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Results show that PlexinA4, a transmembrane protein known to be a co-receptor for class III semaphorins, acts downstream of Islet2 to promote branching of the peripheral axons of the primary sensory neurons.
Both CLU and PLXNA4 have been genetically associated with Alzheimer disease (AD) risk and our data thus provide a direct relationship between two AD risk genes. Our data suggest that increasing the levels of PLXNA4 or targeting CLU-PLXNA4 interactions may have therapeutic value in AD.
Data indicate that plexin A1-4 (PLXNA1-4) mediation of neuroanatomical traits can be detected using in vivo neuroimaging techniques.
There is a significant association between Alzheimer's disease risk and SNPs in PLXNA4.
Rare variants in PLXNA4 and Parkinson's disease.
Plexin-A4 promotes tumor progression and tumor angiogenesis by enhancement of VEGF and bFGF signaling.
These findings implicate Semaphorin-6A - Plexin-A2/Plexin-A4 interactions in dorsal lateral geniculate nucleus axon guidance and in the spatiotemporal organization of guidepost cell populations in the mammalian subpallium.
These findings suggest that by interacting with PlexA4, TrkA plays a crucial role in redirecting local Sema3A signaling to retrograde axonal transport, thereby regulating dendritic GluA2 localization and patterning.
work reveals a 2-fold role of the PlxnA ectodomains: imposing a pre-signaling autoinhibitory separation for the cytoplasmic domains via intermolecular head-to-stalk interactions and supporting dimerization-based PlxnA activation upon ligand binding.
Results suggest that semaphoring 6a activates plexin 4a by disrupting an inhibitory plexin dimer and inducing the active dimer
Distinct cytoplasmic domains in Plexin-A4 mediate diverse responses to semaphorin 3A in developing mammalian neurons.
results suggest that Plexin-A4 is involved in the precise positioning of oligodendrocyte precursor cells in developing cerebral cortex.
null mutations in Sema6A or PlexinA4 (PlexA4) exhibit a pronounced defect in OPL stratification of horizontal cell axons without any apparent deficits in bipolar cell dendrite or photoreceptor axon targeting.
Findings suggest plexin-A4 and Sema3A as new intervention points for treating sepsis.
It regulates lamina-restricted projection of hippocampal mossy fiber. (review)
suggesting that a Semaphorin6A-Plexin-A4 cis interaction serves as an inhibitory mechanism.
plexin-A4 was expressed in the developing nervous system with a pattern different to that of other members of the plexin-A subfamily (plexin-A1, plexin-A2 and plexin-A3)
PlexA4 expressed in oligodendrocyte precursor cells acts as a mediator of semaphorin signals
plexin-A4, as a component of the receptor complex for class III semaphorins, negatively regulates T cell-mediated immune responses
plexin-A3 and plexin-A4 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 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, and Sema6A is at least partially required for dorsal turning of the corticospinal tract axons
The combined loss of PLXNA3 and PLXNA4 impaired facial branchiomotor axon guidance more severely than loss of either plexin alone, suggesting that SEMA3A and SEMA3F signals, even though both essential, are partially redundant.
Involved in the development of primary sensory neurons especially in branching of the peripheral axons. Interacts with the SLIT2 signaling specifically to promote axonal branching of Rohon-Beard neurons and the trigeminal sensory ganglion neurons.
, plexin A4, A
, plexin A4
, putative plexin 2