Disease relevance of Nrp2

• Npn-2 is required for the organization and fasciculation of several cranial nerves and spinal nerves [1].
• We also found that Sema3G binds Neuropilin-2, but not Neuropilin-1, and induces the repulsion of sympathetic axons, but not dorsal root ganglion axons, indicating that Sema3G utilizes Neuropilin-2 as a receptor to repel specific types of axons [2].
• The whole-animal distribution of 90Y-labeled anti-carcinoembryonic antigen monoclonal antibody NP-2 was evaluated by WBAR in nude mice bearing s.c. implants of GW-39 colon cancer and revealed antitumor uptake specifically as well as significant accumulation of 90Y in the bones [3].

High impact information on Nrp2

• Thus, Sema3A-Npn-1 and Sema3F-Npn-2 signaling control distinct steps of motor axon growth and guidance during the formation of spinal motor connections [4].
• In contrast, Sema3F-Npn-2 signaling guides the axons of a medial subset of LMC neurons to the ventral limb, but plays no major role in regulating their fasciculation [4].
• NrCAM, an immunoglobulin superfamily adhesion molecule of the L1 subfamily, associates with neuropilin-2 and is a component of a receptor complex for Sema3B and Sema3F [5].
• Thus, Npn-2 and candidate pheromone receptors play distinct and complementary roles in promoting the wiring and patterning of sensory neurons in the accessory olfactory system [6].
• Analysis of the vomeronasal nerve in neuropilin-2 (npn-2) mutant mice reveals pathfinding defects at multiple choice points [6].

Biological context of Nrp2

• Compared with littermate controls, mice deficient in Npn2 had significantly less ischemia-induced retinal NV and very little subretinal NV due to expression of a Vegf transgene [7].
• RESULTS: We examined the gene expression of Sema3A, Sema3C, Sema3F and their receptors, NP-1, NP-2 and plexin-A1 by in situ hybridization [8].

Anatomical context of Nrp2

• Homozygous Nrp2 mutants show absence or severe reduction of small lymphatic vessels and capillaries during development [9].
• Neuropilin-2 regulates the development of selective cranial and sensory nerves and hippocampal mossy fiber projections [10].
• Guidance of trunk neural crest migration requires neuropilin 2/semaphorin 3F signaling [11].
• These data show that Npn2/Sema3f signaling guides neural crest migration through the somite [11].
• Arteries, veins and larger, collecting lymphatic vessels developed normally, suggesting that neuropilin 2 is selectively required for the formation of small lymphatic vessels and capillaries [9].

Associations of Nrp2 with chemical compounds

• The gradients of Msx1 and Neuropilin-2 expression in basal cells and neurons, respectively, correlated with expression of a retinoic acid-synthesizing enzyme (RALDH2) in lamina propria [12].

Other interactions of Nrp2

• These results suggest that NRPs are early genes in embryonic vessel development and that both NP1 and NP2 are required [13].
• Targeting of both mouse neuropilin-1 and neuropilin-2 genes severely impairs developmental yolk sac and embryonic angiogenesis [13].
• Neuropilin-2 mutant mice exhibit profound and distinct effects on target innervation within the olfactory bulb [14].

Analytical, diagnostic and therapeutic context of Nrp2

• To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry [15].
• We generated a knock-out mutation in the neuropilin-2 gene by gene targeting in embryonic stem cells [14].

References