sensitivity. Obesity and glucose intolerance return when ad lib feeding is restored to the diet-restricted mice, indicating that glucose dysregulation is secondary to obesity in ksr2(-/-) mice. The phenotype of C57BL/6 ksr2(-/-) mice, including obesity and obesity-related dysregulation of glucose homeostasis, recapitulates that of humans with KSR2 mutations, demonstrating the applicability of the C57BL/6 ksr2(-/-) mouse model to the study of the pathogenesis of human disease. These data implicate KSR2 as a physiological regulator of glucose metabolism during development affecting energy sensing, insulin signaling, and lipid storage, and demonstrate the value of the C57BL/6 ksr2(-/-) mouse model as a unique and relevant model system in which to develop and test therapeutic targets for the prevention and treatment of obesity, type 2 diabetes, and obesity-related metabolic disorders.
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Registered trials
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