SEMA4A
SEMA4A (semaphorin 4A, also known as SemB, SEMAB and CORD10) is a transmembrane member of the semaphorin family that acts as a cell surface receptor for plexins. It contributes to cell-cell signalling in synapse development, axon guidance, angiogenesis and adaptive immunity. Browse Assay Genie's current range of SEMA4A research reagents below, or read on for the biology behind the target.
SEMA4A is a cell surface receptor for PLXNB1, PLXNB2, PLXNB3 and PLXND1 and plays an important role in cell-cell signalling. In the nervous system it regulates the development of glutamatergic and GABAergic synapses: it promotes inhibitory synapses in a PLXNB1-dependent manner and excitatory synapses in a PLXNB2-dependent manner. It also promotes axon growth cone collapse and inhibits axonal extension by providing local signals that specify territories inaccessible to growing axons.
Outside the nervous system, SEMA4A has roles in immunity and vascular biology. It helps prime antigen-specific T-cells, promotes differentiation of Th1 T-helper cells and so contributes to adaptive immunity, and it promotes phosphorylation of TIMD2. It inhibits angiogenesis, suppressing vascular endothelial growth factor (VEGF)-mediated endothelial cell migration and proliferation in vitro and angiogenesis in vivo.
The SEMA4A gene encodes a single-pass type I membrane protein containing an immunoglobulin-like C2-type domain, a PSI domain and a sema domain. Semaphorins are a family of soluble and transmembrane proteins involved in axon guidance, morphogenesis, carcinogenesis and immunomodulation. Mutations in the SEMA4A gene are associated with retinal degenerative diseases, including retinitis pigmentosa type 35 (RP35) and cone-rod dystrophy type 10 (CORD10). Multiple alternatively spliced transcript variants encoding different isoforms have been identified. The mouse ortholog is Sema4a. The HGNC previous name describes its sema, immunoglobulin, transmembrane and short cytoplasmic domains.
SEMA4A regulates glutamatergic and GABAergic synapse development through distinct plexin-B partners, making it relevant to studies of excitatory and inhibitory balance.
SEMA4A promotes growth cone collapse and inhibits axonal extension, helping to define territories that growing axons cannot enter.
SEMA4A helps prime antigen-specific T-cells and promotes Th1 differentiation, linking it to adaptive immune responses.
SEMA4A suppresses VEGF-driven endothelial migration and proliferation, and mutations are linked to retinitis pigmentosa and cone-rod dystrophy.
SEMA4A is a cell surface receptor for PLXNB1, PLXNB2, PLXNB3 and PLXND1. It regulates synapse development, promotes axon growth cone collapse, inhibits angiogenesis and supports T-cell priming and Th1 differentiation, contributing to adaptive immunity.
SEMA4A is also called SemB, SEMAB, FLJ12287 and CORD10. The previous HGNC name was sema domain, immunoglobulin domain (Ig), transmembrane domain (TM) and short cytoplasmic domain, (semaphorin) 4A. Multiple alternatively spliced transcript variants encode different isoforms.
Mutations in the SEMA4A gene are associated with retinal degenerative diseases, including retinitis pigmentosa type 35 and cone-rod dystrophy type 10. The mouse ortholog is Sema4a; check the datasheet of any product for its validated reactivity.
Other semaphorin family members involved in axon guidance, immune regulation and angiogenesis, with products at Assay Genie.
Gene and protein annotations from HGNC, NCBI Gene and UniProt Q9H3S1; product specifications from Assay Genie datasheets.