ArticleThe Journal of biological chemistry2015
SH2B1 and IRSp53 proteins promote the formation of dendrites and dendritic branches.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Insulin and IGF signaling in the brain: multilevel regulation of synaptic and network homeostasis.Frontiers in endocrinology · 2026Review
- Timely expression of PGAM5 and its cleavage control mitochondrial homeostasis during neurite re-growth after traumatic brain injury.Cell & bioscience · 2023Article
- Role of the Beta and Gamma Isoforms of the Adapter Protein SH2B1 in Regulating Energy Balance.Endocrinology · 2023Article
- Lead Disrupts Mitochondrial Morphology and Function through Induction of ER Stress in Model of Neurotoxicity.International journal of molecular sciences · 2022Article
- The nucleolar δ isoform of adapter protein SH2B1 enhances morphological complexity and function of cultured neurons.Journal of cell science · 2022Article
- Dendrite tapering actuates a self-organizing signaling circuit for stochastic filopodia initiation in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Deletion of the Brain-Specific α and δ Isoforms of Adapter Protein SH2B1 Protects Mice From Obesity.Diabetes · 2021Article
- Epigenetic Regulation ofInternational journal of molecular sciences · 2020Article
- WNT3A Promotes Neuronal Regeneration upon Traumatic Brain Injury.International journal of molecular sciences · 2020Article
- Brain somatic mutations in MTOR reveal translational dysregulations underlying intractable focal epilepsy.The Journal of clinical investigation · 2019Article
- Filopodia and focal adhesions: An integrated system driving branching morphogenesis in neuronal pathfinding and angiogenesis.Developmental biology · 2019Review
- SH2B1 promotes epithelial-mesenchymal transition through the IRS1/β-catenin signaling axis in lung adenocarcinoma.Molecular carcinogenesis · 2018Article
- Low-dose ionizing radiation induces mitochondrial fusion and increases expression of mitochondrial complexes I and III in hippocampal neurons.Oncotarget · 2015Article
- Quantitative proteomics analysis of CaMKII phosphorylation and the CaMKII interactome in the mouse forebrain.ACS chemical neuroscience · 2015Article
- SH2B1 orchestrates signaling events to filopodium formation during neurite outgrowth.Communicative & integrative biologyArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SH2B1 is an adaptor protein known to enhance neurite outgrowth. In this study, we provide evidence suggesting that the SH2B1 level is increased during in vitro culture of hippocampal neurons, and the β isoform (SH2B1β) is the predominant isoform. The fact that formation of filopodia is prerequisite for neurite initiation suggests that SH2B1 may regulate filopodium formation and thus neurite initiation. To investigate whether SH2B1 may regulate filopodium formation, the effect of SH2B1 and a membrane and actin regulator, IRSp53 (insulin receptor tyrosine kinase substrate p53), is investigated. Overexpressing both SH2B1β and IRSp53 significantly enhances filopodium formation, neurite outgrowth, and branching. Both in vivo and in vitro data show that SH2B1 interacts with IRSp53 in hippocampal neurons. This interaction depends on the N-terminal proline-rich domains of SH2B1. In addition, SH2B1 and IRSp53 co-localize at the plasma membrane, and their levels increase in the Triton X-100-insoluble fraction of developing neurons. These findings suggest that SH2B1-IRSp53 complexes promote the formation of filopodia, neurite initiation, and neuronal branching.
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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 Socratic graph.