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Validated All-in-One™ qPCR Primer for SEMA3A(NM_006080.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene is a member of the semaphorin family and encodes a protein with an Ig-like C2-type (immunoglobulin-like) domain, a PSI domain and a Sema domain. This secreted protein can function as either a chemorepulsive agent, inhibiting axonal outgrowth, or as a chemoattractive agent, stimulating the growth of apical dendrites.
Gene References into function
- sema3A is elevated in schizophrenia, and is associated with downregulation of genes involved in synaptic formation and maintenance.
- human glioma cells express class 3 semaphorins and receptors for soluble and membrane-bound semaphorins, suggesting a possible role of the semaphorin/neuropilin system in the interactions of human malignant glioma with the nervous and immune systems.
- during vascular development and experimental angiogenesis, endothelial cells generate autocrine chemorepulsive signals of class 3 semaphorins (SEMA3 proteins) that localize at nascent adhesive sites in spreading endothelial cells
- Breast carcinoma cells support an autocrine pathway involving SEMA3A, plexin-A1, and NP1 that impedes their ability to chemotax.
- new role of Sema-3A in VEGF function mediated by p38 MAPK and suggest that the abrogation of regulated Sema-3A expression is responsible for VEGF-driven growth of tumor cells
- the chemorepulsive signals mediated by Sema 3A play an important role in preventing nerve fibers growth in the umbilical cord and in gestational uterine tissues.
- extensive inhibition of platelet function by Sema3A appears to be mediated, at least in part, through impairment of agonist-induced Rac1-dependent actin rearrangement
- Down-regulation of NRP1 by NRSF overexpression reduced Sema3A activity. It was concluded that NRSF is a transcription factor that silences NRP1 expression and thereby diminishes the Sema3A mediated inhibition of HaCaT keratinocyte migration
- Vascular endothelial growth factor165 (VEGF165) and semaphorin3A (SEMA3A) elicit pro- and antiangiogenic signals respectively in endothelial cells (ECs) by binding to their receptors VEGFR-2, neuropilin-1 and plexin-a.
- In the regulation of the immune response Sema-3A plays a novel role as a modulator of cross-talk between activated dendritic cells and T cells.
- NP-1/Sema-3A-mediated interactions participate in the control of human thymocyte development
- sema3A and sema3C have opposite roles in neoplasm invasiveness and adhesion
- combinations of sema3A and sema3F may be able to inhibit tumor angiogenesis more effectively than single semaphorins.
- This review highlights the effect of Sema3A on axonal growth cones, the intracellular signaling pathways that lead to the cellular effects, and the evidence for collapsin-response-mediator proteins (CRMPs) as a component of the Sema3A signaling cascade.
- Overexpression of SEMA3A may favor malignant activities of tumor cells. Negative clinicopathol correlations suggest that SEMA3A might represent a novel intervention target for pancreatic cancer patients.
- structural analysis of semaphorin and VEGF binding
- Semaphorin3A (Sema3A) triggers a proapoptotic program that sensitizes leukemic T cells to Fas (CD95)-mediated apoptosis.
- Human neuroma contains increased levels of semaphorin 3A, which surrounds nerve fibers and reduces neurite extension in vitro.
- The sulfated polysaccharides dextran sulfate and fucoidan, but not others, reduce endothelial cell-surface levels of NRP1, NRP2, and to a lesser extent VEGFR-1 and VEGFR-2, and block the binding and in vitro function of semaphorin3A and VEGF(165).
- The role of semaphorins and their receptors in the progression of lung cancer was studied.
- Sema3A inhibits tumor development from MDA-MB-231 and MCF-7 cancer cells, but not from MDA-MB-435 or MDA-MB-468. It inhibits tumor angiogenesis in all of the formed tumors. The inhibition is correlated with the expression of NRP-1 of the tumors cells.
- These findings indicate that EGF released from corneal epithelial cells up-regulates the expression of Sema3A in corneal fibroblasts.
