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Data indicate that plexin A1 (zeige PLXNA1 Proteine)-4 (PLXNA1 (zeige PLXNA1 Proteine)-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 (zeige SEMA3A Proteine) receptors (neuropilin-1 (NRP-1 (zeige NRP1 Proteine)), NRP-2 (zeige NELL2 Proteine), plexin A1 (zeige PLXNA1 Proteine), plexin A2 (zeige Plxna2 Proteine), and plexin A3) significantly increased during M-CSF (zeige CSF1 Proteine)-mediated differentiation of monocytes into macrophages.
genetic findings demonstrate that Sema3a (zeige SEMA3A Proteine) repellent signaling plays a role in the establishment of proper afferent projections in SAG (zeige RNF7 Proteine) neurons, and this signaling likely occurs through a receptor complex involving Npn1 (zeige NRP1 Proteine) and either plexinA1 (zeige PLXNA1 Proteine) or plexinA3
plexin-A3 and plexin-A4 (zeige PLXNA4 Proteine) 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 (zeige CORT Proteine) 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 (zeige PLXNA4 Proteine), and Sema6A (zeige SEMA6A Proteine) is at least partially required for dorsal turning of the corticospinal tract axons
The combined loss of PLXNA3 and PLXNA4 (zeige PLXNA4 Proteine) impaired facial branchiomotor axon guidance more severely than loss of either plexin alone, suggesting that SEMA3A (zeige SEMA3A Proteine) and SEMA3F (zeige SEMA3F Proteine) signals, even though both essential, are partially redundant.
the plexin A3 GAP domain adopts a closed conformation and cannot accommodate R-Ras/M-Ras (zeige MRAS Proteine) 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 (zeige SEMA3F Proteine) and co-receptor neuropilin (zeige NRP1 Proteine)-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 (zeige TH Proteine) 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