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Data indicate that plexin A1 (show PLXNA1 Proteins)-4 (PLXNA1 (show PLXNA1 Proteins)-4) mediation of neuroanatomical traits can be detected using in vivo neuroimaging techniques.
in vitro analysis on PLXNA3 also suggest that this gene may have some form of growth suppressive role in breast cancer, in addition to a similar role for the gene previously reported in ovarian cancer.
Data show that the expression of Sema3A (show SEMA3A Proteins) receptors (neuropilin-1 (NRP-1 (show NRP1 Proteins)), NRP-2 (show NELL2 Proteins), plexin A1 (show PLXNA1 Proteins), plexin A2 (show Plxna2 Proteins), and plexin A3) significantly increased during M-CSF (show CSF1 Proteins)-mediated differentiation of monocytes into macrophages.
genetic findings demonstrate that Sema3a (show SEMA3A Proteins) repellent signaling plays a role in the establishment of proper afferent projections in SAG (show RNF7 Proteins) neurons, and this signaling likely occurs through a receptor complex involving Npn1 (show NRP1 Proteins) and either plexinA1 (show PLXNA1 Proteins) or plexinA3
plexin-A3 and plexin-A4 (show PLXNA4 Proteins) are expressed in newly-differentiated sympathetic neurons, but not their neural crest precursors. They function cooperatively to regulate the migration of sympathetic neurons and then differentially to guide the sympathetic axons.
These results indicate that the stereotyped pruning of the visual and motor CST (show CORT Proteins) axon collaterals is differentially regulated and that this specificity arises from the differential expression of plexin receptors in the cortex.
the signaling of plexin-A3, plexin-A4 (show PLXNA4 Proteins), and Sema6A (show SEMA6A Proteins) is at least partially required for dorsal turning of the corticospinal tract axons
The combined loss of PLXNA3 and PLXNA4 (show PLXNA4 Proteins) impaired facial branchiomotor axon guidance more severely than loss of either plexin alone, suggesting that SEMA3A (show SEMA3A Proteins) and SEMA3F (show SEMA3F Proteins) signals, even though both essential, are partially redundant.
the plexin A3 GAP domain adopts a closed conformation and cannot accommodate R-Ras/M-Ras (show MRAS Proteins) in its substrate-binding site, providing a structural basis for the autoinhibited state of plexins
\Homodimerization of PlxnA3 caused by mutation M1281L remains in the presence of ligand semaphorin 3F (show SEMA3F Proteins) and co-receptor neuropilin (show NRP1 Proteins)-2a.
Data show that null mutants of the guidance receptor plexin A3 display motor axon branching defects.
in vivo demonstration of the intersection of spontaneous electrical activity with the PlexinA3 guidance molecule receptor in regulation of axon pathfinding
study shows plexinA3 is a crucial receptor for axon guidance cues in primary motor neurons
Plexin A3 plays an additional role in motor axonal morphogenesis.
Plxna3 acts with its ligand Sema3a1 for fasciculation and correct target selection of the Vp and VII (show TH Proteins) motor axons.
The protein encoded by this gene is a member of the plexin class of proteins. The encoded protein is a transmembrane protein that is exposed on the cell surface. This gene is thought to be involved in epithelial and neural tissue development.
, Sex chromosome X transmembrane protein of HGF receptor family 3
, semaphorin receptor SEX
, plexin 3
, Plexin 4, SEX, homolog to the cMet/HGF receptors