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Gene Review

PLXNA1  -  plexin A1

Homo sapiens

Synonyms: NOV, NOVP, PLEXIN-A1, PLXN1, Plexin-A1, ...
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Disease relevance of PLXNA1


High impact information on PLXNA1

  • In our study we observed eight male HD patients who were treated with NOVP (Novanthrone, Oncovin, Vinblastine, Prednisone) chemotherapy [5].
  • Winberg et al. present evidence that the transmembrane protein Off-track (OTK) interacts biochemically and genetically with Plexin A and is important for Sema 1a repulsive signaling [6].
  • Northern blot analysis revealed different expression of the SEX family of genes in fetal tissues, with SEX, OCT, and NOV predominantly expressed in brain, and SEP expressed at highest levels in kidney [7].
  • Reducing SEMA3A or NP1 expression by RNA interference or inhibiting plexin-A1 signaling enhanced migration [8].
  • Conversely, expression of constitutively active plexin-A1 impaired chemotaxis [8].

Chemical compound and disease context of PLXNA1

  • PURPOSE: Because the effects of mitoxantrone on human male fertility were unknown, we determined prospectively the effects of three courses of mitoxantrone (Novantrone), vincristine (Oncovin), vinblastine, prednisone (NOVP) chemotherapy on the potential for fertility of men with Hodgkin's disease (HD) [9].
  • To better define the importance of the GS in predicting treatment results in a group of patients treated with uniform therapy, we performed GS prior to treatment in 46 patients with pathologically or clinically staged I-III Hodgkin's disease who received three cycles of NOVP (Novantrone, vincristine, vinblastine, prednisone) followed by XRT [10].
  • NOVP has also been reported to produce limited toxicity in this trial and should be considered as an alternative to MOPP or doxorubicin-containing regimens in treatment of patients with early-staged disease and LMA greater than 10 cm [11].

Biological context of PLXNA1

  • We have analyzed the expression of Neuropilin-1, Plexin-A1, and Semaphorin 3A in the above-mentioned tissues on the hypothesis that these molecules could regulate innervation in these organs during gestation [12].
  • This chapter describes the optimization of this assay and outlines the subtle differences required to enable Sema3A-Fc and Sema4D-Fc to induce identical collapse phenotypes in COS cells expressing Plexin-A1 and neuropilin-1, or Plexin-B1, respectively [13].
  • Using an in vivo model of microglia activation by striatal injection of lipopolysaccharide demonstrated a corresponding upregulation of Plexin-A1 and Neuropilin-1 in activated microglia and enhanced production of Sema3A by stressed adult neurons [14].
  • Plexin-A1 can function as a signal transducing subunit for the neuronal neuropilin receptor, and its gene is located in the linkage interval for hereditary congenital facial paresis at chromosome 3q21-q22 (MIM601471), making it an excellent candidate gene for this disorder [2].
  • We therefore conclude that it is highly unlikely that Plexin-A1 is involved in the pathogenicity of hereditary congenital facial paresis [2].

Anatomical context of PLXNA1

  • Sema3A/Plexin-A1-induced growth cone collapse, for example, requires Rac activity, which is a surprising result given that this GTPase is usually associated with membrane protrusions [15].
  • We show here that Sema3A-induced collapse of COS-7 cells expressing Plexin-A1 also requires Rac but not Rho activity and that the cytoplasmic tail of Plexin-A1 interacts directly with activated Rac [15].
  • RanBPM has the potential to link Plexin-A receptors to retrograde transport and microtubule function in axonal guidance [16].
  • During mouse embryogenesis, the murine ortholog of plexin-A1 gene showed restricted spatial and temporal expression in the hindbrain, consistent with a role in cell body movement, or axonal guidance during facial nerve development [2].
  • Differentiated podocytes expressed 2-4-fold higher plexin A1, A2, and A3 mRNA levels than undifferentiated podocytes [17].

Associations of PLXNA1 with chemical compounds


Regulatory relationships of PLXNA1

  • Recruitment of active Rnd1 is sufficient to trigger signaling by Plexin-A1, even in the absence of Sema3A, and initiates cytoskeletal collapse by activating its cytoplasmic domain [20].

Other interactions of PLXNA1

  • Thus, the antagonism of two GTPases regulates the activity of the Sema3A receptor, and activation by Rnd1 appears to be an essential step in signaling by Plexin-A1 [20].
  • CIITA also regulates the gene expression of plexna-1, which encodes a semaphorin receptor, plexin-A1, that might be involved in the interaction with T-cells through an unknown ligand for plexin-A1 [21].
  • Reducing plexin-A1 expression with shRNA greatly reduced actin polarization as well as Rho activation without affecting Rac or Cdc42 activation [22].

Analytical, diagnostic and therapeutic context of PLXNA1


  1. Human malignant glioma cells express semaphorins and their receptors, neuropilins and plexins. Rieger, J., Wick, W., Weller, M. Glia (2003) [Pubmed]
  2. Nucleotide variation analysis does not support a causal role for plexin-A1 in hereditary congenital facial paresis. van der Zwaag, B., Burbach, J.P., Brunner, H.G., van Bokhoven, H., Padberg, G.W. Brain Res. Dev. Brain Res. (2005) [Pubmed]
  3. NOVP chemotherapy for Hodgkin's disease transiently induces sperm aneuploidies associated with the major clinical aneuploidy syndromes involving chromosomes X, Y, 18, and 21. Frias, S., Van Hummelen, P., Meistrich, M.L., Lowe, X.R., Hagemeister, F.B., Shelby, M.D., Bishop, J.B., Wyrobek, A.J. Cancer Res. (2003) [Pubmed]
  4. NOVP: a novel chemotherapeutic regimen with minimal toxicity for treatment of Hodgkin's disease. Hagemeister, F.B., Cabanillas, F., Velásquez, W.S., Meistrich, M.L., Liang, J.C., McLaughlin, P., Redman, J.R., Romaguera, J.E., Rodríguez, M.A., Swan, F. Semin. Oncol. (1990) [Pubmed]
  5. Chemotherapy induces transient sex chromosomal and autosomal aneuploidy in human sperm. Robbins, W.A., Meistrich, M.L., Moore, D., Hagemeister, F.B., Weier, H.U., Cassel, M.J., Wilson, G., Eskenazi, B., Wyrobek, A.J. Nat. Genet. (1997) [Pubmed]
  6. Plexin signaling via off-track and rho family GTPases. Whitford, K.L., Ghosh, A. Neuron (2001) [Pubmed]
  7. A family of transmembrane proteins with homology to the MET-hepatocyte growth factor receptor. Maestrini, E., Tamagnone, L., Longati, P., Cremona, O., Gulisano, M., Bione, S., Tamanini, F., Neel, B.G., Toniolo, D., Comoglio, P.M. Proc. Natl. Acad. Sci. U.S.A. (1996) [Pubmed]
  8. Competing autocrine pathways involving alternative neuropilin-1 ligands regulate chemotaxis of carcinoma cells. Bachelder, R.E., Lipscomb, E.A., Lin, X., Wendt, M.A., Chadborn, N.H., Eickholt, B.J., Mercurio, A.M. Cancer Res. (2003) [Pubmed]
  9. Rapid recovery of spermatogenesis after mitoxantrone, vincristine, vinblastine, and prednisone chemotherapy for Hodgkin's disease. Meistrich, M.L., Wilson, G., Mathur, K., Fuller, L.M., Rodriguez, M.A., McLaughlin, P., Romaguera, J.E., Cabanillas, F.F., Ha, C.S., Lipshultz, L.I., Hagemeister, F.B. J. Clin. Oncol. (1997) [Pubmed]
  10. The gallium scan predicts relapse in patients with Hodgkin's disease treated with combined modality therapy. Hagemeister, F.B., Purugganan, R., Podoloff, D.A., Hess, M., Rodriguez, M.A., McLaughlin, P., Swan, F., Romaguera, J.E., Cabanillas, F. Ann. Oncol. (1994) [Pubmed]
  11. Hodgkin's disease with a mediastinal mass greater than 10 cm: results of four different treatment approaches. Preti, A., Hagemeister, F.B., McLaughlin, P., Swan, F., Rodriguez, A., Besa, P., Cox, J.D., Allen, P.K., Cabanillas, F. Ann. Oncol. (1994) [Pubmed]
  12. Restricted innervation of uterus and placenta during pregnancy: evidence for a role of the repelling signal Semaphorin 3A. Marzioni, D., Tamagnone, L., Capparuccia, L., Marchini, C., Amici, A., Todros, T., Bischof, P., Neidhart, S., Grenningloh, G., Castellucci, M. Dev. Dyn. (2004) [Pubmed]
  13. Plexin-induced collapse assay in COS cells. Turner, L.J., Hall, A. Meth. Enzymol. (2006) [Pubmed]
  14. A novel role for Sema3A in neuroprotection from injury mediated by activated microglia. Majed, H.H., Chandran, S., Niclou, S.P., Nicholas, R.S., Wilkins, A., Wing, M.G., Rhodes, K.E., Spillantini, M.G., Compston, A. J. Neurosci. (2006) [Pubmed]
  15. The activity of the plexin-A1 receptor is regulated by Rac. Turner, L.J., Nicholls, S., Hall, A. J. Biol. Chem. (2004) [Pubmed]
  16. RanBPM contributes to Semaphorin3A signaling through plexin-A receptors. Togashi, H., Schmidt, E.F., Strittmatter, S.M. J. Neurosci. (2006) [Pubmed]
  17. Autocrine class 3 semaphorin system regulates slit diaphragm proteins and podocyte survival. Guan, F., Villegas, G., Teichman, J., Mundel, P., Tufro, A. Kidney Int. (2006) [Pubmed]
  18. Recovery of sperm production following radiation therapy for Hodgkin's disease after induction chemotherapy with mitoxantrone, vincristine, vinblastine, and prednisone (NOVP). Dubey, P., Wilson, G., Mathur, K.K., Hagemeister, F.B., Fuller, L.M., Ha, C.S., Cox, J.D., Meistrich, M.L. Int. J. Radiat. Oncol. Biol. Phys. (2000) [Pubmed]
  19. A new chemotherapy regimen for treatment of Hodgkin's disease associated with minimal genotoxicity. Liang, J.C., Bailey, N.M., Gabriel, G.J., Kattan, M.W., Wang, R.Y., Hagemeister, F.B., Cabanillas, F.F., Fuller, L.M. Leuk. Lymphoma (1993) [Pubmed]
  20. Antagonistic effects of Rnd1 and RhoD GTPases regulate receptor activity in Semaphorin 3A-induced cytoskeletal collapse. Zanata, S.M., Hovatta, I., Rohm, B., Püschel, A.W. J. Neurosci. (2002) [Pubmed]
  21. Antigen recognition and presentation by dendritic cells. Inaba, K., Inaba, M. Int. J. Hematol. (2005) [Pubmed]
  22. Cutting edge: rho activation and actin polarization are dependent on plexin-A1 in dendritic cells. Eun, S.Y., O'connor, B.P., Wong, A.W., van Deventer, H.W., Taxman, D.J., Reed, W., Li, P., Blum, J.S., McKinnon, K.P., Ting, J.P. J. Immunol. (2006) [Pubmed]
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