High impact information on Plxna1

• Expression of a dominant-negative Plex 1 in sensory neurons blocks Sema3A-induced growth cone collapse [1].
• CIITA-regulated plexin-A1 affects T-cell-dendritic cell interactions [2].
• These data indicate involvement of plexin-A1 in T cell-DC interactions but not antigen processing or binding [2].
• RNA interference by short hairpin RNA specific for plexin-A1, but not a single-nucleotide mutant, greatly reduced plexin-A1 expression and T cell stimulation by protein- or peptide-antigen-pulsed DCs.Plexin-A1 is not required for peptide binding to MHC [2].
• Sema3A, a prototypical semaphorin, acts as a chemorepellent or a chemoattractant for axons by activating a receptor complex comprising neuropilin-1 as the ligand-binding subunit and plexin-A1 as the signal-transducing subunit [3].

Biological context of Plxna1

• All the mouse and rat plexin A genes were localized to chromosome regions where conserved homology has been identified among human, mouse and rat [4].
• RESULTS: We examined the gene expression of Sema3A, Sema3C, Sema3F and their receptors, NP-1, NP-2 and plexin-A1 by in situ hybridization [5].
• We obtained mouse plexin 3 cDNA clones in which a part of protein-coding region was deleted [6].
• The expression and function of plexins in non-neuronal tissues has been poorly characterized, although Plexin-A1 has been shown to have a role during lung and cardiac morphogenesis [7].
• Plexin-A1 and its interaction with DAP12 in immune responses and bone homeostasis [8].

Anatomical context of Plxna1

• In the testis, Plxna1, Plxnb1 and Plxnc1 are expressed in the developing sex chords [7].
• In the tooth bud, Plxna1 and Plxnb1 are expressed in the oral epithelium, enamel knot and in both the inner and outer enamel epithelium, whereas the expression of Plxnb2 is more restricted to the inner enamel epithelium [7].
• Deletion of the highly conserved cytoplasmic domain of Plexin-A1 or -A2 creates a dominant negative Sema3A receptor that renders sensory axons resistant to the repulsive effects of Sema3A when expressed in sensory ganglia [9].
• Stereotyped axon pruning via plexin signaling is associated with synaptic complex elimination in the hippocampus [10].
• Additionally, plexin-A1 has been implicated in dendritic cell function in the immune system [8].

Associations of Plxna1 with chemical compounds

• Moreover, putative extracellular segments of these two proteins had three repeats of a cysteine-rich domain which is a common motif for plexin proteins [6].
• Furthermore, we show that plexin-A1 associates with the triggering receptor expressed on myeloid cells-2 (Trem-2), linking semaphorin-signalling to the immuno-receptor tyrosine-based activation motif (ITAM)-bearing adaptor protein, DAP12 [8].
• Interestingly, integrin-based focal adhesive structures are disassembled within minutes upon plexin activation; this is followed by actin depolymerization and, eventually, by cellular collapse [11].

Physical interactions of Plxna1

• Plexin/neuropilin complexes mediate repulsion by the axonal guidance signal semaphorin 3A [9].

Regulatory relationships of Plxna1

• Here, we show that plexin-A3 is the most ubiquitously expressed plexin family member within regions of the developing mammalian nervous system known to contain semaphorin-responsive neurons [12].

Other interactions of Plxna1

• Identification and characterization of a novel mouse plexin, plexin-A4 [13].
• It has been proposed that four members of the plexin A subfamily (plexin-As; plexin-A1, -A2, -A3, and -A4) and two neuropilins (neuropilin-1 and neuropilin-2) form complexes and serve as receptors for class 3 secreted semaphorins (Semas), potent neural chemorepellents [14].
• Thus, we named these two proteins mouse plexin 2 and mouse plexin 3 [6].
• A physical and functional association between Met and Plexin B1, the prototype of class B Plexin subfamily, has been previously demonstrated [15].
• We found the semaphorin receptor plexin-A1 was expressed in DCs, but not in other immune cells, and was strongly induced by CIITA [2].

Analytical, diagnostic and therapeutic context of Plxna1

• Northern blot analysis indicated that mouse plexin 1 was predominantly expressed in the brain [16].
• MATERIALS AND METHODS: ATDC5 cells and primary chondrocytes were either treated with NOV recombinant protein or transfected with a NOV-specific siRNA to determine, using quantitative RT-PCR, the effect of NOV on the expression of several molecules involved in chondrocyte differentiation [17].
• Hybridoma antibodies which reacted against the nonoccluded form (NOV) of AcNPV in an ELISA test expressed different specificities for the occluded form of the virus (OV), a mutant strain of AcNPV, and CfNPV [18].
• The polypeptide specificity of 19 of 28 hybridoma antibodies which reacted with OV and NOV of AcNPV was assigned using Western blot analysis [18].

References