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Gene Review

PLXNB2  -  plexin B2

Homo sapiens

Synonyms: KIAA0315, MM1, Nbla00445, PLEXB2, Plexin-B2, ...
 
 
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Disease relevance of PLXNB2

 

Psychiatry related information on PLXNB2

 

High impact information on PLXNB2

  • CONCLUSIONS: Effective early noninvasive diagnosis of patency after thrombolysis is possible in patients treated > 3 hours after symptom onset by use of criteria derived from the relative increase over 90 minutes in plasma markers, particularly myoglobin, troponin T, and MM3/MM1 creatine kinase isoforms [6].
  • The expression pattern of MM1 was similar to normal PCs and MGUS, whereas MM4 was similar to MM cell lines [7].
  • Also, genes involved in DNA metabolism and cell cycle control were overexpressed in a comparison of MM1 and MM4 [7].
  • Here we show that plexin-B1 and plexin-B2 undergo proteolytic processing in their extracellular portion, thereby converting single-chain precursors into non-disulfide-linked, heterodimeric receptors [8].
  • Furthermore, 15 MN7-specific protein spots were localized after comparison with two-dimensional PAGE patterns from the conditioned medium of the nonosteogenic stromal cell lines MM1 and MV1 [9].
 

Chemical compound and disease context of PLXNB2

  • Moreover, we reported that palmitoyl-cyclic phosphatidic acid (Pal-cPA), a structural analogue of LPA, inhibits LPA-induced migration of MM1 cells and experimental metastasis of B16 murine melanoma cells [10].
  • A randomized study (WOS MM1) comparing the oral regime Z-Dex (idarubicin and dexamethasone) with vincristine, adriamycin and dexamethasone as induction therapy for newly diagnosed patients with multiple myeloma [11].
  • Among the glycosides tested, ginsenoside Rg3 was found to be a potent inhibitor of invasion by rat ascites hepatoma cells (MM1), B16FE7 melanoma cells, human small cell lung carcinoma (OC10), and human pancreatic adenocarcinoma (PSN-1) cells, when examined in a cell monolayer invasion model [12].
  • Carba derivatives, in which the phosphate oxygen was replaced with a methylene group at either the sn-2 or the sn-3 position, showed much more potent inhibitory effects on MM1 tumor cell transcellular migration and the pulmonary metastasis of B16-F0 melanoma than the natural pal-cPA [13].
 

Biological context of PLXNB2

 

Anatomical context of PLXNB2

  • Whereas low level expression was seen in kidney, esophagus, liver, lymph node, ovary and testis, none of the other tissues from a total of 18 different human organs showed any MM1 expression [1].
  • Using thin-film agarose gels and a rapid isoelectric focusing technique, we separated the MM isoforms into MM3 (skeletal muscle form), MM2, and MM1 (in vivo conversion forms) [16].
  • Although the coculture of the highly invasive clone (MM1) of AH130 cells and the mesothelial cell layer or endothelial cell layer in modified minimum essential medium supplemented with 10% FCS resulted in extensive penetration of the layer by the tumor cells, the omission of FCS resulted in an almost complete elimination of the in vitro invasion [17].
  • Although no VV1, VV2 or MV2 cases were included in our study, we suggest that stereotypic accumulation of PrP is a consistent pathologic feature of sCJD and that the spinal cord remains relatively resistant to the pathologic process of sCJD, at least in patients with MM1 sCJD [18].
  • To investigate the role of RhoA on the intracellular membrane dynamics of lysosomes in rat hepatoma cells (MM1), we analyzed the localization of lysosomal aspartic proteinase cathepsin D by confocal immunofluorescence microscopy in the dominant active RhoA-transfected cells [19].
 

Associations of PLXNB2 with chemical compounds

  • The addition of dibutyryl cAMP significantly abrogated LPA-induced invasion by MM1 cells and actin polymerization in the cells [20].
  • Fluvastatin and lovastatin inhibited LPA-induced MM1 cell invasion in a dose-dependent manner [21].
  • The theoretical docking studies showed that MM1 acts on the same site of the receptor as losartan [22].
  • However, EDTA stabilized the labile MM and MM1 sub-bands, which are the first to appear in the blood after the release from the damaged tissue and its addition to blood samples intended for determining the MM sub-band pattern is recommended [23].
  • The enzyme sequentially converts creatine kinase MM3 to MM2 and MM1 and hydrolyzes lysine and arginine from hippuryl-L-lysine and hippuryl-L-arginine [24].
 

Analytical, diagnostic and therapeutic context of PLXNB2

  • The detection of periodic sharp and slow wave complexes in the EEG is reliable in the clinical diagnosis of MM1 and MV1 patients only [25].
  • The median time to peak MM3/MM1 and total CK-MB activity was 2 and 8 h after reperfusion, respectively, returning to baseline values by 2 and 5 days, respectively [26].
  • Creatine kinase isoforms markers, including MB2 concentration, MB2/MB1 and MM3/MM1 ratios, and MT index (based on the "tissue" M subunits), were measured in serial specimens from 207 patients receiving thrombolytic therapy followed by acute angiography [27].
  • MM1 immunoreactivity in Western blotting involved bands in the range of M(r) 33-226 kDa, in both arterial and venous SM tissues [28].
  • However, immunoprecipitation experiments revealed that MM1 bound to a 100-kDa polypeptide that was present only in the arterial SM extract [28].

References

  1. Identification and partial sequence of a cDNA that is differentially expressed in human brain tumors. Shinoura, N., Shamraj, O.I., Hugenholz, H., Zhu, J.G., McBlack, P., Warnick, R., Tew, J.J., Wani, M.A., Menon, A.G. Cancer Lett. (1995) [Pubmed]
  2. Creatine kinase isoform analysis in the detection and assessment of thrombolysis in man. Puleo, P.R., Perryman, M.B., Bresser, M.A., Rokey, R., Pratt, C.M., Roberts, R. Circulation (1987) [Pubmed]
  3. Biological behavior of MM1 hamster melanoma. Stanberry, L.R., Das Gupta, T.K., Beattie, C.W. Cancer Res. (1982) [Pubmed]
  4. Effect of creatine kinase-MM subtype composition on a CK-MB immunoinhibition assay. Morison, I.M., Clayson, K.J., Fine, J.S. Clin. Chem. (1988) [Pubmed]
  5. Sporadic Creutzfeldt-Jakob disease with MM1-type prion protein and plaques. Puoti, G., Limido, L., Cotrufo, R., Di Fede, G., Tagliavini, F. Neurology (2004) [Pubmed]
  6. A study of biochemical markers of reperfusion early after thrombolysis for acute myocardial infarction. The PERM Study Group. Prospective Evaluation of Reperfusion Markers. Laperche, T., Steg, P.G., Dehoux, M., Benessiano, J., Grollier, G., Aliot, E., Mossard, J.M., Aubry, P., Coisne, D., Hanssen, M. Circulation (1995) [Pubmed]
  7. Global gene expression profiling of multiple myeloma, monoclonal gammopathy of undetermined significance, and normal bone marrow plasma cells. Zhan, F., Hardin, J., Kordsmeier, B., Bumm, K., Zheng, M., Tian, E., Sanderson, R., Yang, Y., Wilson, C., Zangari, M., Anaissie, E., Morris, C., Muwalla, F., van Rhee, F., Fassas, A., Crowley, J., Tricot, G., Barlogie, B., Shaughnessy, J. Blood (2002) [Pubmed]
  8. Functional regulation of semaphorin receptors by proprotein convertases. Artigiani, S., Barberis, D., Fazzari, P., Longati, P., Angelini, P., van de Loo, J.W., Comoglio, P.M., Tamagnone, L. J. Biol. Chem. (2003) [Pubmed]
  9. Characterization of the osteogenic stromal cell line MN7: identification of secreted MN7 proteins using two-dimensional polyacrylamide gel electrophoresis, western blotting, and microsequencing. Mathieu, E., Meheus, L., Raymackers, J., Merregaert, J. J. Bone Miner. Res. (1994) [Pubmed]
  10. Cyclic phosphatidic acid inhibits RhoA-mediated autophosphorylation of FAK at Tyr-397 and subsequent tumor-cell invasion. Mukai, M., Iwasaki, T., Tatsuta, M., Togawa, A., Nakamura, H., Murakami-Murofushi, K., Kobayashi, S., Imamura, F., Inoue, M. Int. J. Oncol. (2003) [Pubmed]
  11. A randomized study (WOS MM1) comparing the oral regime Z-Dex (idarubicin and dexamethasone) with vincristine, adriamycin and dexamethasone as induction therapy for newly diagnosed patients with multiple myeloma. Cook, G., Clark, R.E., Morris, T.C., Robertson, M., Lucie, N.P., Anderson, S., Paul, J., Franklin, I.M. Br. J. Haematol. (2004) [Pubmed]
  12. Inhibition of in vitro tumor cell invasion by ginsenoside Rg3. Shinkai, K., Akedo, H., Mukai, M., Imamura, F., Isoai, A., Kobayashi, M., Kitagawa, I. Jpn. J. Cancer Res. (1996) [Pubmed]
  13. Inhibition of transcellular tumor cell migration and metastasis by novel carba-derivatives of cyclic phosphatidic acid. Uchiyama, A., Mukai, M., Fujiwara, Y., Kobayashi, S., Kawai, N., Murofushi, H., Inoue, M., Enoki, S., Tanaka, Y., Niki, T., Kobayashi, T., Tigyi, G., Murakami-Murofushi, K. Biochim. Biophys. Acta (2007) [Pubmed]
  14. Lysogeny of Streptococcus pneumoniae with MM1 phage: improved adherence and other phenotypic changes. Loeffler, J.M., Fischetti, V.A. Infect. Immun. (2006) [Pubmed]
  15. Mesothelial differentiation as reflected by differential gene expression. Sun, X., Gulyás, M., Hjerpe, A. Am. J. Respir. Cell Mol. Biol. (2004) [Pubmed]
  16. Early detection of skeletal muscle injury by assay of creatine kinase MM isoforms in serum after acute exercise. Apple, F.S., Hellsten, Y., Clarkson, P.M. Clin. Chem. (1988) [Pubmed]
  17. Serum requirement for in vitro invasion by tumor cells. Imamura, F., Horai, T., Mukai, M., Shinkai, K., Akedo, H. Jpn. J. Cancer Res. (1991) [Pubmed]
  18. Neuropathologic characteristics of spinal cord lesions in sporadic Creutzfeldt-Jakob disease. Iwasaki, Y., Yoshida, M., Hashizume, Y., Kitamoto, T., Sobue, G. Acta Neuropathol. (2005) [Pubmed]
  19. Small guanosine triphosphatase Rho/Rho-associated kinase as a novel regulator of intracellular redistribution of lysosomes in invasive tumor cells. Nishimura, Y., Itoh, K., Yoshioka, K., Uehata, M., Himeno, M. Cell Tissue Res. (2000) [Pubmed]
  20. Inhibition of tumor invasion and metastasis by a novel lysophosphatidic acid (cyclic LPA). Mukai, M., Imamura, F., Ayaki, M., Shinkai, K., Iwasaki, T., Murakami-Murofushi, K., Murofushi, H., Kobayashi, S., Yamamoto, T., Nakamura, H., Akedo, H. Int. J. Cancer (1999) [Pubmed]
  21. Inhibition of lysophosphatidic acid-induced RhoA activation and tumor cell invasion by 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors. Kusama, T., Mukai, M., Ayaki, M., Imamura, F., Tatsuta, M., Matsumoto, Y., Nakamura, H., Inoue, M. Int. J. Oncol. (2003) [Pubmed]
  22. Synthesis, binding studies and in vivo biological evaluation of novel non-peptide antihypertensive analogues. Mavromoustakos, T., Moutevelis-Minakakis, P., Kokotos, C.G., Kontogianni, P., Politi, A., Zoumpoulakis, P., Findlay, J., Cox, A., Balmforth, A., Zoga, A., Iliodromitis, E. Bioorg. Med. Chem. (2006) [Pubmed]
  23. The protection of creatine kinase MM sub-bands by EDTA during storage. Chapelle, J.P., Bertrand, A., Heusghem, C. Clin. Chim. Acta (1981) [Pubmed]
  24. Isolation and purification of creatine kinase conversion factor from human serum and its identification as carboxypeptidase N. Michelutti, L., Falter, H., Certossi, S., Marcotte, B., Mazzuchin, A. Clin. Biochem. (1987) [Pubmed]
  25. Current clinical diagnosis in Creutzfeldt-Jakob disease: identification of uncommon variants. Zerr, I., Schulz-Schaeffer, W.J., Giese, A., Bodemer, M., Schröter, A., Henkel, K., Tschampa, H.J., Windl, O., Pfahlberg, A., Steinhoff, B.J., Gefeller, O., Kretzschmar, H.A., Poser, S. Ann. Neurol. (2000) [Pubmed]
  26. Creatine kinase MB isoforms: sensitive markers of ischemic myocardial damage. Hossein-Nia, M., Kallis, P., Brown, P.A., Chester, M.R., Kaski, J.C., Murday, A.J., Treasure, T., Holt, D.W. Clin. Chem. (1994) [Pubmed]
  27. Creatine kinase MM and MB isoforms in patients receiving thrombolytic therapy and acute angiography. TAMI Study Group. Christenson, R.H., Ohman, E.M., Topol, E.J., O'Hanesian, M.A., Sigmon, K.N., Duh, S.H., Kereiakes, D., Worley, S.J., George, B.S., Pizzo, C.K. Clin. Chem. (1995) [Pubmed]
  28. Differential availability/processing of decorin precursor in arterial and venous smooth muscle cells. Franch, R., Chiavegato, A., Maraschin, M., Candeo, S., Ausoni, S., Villa, A., Gerosa, G., Gasparotto, L., Parnigotto, P., Sartore, S. J. Anat. (2006) [Pubmed]
 
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