NME2 associates with PTPσ to transduce signals from chondroitin sulfate proteoglycans

Hamasaki, Hajime; Fujitani, Masashi; Yamashita, Toshio

doi:10.1016/j.bbrc.2016.02.042

Cited by 3 publications

(4 citation statements)

References 24 publications

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“…The inhibition of dendritic formation mediated by PTPRS depends on its direct interaction with its ligand CSPG, which induces PTPRS-mediated TrkB dephosphorylation, thereby suppressing dendritic spine growth ( Figure 3A ) ( Kurihara and Yamashita, 2012 ; Lesnikova et al, 2020 ). Neurite outgrowth inhibition induced by CSPGs also appears to be mediated by the intracellular interaction between PTPRS and the nucleoside diphosphate kinase 2 NME2 ( Figure 3A ) ( Hamasaki et al, 2016 ).…”

Section: Lar-rptps In Neurite Growth and Axon Guidancementioning

confidence: 99%

LAR Receptor Tyrosine Phosphatase Family in Healthy and Diseased Brain

Cornejo

Cortés

Findlay

et al. 2021

Front. Cell Dev. Biol.

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Protein phosphatases are major regulators of signal transduction and they are involved in key cellular mechanisms such as proliferation, differentiation, and cell survival. Here we focus on one class of protein phosphatases, the type IIA Receptor-type Protein Tyrosine Phosphatases (RPTPs), or LAR-RPTP subfamily. In the last decade, LAR-RPTPs have been demonstrated to have great importance in neurobiology, from neurodevelopment to brain disorders. In vertebrates, the LAR-RPTP subfamily is composed of three members: PTPRF (LAR), PTPRD (PTPδ) and PTPRS (PTPσ), and all participate in several brain functions. In this review we describe the structure and proteolytic processing of the LAR-RPTP subfamily, their alternative splicing and enzymatic regulation. Also, we review the role of the LAR-RPTP subfamily in neural function such as dendrite and axon growth and guidance, synapse formation and differentiation, their participation in synaptic activity, and in brain development, discussing controversial findings and commenting on the most recent studies in the field. Finally, we discuss the clinical outcomes of LAR-RPTP mutations, which are associated with several brain disorders.

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Section: Lar-rptps In Neurite Growth and Axon Guidancementioning

confidence: 99%

LAR Receptor Tyrosine Phosphatase Family in Healthy and Diseased Brain

Cornejo

Cortés

Findlay

et al. 2021

Front. Cell Dev. Biol.

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“…Several other proteins have been reported to function as signals downstream of PTPσ. NDPK2 (nucleoside diphosphate kinase 2) interacts with PTPσ and NDPK2 knockdown in cortical neurons overcomes inhibition by CSPGs (Hamasaki et al, 2016 ). Ezrin, a linker protein between the plasma membrane and actin cytoskeleton, is a substrate of PTPσ and regulates migration and organization of cells by altering adhesion of their surface structures (Doody et al, 2015 ).…”

Section: Two Rptps Use Both Convergent and Divergent Signaling Pathwamentioning

confidence: 99%

Advances in the Signaling Pathways Downstream of Glial-Scar Axon Growth Inhibitors

Sami

Selzer

2020

Front. Cell. Neurosci.

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Axon growth inhibitors generated by reactive glial scars play an important role in failure of axon regeneration after CNS injury in mature mammals. Among the inhibitory factors, chondroitin sulfate proteoglycans (CSPGs) are potent suppressors of axon regeneration and are important molecular targets for designing effective therapies for traumatic brain injury or spinal cord injury (SCI). CSPGs bind with high affinity to several transmembrane receptors, including two members of the leukocyte common antigen related (LAR) subfamily of receptor protein tyrosine phosphatases (RPTPs). Recent studies demonstrate that multiple intracellular signaling pathways downstream of these two RPTPs mediate the growth-inhibitory actions of CSPGs. A better understanding of these signaling pathways may facilitate development of new and effective therapies for CNS disorders characterized by axonal disconnections. This review will focus on recent advances in the downstream signaling pathways of scar-mediated inhibition and their potential as the molecular targets for CNS repair.

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“…CA2 is spatially divided into two subclusters on the UMAP (fig. S2A): One of them is marked by the expression of Rps6 , encoding the 40 S ribosomal protein S6, whose phosphorylation indicates neuronal activity during synaptic plasticity ( 37 , 38 ); and the other is marked by the expression of Nme2 , which encodes a nucleoside diphosphate kinase involved in neurite outgrowth inhibition ( 39 ). Loss of KDM5A showed a decrease in the Rps6 cluster accompanied by an increase in the Nme2 cluster (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…When KDM5A is lost, there is a shift in identity of the CA2 cellular subclusters, with a decrease in CA2 neurons expressing Rps6 , a gene known for its function in synaptic plasticity ( 37 , 38 ), and an increase in CA2 neurons expressing Nme2 , a gene known for its role in neurite outgrowth inhibition ( 39 ). We also identified a role for KDM5A in mediating the development of a subtype of CA3 neurons; we found a decrease in the Kdm5a −/− of a CA3 subtype that expresses Shisa6 and markers of mossy fibers.…”

Section: Discussionmentioning

confidence: 99%

Disruption of the autism gene and chromatin regulator KDM5A alters hippocampal cell identity

El Hayek,

DeVries,

Gogate

et al. 2023

Sci. Adv.

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Chromatin regulation plays a pivotal role in establishing and maintaining cellular identity and is one of the top pathways disrupted in autism spectrum disorder (ASD). The hippocampus, composed of distinct cell types, is often affected in patients with ASD. However, the specific hippocampal cell types and their transcriptional programs that are dysregulated in ASD are unknown. Using single-nucleus RNA sequencing, we show that the ASD gene, lysine demethylase 5A ( KDM5A ), regulates the development of specific subtypes of excitatory and inhibitory neurons. We found that KDM5A is essential for establishing hippocampal cell identity by controlling a differentiation switch early in development. Our findings define a role for the chromatin regulator KDM5A in establishing hippocampal cell identity and contribute to the emerging convergent mechanisms across ASD.

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NME2 associates with PTPσ to transduce signals from chondroitin sulfate proteoglycans

Cited by 3 publications

References 24 publications

LAR Receptor Tyrosine Phosphatase Family in Healthy and Diseased Brain

LAR Receptor Tyrosine Phosphatase Family in Healthy and Diseased Brain

Advances in the Signaling Pathways Downstream of Glial-Scar Axon Growth Inhibitors

Disruption of the autism gene and chromatin regulator KDM5A alters hippocampal cell identity

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