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Gene Review

PRB3  -  proline-rich protein BstNI subfamily 3

Homo sapiens

Synonyms: Basic salivary proline-rich protein 3, G1, PRG, Parotid salivary glycoprotein G1, Proline-rich protein G1
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Disease relevance of PRB3


High impact information on PRB3

  • Previous results have demonstrated that AT cells are defective in the G1/S checkpoint activated after radiation damage and that this defect is attributable to a defective p53 signal transduction pathway [6].
  • Saccharomyces cerevisiae cells treated with rapamycin irreversibly arrested in the G1 phase of the cell cycle [7].
  • The resulting lymphoblastoid cell line has secreted immunoglobulin G1 of the kappa type continuously for 2 years [8].
  • Increased cytokine secretion was specifically inhibited by G1, an anti-P-selectin mAb that prevents P-selectin from binding to its ligand (P-selectin glycoprotein ligand-1) on myeloid cells [9].
  • Thus, the progression of resting B lymphocytes into the G1 phase of the cell cycle can be reconstituted in the absence of virus by the cooperation of two of the six viral genes required for immortalization [2].

Chemical compound and disease context of PRB3


Biological context of PRB3

  • The amino terminus contained repeating sequences of Ser-Gln-Gly-Pro-Pro-Pro-Arg-Pro-Gly-Lys-Pro-Glu-Gly-Pro-Pro-Pro- Gln-Gly that had significant compositional and sequence homology to that encoded by exon 3 of the PRB3 gene [14].
  • This C nucleotide insertion leads to a frameshift with a premature termination codon that probably results in markedly reduced or absent PRB3 gene expression [1].
  • The four exons, including splice junctions, for both PRB3 alleles of this subject were completely sequenced [1].
  • The amino acid sequence G(1)-P(2)-P(3)-P(4)-H(5)-P(6)-G(7)-K(8)-P(9) occurs twice in the proline-rich glycoprotein (PRG) found in human parotid saliva [15].
  • Each of these two amino acid changes reduced the beta G1 activity of the corresponding mutant beta G1 expressed following transfection of COS cells with expression vectors harboring the mutated cDNAs [4].

Anatomical context of PRB3

  • Together, these results suggest that this subject does not express the PRB3 gene and that one of the consequences is an altered ability to interact with a bacterium known to colonize the oral cavity [1].
  • Mechanisms for this chemoprevention are previously linked to all-trans retinoic acid (RA) signaling growth inhibition at G1 in carcinogen-exposed immortalized human bronchial epithelial cells [16].
  • Mutated cDNA clones, including the entire coding sequence, were isolated using the polymerase chain reaction (PCR) products derived from beta G1-deficient fibroblasts [4].
  • In contrast, expression in proliferating embryonic peripheral nervous system cells occurs during interphase as a brief pulse that initiates before and overlaps with S phase, demonstrating the presence of a G1 phase in these embryonic neural cell cycles [17].
  • G1, G2, and G4 co-immunoprecipitated with G5, and G4 co-immunoprecipitated with G8, but the putative dimers were retained in the endoplasmic reticulum (ER) [18].

Associations of PRB3 with chemical compounds

  • Alleles at the PRB3 locus coding for a disulfide-bonded human salivary proline-rich glycoprotein (Gl 8) and a null in an Ashkenazi Jew [19].
  • (formula; see text) To understand the structural basis of F. nucleatum binding, we screened glycolipids and neoglycolipids carrying carbohydrate structures related to those of the PRG for receptor activity; components with unsubstituted terminal lactosamine residues best supported adherence [14].
  • Amino acid analysis of the protein core showed predominantly proline, glycine, and glutamic acid/glutamine, a characteristic of proline-rich glycoproteins (PRG) [14].
  • Since proline is the major amino acid present in native PRG, these localized conformations may contribute to PRG's global conformation and act as a primary force in determining its biological activities [20].
  • Exchange lifetime data and previously reported hydrogen----deuterium exchange experiments suggest that the PRG histidine N tau H protons are not involved in hydrogen-bonds [21].

Analytical, diagnostic and therapeutic context of PRB3


  1. PRB3 null mutations result in absence of the proline-rich glycoprotein Gl and abolish Fusobacterium nucleatum interactions with saliva in vitro. Azen, E., Prakobphol, A., Fisher, S.J. Infect. Immun. (1993) [Pubmed]
  2. EBNA-2 and EBNA-LP cooperate to cause G0 to G1 transition during immortalization of resting human B lymphocytes by Epstein-Barr virus. Sinclair, A.J., Palmero, I., Peters, G., Farrell, P.J. EMBO J. (1994) [Pubmed]
  3. Altered regulation of G1 cyclins in senescent human diploid fibroblasts: accumulation of inactive cyclin E-Cdk2 and cyclin D1-Cdk2 complexes. Dulić, V., Drullinger, L.F., Lees, E., Reed, S.I., Stein, G.H. Proc. Natl. Acad. Sci. U.S.A. (1993) [Pubmed]
  4. Mucopolysaccharidosis type VII: characterization of mutations and molecular heterogeneity. Tomatsu, S., Fukuda, S., Sukegawa, K., Ikedo, Y., Yamada, S., Yamada, Y., Sasaki, T., Okamoto, H., Kuwahara, T., Yamaguchi, S. Am. J. Hum. Genet. (1991) [Pubmed]
  5. Immunoscintigraphy of human mammary carcinoma xenografts using monoclonal antibodies 12H12 and BM-2 labeled with 99mTc and radioiodine. Brümmendorf, T.H., Kaul, S., Schuhmacher, J., Baum, R.P., Matys, R., Klivényi, G., Adams, S., Bastert, G. Cancer Res. (1994) [Pubmed]
  6. ATM associates with and phosphorylates p53: mapping the region of interaction. Khanna, K.K., Keating, K.E., Kozlov, S., Scott, S., Gatei, M., Hobson, K., Taya, Y., Gabrielli, B., Chan, D., Lees-Miller, S.P., Lavin, M.F. Nat. Genet. (1998) [Pubmed]
  7. Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast. Heitman, J., Movva, N.R., Hall, M.N. Science (1991) [Pubmed]
  8. Herpes simplex virus glycoprotein D: human monoclonal antibody produced by bone marrow cell line. Seigneurin, J.M., Desgranges, C., Seigneurin, D., Paire, J., Renversez, J.C., Jacquemont, B., Micouin, C. Science (1983) [Pubmed]
  9. Monocyte tethering by P-selectin regulates monocyte chemotactic protein-1 and tumor necrosis factor-alpha secretion. Signal integration and NF-kappa B translocation. Weyrich, A.S., McIntyre, T.M., McEver, R.P., Prescott, S.M., Zimmerman, G.A. J. Clin. Invest. (1995) [Pubmed]
  10. Complete nucleotide sequence of the M RNA segment of Andes virus and analysis of the variability of the termini of the virus S, M and L RNA segments. Padula, P.J., Sanchez, A.J., Edelstein, A., Nichol, S.T. J. Gen. Virol. (2002) [Pubmed]
  11. Valproic acid suppresses G1 phase-dependent sialylation of a 65kDa glycoprotein in the C6 glioma cell cycle. Bacon, C.L., O'Driscoll, E., Regan, C.M. Int. J. Dev. Neurosci. (1997) [Pubmed]
  12. Bufalin induces apoptosis and the G0/G1 cell cycle arrest of endometriotic stromal cells: a promising agent for the treatment of endometriosis. Nasu, K., Nishida, M., Ueda, T., Takai, N., Bing, S., Narahara, H., Miyakawa, I. Mol. Hum. Reprod. (2005) [Pubmed]
  13. P-glycoprotein expression is induced in human pancreatic cancer xenografts during treatment with a cell cycle regulator, mimosine. Zalatnai, A. Pathol. Oncol. Res. (2005) [Pubmed]
  14. Structure and bacterial receptor activity of a human salivary proline-rich glycoprotein. Gillece-Castro, B.L., Prakobphol, A., Burlingame, A.L., Leffler, H., Fisher, S.J. J. Biol. Chem. (1991) [Pubmed]
  15. N.m.r. and computer-simulated conformational analyses of a nonapeptide found in a human salivary proline-rich glycoprotein. Loomis, R.E., Tseng, C.C., Bergey, E.J., Levine, M.J. Int. J. Pept. Protein Res. (1988) [Pubmed]
  16. Posttranslational regulation of cyclin D1 by retinoic acid: a chemoprevention mechanism. Langenfeld, J., Kiyokawa, H., Sekula, D., Boyle, J., Dmitrovsky, E. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  17. A Drosophila G1-specific cyclin E homolog exhibits different modes of expression during embryogenesis. Richardson, H.E., O'Keefe, L.V., Reed, S.I., Saint, R. Development (1993) [Pubmed]
  18. ABCG5 and ABCG8 are obligate heterodimers for protein trafficking and biliary cholesterol excretion. Graf, G.A., Yu, L., Li, W.P., Gerard, R., Tuma, P.L., Cohen, J.C., Hobbs, H.H. J. Biol. Chem. (2003) [Pubmed]
  19. Alleles at the PRB3 locus coding for a disulfide-bonded human salivary proline-rich glycoprotein (Gl 8) and a null in an Ashkenazi Jew. Azen, E.A., Minaguchi, K., Latreille, P., Kim, H.S. Am. J. Hum. Genet. (1990) [Pubmed]
  20. Investigation of cis/trans proline isomerism in a multiply occurring peptide fragment from human salivary proline-rich glycoprotein. Loomis, R.E., Gonzalez, M., Loomis, P.M. Int. J. Pept. Protein Res. (1991) [Pubmed]
  21. N.m.r. analyses of the histidine microenvironments in a human salivary proline-rich glycoprotein. Loomis, R.E., Tseng, C.C., Levine, M.J. Int. J. Pept. Protein Res. (1988) [Pubmed]
  22. Occurrence and significance of D-methotrexate as a contaminant of commercial methotrexate. Cramer, S.M., Schornagel, J.H., Kalghatgi, K.K., Bertino, J.R., Horváth, C. Cancer Res. (1984) [Pubmed]
  23. A new C-type cyclin-dependent kinase from tomato expressed in dividing tissues does not interact with mitotic and G1 cyclins. Joubès, J., Lemaire-Chamley, M., Delmas, F., Walter, J., Hernould, M., Mouras, A., Raymond, P., Chevalier, C. Plant Physiol. (2001) [Pubmed]
  24. p53-dependent apoptosis in melanoma cells after treatment with camptothecin. Li, G., Bush, J.A., Ho, V.C. J. Invest. Dermatol. (2000) [Pubmed]
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