ArticleMolecular endocrinology (Baltimore, Md.)2009
Nucleocytoplasmic shuttling of the adapter protein SH2B1beta (SH2-Bbeta) is required for nerve growth factor (NGF)-dependent neurite outgrowth and enhancement of expression of a subset of NGF-responsive genes.
Article in Molecular endocrinology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Identification of βIIΣ1-Spectrin as a Binding Partner of the GH-regulated Human Obesity Scaffold Protein SH2B1.Endocrinology · 2025Article
- 2022 Cannon lecture: an ode to signal transduction: how the growth hormone pathway revealed insight into height, malignancy, and obesity.American journal of physiology. Endocrinology and metabolism · 2023Review
- The nucleolar δ isoform of adapter protein SH2B1 enhances morphological complexity and function of cultured neurons.Journal of cell science · 2022Article
- Shuttling of cellular proteins between the plasma membrane and nucleus (Review).Molecular medicine reports · 2022Review
- Neural Stem Cells Overexpressing Nerve Growth Factor Improve Functional Recovery in Rats Following Spinal Cord Injury via Modulating Microenvironment and Enhancing Endogenous Neurogenesis.Frontiers in cellular neuroscience · 2021Article
- Article
- Phosphorylation of the Unique C-Terminal Tail of the Alpha Isoform of the Scaffold Protein SH2B1 Controls the Ability of SH2B1α To Enhance Nerve Growth Factor Function.Molecular and cellular biology · 2018Article
- The Dyslexia-susceptibility Protein KIAA0319 Inhibits Axon Growth Through Smad2 Signaling.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- LNK (SH2B3): paradoxical effects in ovarian cancer.Oncogene · 2015Article
- SH2B1 and IRSp53 proteins promote the formation of dendrites and dendritic branches.The Journal of biological chemistry · 2015Article
- Functional characterization of obesity-associated variants involving the α and β isoforms of human SH2B1.Endocrinology · 2014Article
- SH2B1 regulation of energy balance, body weight, and glucose metabolism.World journal of diabetes · 2014Review
- SH2B1β interacts with STAT3 and enhances fibroblast growth factor 1-induced gene expression during neuronal differentiation.Molecular and cellular biology · 2014Article
- Phosphorylation of the adaptor protein SH2B1β regulates its ability to enhance growth hormone-dependent macrophage motility.Journal of cell science · 2013Article
- Human SH2B1 mutations are associated with maladaptive behaviors and obesity.The Journal of clinical investigation · 2012Article
- The plasminogen activation system and the regulation of catecholaminergic function.Journal of biomedicine & biotechnology · 2012Review
- Identification of SH2B1β as a focal adhesion protein that regulates focal adhesion size and number.Journal of cell science · 2011Article
- Phosphorylation controls a dual-function polybasic nuclear localization sequence in the adapter protein SH2B1β to regulate its cellular function and distribution.Journal of cell science · 2011Article
- Critical role of the Src homology 2 (SH2) domain of neuronal SH2B1 in the regulation of body weight and glucose homeostasis in mice.Endocrinology · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The adapter protein SH2B1 (SH2-B, PSM) is recruited to multiple ligand-activated receptor tyrosine kinases, including the receptors for nerve growth factor (NGF), insulin, and IGF-I as well as the cytokine receptor-associated Janus kinase family kinases. In this study, we examine SH2B1's function in NGF signaling. We show that depleting endogenous SH2B1 using short hairpin RNA against SH2B1 inhibits NGF-dependent neurite outgrowth, but not NGF-mediated phosphorylation of Akt or ERKs 1/2. SH2B1 has been hypothesized to localize and function at the plasma membrane. We identify a nuclear localization signal within SH2B1 and show that it is required for nuclear translocation of SH2B1beta. Mutation of the nuclear localization signal has no effect on NGF-induced activation of TrkA and ERKs 1/2 but prevents SH2B1beta from enhancing NGF-induced neurite outgrowth. Disruption of SH2B1beta nuclear import also prevents SH2B1beta from enhancing NGF-induced transcription of genes important for neuronal differentiation, including those encoding urokinase plasminogen activator receptor, and matrix metalloproteinases 3 and 10. Disruption of SH2B1beta nuclear export by mutation of its nuclear export sequence similarly prevents SH2B1beta enhancement of NGF-induced transcription of those genes. Nuclear translocation of the highly homologous family member SH2B2(APS) was not observed. Together, these data suggest that rather than simply acting as an adapter protein linking signaling proteins to the activated TrkA receptor at the plasma membrane, SH2B1beta must shuttle between the plasma membrane and nucleus to function as a critical component of NGF-induced gene expression and neuronal differentiation.
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