Semaphorin7A and its receptors: Pleiotropic regulators of immune cell function, bone homeostasis, and neural development

Jongbloets, Bart C.; Ramakers, G.J.A.; Pasterkamp, R. Jeroen

doi:10.1016/j.semcdb.2013.01.002

Cited by 38 publications

(44 citation statements)

References 99 publications

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“…Rather, the cells expressing high levels of Sema7A in S1 (spiny stellate cells and GABAergic neurons) appear to show the strongest phenotypes in its absence. Downstream mechanisms are likely to be complex, because Sema7A can signal via β1-integrins and Plexin C1 alone and together in cis, in trans, or in a local autocrine fashion following cleavage (33)(34)(35).…”

Section: Discussionmentioning

confidence: 99%

Maturation of cortical circuits requires Semaphorin 7A

Carcea

Patil²,

Robison

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Abnormal cortical circuits underlie some cognitive and psychiatric disorders, yet the molecular signals that generate normal cortical networks remain poorly understood. Semaphorin 7A (Sema7A) is an atypical member of the semaphorin family that is GPI-linked, expressed principally postnatally, and enriched in sensory cortex. Significantly, SEMA7A is deleted in individuals with 15q24 microdeletion syndrome, characterized by developmental delay, autism, and sensory perceptual deficits. We studied the role that Sema7A plays in establishing functional cortical circuitry in mouse somatosensory barrel cortex. We found that Sema7A is expressed in spiny stellate cells and GABAergic interneurons and that its absence disrupts barrel cytoarchitecture, reduces asymmetrical orientation of spiny stellate cell dendrites, and functionally impairs thalamocortically evoked synaptic responses, with reduced feed-forward GABAergic inhibition. These data identify Sema7A as a regulator of thalamocortical and local circuit development in layer 4 and provide a molecular handle that can be used to explore the coordinated generation of excitatory and inhibitory cortical circuits.E/I balance | critical period | EPSPs | IPSPs | thalamocortical

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Section: Discussionmentioning

confidence: 99%

Maturation of cortical circuits requires Semaphorin 7A

Carcea

Patil²,

Robison

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…[16][17][18] Sema7A regulates bone homeostasis. 19 Interestingly, our recent study showed that Sema3A could regulate bone remodeling indirectly by modulating sensory nerve development. 20 Therefore, in this review, we will focus on Sema3A as a example to highlight the key role of semaphorins in the regulation of bone remodeling.…”

Section: Semaphorin Signaling Semaphorin Family and The Receptorsmentioning

confidence: 99%

Semaphorin 3A

2013

Cell Adhesion & Migration

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“…The pleiotropic functions of semaphorin proteins range from axon outgrowth, angiogenesis, bone differentiation, and immune regulation to tumor metastasis. Semaphorin7A (Sema7A; also known as CD108 or SemaK1) is the only GPI-anchored semaphoring; thus, it lacks a cytoplasmic domain (13,14). The extracellular domain of Sema7A contains a conserved Sema domain bearing an RGD motif, a "plexins semaphorins integrins" domain, and an Ig domain.…”

mentioning

confidence: 99%

Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration

Rijn

Paulis

Riet

et al. 2016

The Journal of Immunology

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Dendritic cell (DC) migration is essential for efficient host defense against pathogens and cancer, as well as for the efficacy of DC-based immunotherapies. However, the molecules that induce the migratory phenotype of DCs are poorly defined. Based on a large-scale proteome analysis of maturing DCs, we identified the GPI-anchored protein semaphorin 7A (Sema7A) as being highly expressed on activated primary myeloid and plasmacytoid DCs in human and mouse. We demonstrate that Sema7A deficiency results in impaired chemokine CCL21-driven DC migration in vivo. Impaired formation of actin-based protrusions, resulting in slower three-dimensional migration, was identified as the mechanism underlying the DC migration defect. Furthermore, we show, by atomic force microscopy, that Sema7A decreases adhesion strength to extracellular matrix while increasing the connectivity of adhesion receptors to the actin cytoskeleton. This study demonstrates that Sema7A controls the assembly of actin-based protrusions that drive DC migration in response to CCL21.

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Semaphorin7A and its receptors: Pleiotropic regulators of immune cell function, bone homeostasis, and neural development

Cited by 38 publications

References 99 publications

Maturation of cortical circuits requires Semaphorin 7A

Maturation of cortical circuits requires Semaphorin 7A

Semaphorin 3A

Semaphorin 7A Promotes Chemokine-Driven Dendritic Cell Migration

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