Disease relevance of Plxnc1

• The poxvirus A39R protein is a member of the semaphorin family previously reported to bind plexin C1 [1].
• Finally, in vivo T cell responses to ovalbumin peptide and contact hypersensitivity to dinitrofluorobenzene were slightly decreased in Plexin C1(-/-) mice [2].

High impact information on Plxnc1

• A39R binding to plexin C1 on DCs inhibited integrin-mediated adhesion and spreading in vitro [1].
• Furthermore, A39R binding to plexin C1 inhibited chemokine-induced migration of DCs in vitro, suggesting that plexins and semaphorins could be involved in the regulation of leukocyte movement [1].
• We show that, in the mouse, plexin C1 is expressed on dendritic cells (DCs) and neutrophils and is the only receptor for A39R on these cells [1].
• The A39R effect on DC adhesion was blocked by a specific inhibitor of cofilin phosphorylation, suggesting that the regulation of F-actin turnover by plexin C1 was essential to induce cellular retraction [1].
• The poxvirus A39R protein is a member of the semaphorin family that binds to Plexin C1, a molecule expressed on neutrophils and dendritic cells (DC) [3].

Biological context of Plxnc1

• We found that A39R treatment strongly inhibits phagocytosis by DC and neutrophils in vitro in a Plexin C1-dependent fashion [3].

Anatomical context of Plxnc1

• In the testis, Plxna1, Plxnb1 and Plxnc1 are expressed in the developing sex chords [4].
• Plexin C1 engagement on mouse dendritic cells by viral semaphorin A39R induces actin cytoskeleton rearrangement and inhibits integrin-mediated adhesion and chemokine-induced migration [1].
• Plexin C1(-/-) bone marrow-derived DCs induced normal in vitro T cell responses but reduced in vivo T cell responses when injected subcutaneously to WT mice [2].
• In two different in vivo assays, Plexin C1(-/-) DC migration to lymph nodes (LNs) was lower than that of wild-type (WT) DC but this difference was not statistically significant [2].

Other interactions of Plxnc1

• We have done an extensive non-radioactive in situ hybridisation survey of Plxna1-a4, Plxnb1 -b3 and Plxnc1 in E14 mouse embryo [4].
• Structural characterization of the mouse high growth deletion and discovery of a novel fusion transcript between suppressor of cytokine signaling-2 (Socs-2) and viral encoded semaphorin receptor (Plexin C1) [5].

References