ArticleEndocrinology2010
Critical role of the Src homology 2 (SH2) domain of neuronal SH2B1 in the regulation of body weight and glucose homeostasis in mice.
Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 43 citations in OpenAlex.
- Monoallelic SH2B1 Variants in Neurodevelopmental Disorders: Phenotypic Expansion and Functional Characterization of Rare Variants.Molecular genetics & genomic medicine · 2026Article
- Central leptin pathways in metabolic homeostasis.Clinical science (London, England : 1979) · 2025Review
- The Mechanism of the Gut-Brain Axis in Regulating Food Intake.Nutrients · 2023Review
- Review
- STAT3 phosphorylation in central leptin resistance.Nutrition & metabolism · 2021Review
- Leptin: A Potential Link Between Obstructive Sleep Apnea and Obesity.Frontiers in physiology · 2021Article
- Roles of Gangliosides in Hypothalamic Control of Energy Balance: New Insights.International journal of molecular sciences · 2020Review
- Mediation Analysis Supports a Causal Relationship between Maternal Hyperglycemia and Placental DNA Methylation Variations at the Leptin Gene Locus and Cord Blood Leptin Levels.International journal of molecular sciences · 2020Article
- The kinetics of folding of the NSH2 domain from p85.Scientific reports · 2019Article
- Insights into Body Size Evolution: A Comparative Transcriptome Study on Three Species of Asian Sisoridae Catfish.International journal of molecular sciences · 2019Article
- The Effect of SH2B1 Variants on Expression of Leptin- and Insulin-Induced Pathways in Murine Hypothalamus.Obesity facts · 2018Article
- The Leptin Receptor Complex: Heavier Than Expected?Frontiers in endocrinology · 2017Review
- 20 years of leptin: connecting leptin signaling to biological function.The Journal of endocrinology · 2014Review
- SH2B1 regulation of energy balance, body weight, and glucose metabolism.World journal of diabetes · 2014Review
- Review
- Leptin signaling and leptin resistance.Frontiers of medicine · 2013Review
- Implication of a rare deletion at distal 16p11.2 in schizophrenia.JAMA psychiatry · 2013Article
- New function of the adaptor protein SH2B1 in brain-derived neurotrophic factor-induced neurite outgrowth.PloS one · 2013Article
- Article
- Mutation screen in the GWAS derived obesity gene SH2B1 including functional analyses of detected variants.BMC medical genomics · 2012Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
SH2B1 is an SH2 domain-containing adaptor protein that plays a key role in the regulation of energy and glucose metabolism in both rodents and humans. Genetic deletion of SH2B1 in mice results in obesity and type 2 diabetes. Single-nucleotide polymorphisms in the SH2B1 loci and chromosomal deletions of the SH2B1 loci associate with obesity and insulin resistance in humans. In cultured cells, SH2B1 promotes leptin and insulin signaling by binding via its SH2 domain to phosphorylated tyrosines in Janus kinase 2 and the insulin receptor, respectively. Here we generated three lines of mice to analyze the role of the SH2 domain of SH2B1 in the central nervous system. Transgenic mice expressing wild-type, SH2 domain-defective (R555E), or SH2 domain-alone (DeltaN503) forms of SH2B1 specifically in neurons were crossed with SH2B1 knockout mice to generate KO/SH2B1, KO/R555E, or KO/DeltaN503 compound mutant mice. R555E had a replacement of Arg(555) with Glu within the SH2 domain. DeltaN503 contained an intact SH2 domain but lacked amino acids 1-503. Neuron-specific expression of recombinant SH2B1, but not R555E or DeltaN503, corrected hyperphagia, obesity, glucose intolerance, and insulin resistance in SH2B1 null mice. Neuron-specific expression of R555E in wild-type mice promoted obesity and insulin resistance. These results indicate that in addition to the SH2 domain, N-terminal regions of neuronal SH2B1 are also required for the maintenance of normal body weight and glucose metabolism. Additionally, mutations in the SH2 domain of SH2B1 may increase the susceptibility to obesity and type 2 diabetes in a dominant-negative manner.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.