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NOG  -  noggin

Homo sapiens

 
 
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Disease relevance of NOG

 

High impact information on NOG

  • Heterozygous mutations in the gene encoding noggin affect human joint morphogenesis [6].
  • noggin is expressed in the Spemann organizer region of the Xenopus embryo and can promote dorsal cell fates within the mesoderm and neural development within the overlying ectoderm [7].
  • Here, we show that noggin promotes ventral development in Drosophila, specifying ventral ectoderm and CNS in the absence of all endogenous ventral-specific zygotic gene expression [7].
  • They are the components of the Spemann organizer, noggin, chordin, and follistatin, members of the Dan/Cerberus family, and twisted gastrulation [8].
  • Ruiz i Altaba describes a possible model for anteroposterior patterning involving ;lanar signals for amphibian, avian and mammalian embryos, compares the axial patterning of the neural plate with the patterning of insect epithelia, and discussed possible roles of noggin, follistatin and hedgehog-related genes in neural induction and patterning [9].
 

Chemical compound and disease context of NOG

  • In nonobese diabetic/severe combined immunodeficient (NOD/SCID)/gammacnull (NOG) mice, ritonavir very efficiently prevented tumor growth and leukemic infiltration in various organs of NOG mice at the same dose used for treatment of patients with AIDS [10].
  • When a novel spirodiketopiperazine-containing CCR5 inhibitor, AK602/ONO4128/GW873140 (molecular weight, 614), was administered to the NOG mice 1 day after R5 HIV-1 inoculation, the replication and cytopathic effects of R5 HIV-1 were significantly suppressed [11].
 

Biological context of NOG

  • A recent case report described a heterozygous 42-bp deletion in the protein-coding region of the noggin gene in a patient with FOP [12].
  • Among the samples analyzed by SSCP and DNA sequencing was an independently obtained DNA sample from the identical FOP patient previously described with the 42-bp noggin deletion; no mutation was detected [12].
  • Examination of the DNA sequences of 20 cloned noggin PCR products, undertaken to evaluate the possibility of a somatic mutation in the noggin gene which could be carried by a small subset of white blood cells, also failed to detect the presence of the reported 42-bp deletion [12].
  • RESULTS: Three different missense mutations in NOG were found [13].
  • The disease is caused by mutations of the NOG gene, that maps to chromosome 17q22 [14].
 

Anatomical context of NOG

 

Associations of NOG with chemical compounds

  • This new mutation is a guanine to adenine change at nucleotide 283 (283G --> A) of the NOG gene, and is transmitted in the family (in the heterozygote form) by the affected mother to her two affected children [20].
  • Although statins increased BMP-2 expression, the proapoptotic effect of statins was not prevented by the BMP antagonist noggin, and was abolished by mevalonate and geranylgeranylpyrophosphate, suggesting the involvement of defective protein geranylgeranylation [21].
  • Growth factor activity is regulated by binding proteins, and we previously showed that BMPs induce noggin, a glycoprotein that binds and blocks BMP action [22].
  • Dexamethasone treatment, like BMP treatment, also increased expression of the BMP-binding protein noggin [23].
  • The addition of noggin inhibited VPA-induced potentiation of osteogenic differentiation [24].
 

Regulatory relationships of NOG

  • Functional assays indicate that glial-induced dendritic growth is significantly reduced by BMP7 antibodies and completely inhibited by exogenous noggin and follistatin [25].
  • Transfection of C4-2B cells with VEGF partially rescued the C4-2B CM-induced pro-osteoblastic activity from noggin inhibition [26].
  • Mutations in the GDF inhibitor Noggin (NOG) or activating mutations in GDF5 cause proximal symphalangism (SYM1) [27].
  • Here it is reported that in animal cap explants of the amphibian Pleurodeles waltl, noggin can induce upregulation of a FOS-related protein in a calcium-dependent manner [28].
 

Other interactions of NOG

  • We conclude that mutations in the coding region of noggin are not associated with FOP [12].
  • A powerful antagonist of BMP4 is the secreted polypeptide noggin [12].
  • However, addition of ganglionic glia to cultured sympathetic neurons causes a marked increase in BMP proteins coincident with a significant decrease in follistatin and noggin [25].
  • Both noggin alone and anti-VEGF antibody alone diminished C4-2B CM-induced pro-osteoblastic activity [26].
  • The incubation of BVSMCs with noggin, an inhibitor of BMP, decreased RUNX2 expression [29].
 

Analytical, diagnostic and therapeutic context of NOG

  • Thus, the hNOG mice mirror human systemic HIV infection by developing specific antibodies, suggesting that they may have potential as an HIV/AIDS animal model for the study of HIV pathogenesis and immune responses [5].
  • In the present study, we used human recombinant noggin protein to determine whether endogenous BMP-2/4 triggers neuronal differentiation in dissociated cell culture [30].
  • We have also determined a role in postimplantation development of two transcripts identified in a differential display RT-PCR screen of genes induced in ES cells by noggin exposure, Aggf1 and an Est (GenBank AK008955) [31].
  • The paper concludes with recent research on the use of ex vivo and in vivo gene delivery strategies via gene therapy vectors encoding growth promoting and inhibiting molecules (PDGF, BMP, noggin and others) to regenerate periodontal structures including bone, periodontal ligament and cementum [32].
  • The CD19+CD5- BM cells showed to express CD5 after the coculture with NOG spleen cells [33].

References

  1. Autosomal dominant stapes ankylosis with broad thumbs and toes, hyperopia, and skeletal anomalies is caused by heterozygous nonsense and frameshift mutations in NOG, the gene encoding noggin. Brown, D.J., Kim, T.B., Petty, E.M., Downs, C.A., Martin, D.M., Strouse, P.J., Moroi, S.E., Milunsky, J.M., Lesperance, M.M. Am. J. Hum. Genet. (2002) [Pubmed]
  2. Mutations of the NOG gene in individuals with proximal symphalangism and multiple synostosis syndrome. Takahashi, T., Takahashi, I., Komatsu, M., Sawaishi, Y., Higashi, K., Nishimura, G., Saito, H., Takada, G. Clin. Genet. (2001) [Pubmed]
  3. Establishment of a myeloid leukemia cell line, TRL-01, with MLL-ENL fusion gene. Ninomiya, M., Abe, A., Yokozawa, T., Ozeki, K., Yamamoto, K., Ito, M., Ito, M., Kiyoi, H., Emi, N., Naoe, T. Cancer Genet. Cytogenet. (2006) [Pubmed]
  4. Characterization of a stapes ankylosis family with a NOG mutation. Brown, D.J., Kim, T.B., Petty, E.M., Downs, C.A., Martin, D.M., Strouse, P.J., Moroi, S.E., Gebarski, S.S., Lesperance, M.M. Otol. Neurotol. (2003) [Pubmed]
  5. Hematopoietic stem cell-engrafted NOD/SCID/IL2R{gamma}null mice develop human lymphoid systems and induce long-lasting HIV-1 infection with specific humoral immune responses. Watanabe, S., Terashima, K., Ohta, S., Horibata, S., Yajima, M., Shiozawa, Y., Dewan, M.Z., Yu, Z., Ito, M., Morio, T., Shimizu, N., Honda, M., Yamamoto, N. Blood (2007) [Pubmed]
  6. Heterozygous mutations in the gene encoding noggin affect human joint morphogenesis. Gong, Y., Krakow, D., Marcelino, J., Wilkin, D., Chitayat, D., Babul-Hirji, R., Hudgins, L., Cremers, C.W., Cremers, F.P., Brunner, H.G., Reinker, K., Rimoin, D.L., Cohn, D.H., Goodman, F.R., Reardon, W., Patton, M., Francomano, C.A., Warman, M.L. Nat. Genet. (1999) [Pubmed]
  7. The Xenopus dorsalizing factor noggin ventralizes Drosophila embryos by preventing DPP from activating its receptor. Holley, S.A., Neul, J.L., Attisano, L., Wrana, J.L., Sasai, Y., O'Connor, M.B., De Robertis, E.M., Ferguson, E.L. Cell (1996) [Pubmed]
  8. Bone morphogenetic proteins, their antagonists, and the skeleton. Canalis, E., Economides, A.N., Gazzerro, E. Endocr. Rev. (2003) [Pubmed]
  9. Pattern formation in the vertebrate neural plate. Ruiz i Altaba, A. Trends Neurosci. (1994) [Pubmed]
  10. Efficient intervention of growth and infiltration of primary adult T-cell leukemia cells by an HIV protease inhibitor, ritonavir. Dewan, M.Z., Uchihara, J.N., Terashima, K., Honda, M., Sata, T., Ito, M., Fujii, N., Uozumi, K., Tsukasaki, K., Tomonaga, M., Kubuki, Y., Okayama, A., Toi, M., Mori, N., Yamamoto, N. Blood (2006) [Pubmed]
  11. Potent anti-R5 human immunodeficiency virus type 1 effects of a CCR5 antagonist, AK602/ONO4128/GW873140, in a novel human peripheral blood mononuclear cell nonobese diabetic-SCID, interleukin-2 receptor gamma-chain-knocked-out AIDS mouse model. Nakata, H., Maeda, K., Miyakawa, T., Shibayama, S., Matsuo, M., Takaoka, Y., Ito, M., Koyanagi, Y., Mitsuya, H. J. Virol. (2005) [Pubmed]
  12. Linkage exclusion and mutational analysis of the noggin gene in patients with fibrodysplasia ossificans progressiva (FOP). Xu, M.Q., Feldman, G., Le Merrer, M., Shugart, Y.Y., Glaser, D.L., Urtizberea, J.A., Fardeau, M., Connor, J.M., Triffitt, J., Smith, R., Shore, E.M., Kaplan, F.S. Clin. Genet. (2000) [Pubmed]
  13. Identical mutations in NOG can cause either tarsal/carpal coalition syndrome or proximal symphalangism. Dixon, M.E., Armstrong, P., Stevens, D.B., Bamshad, M. Genet. Med. (2001) [Pubmed]
  14. Identification of a novel NOG gene mutation (P35S) in an Italian family with symphalangism. Mangino, M., Flex, E., Digilio, M.C., Giannotti, A., Dallapiccola, B. Hum. Mutat. (2002) [Pubmed]
  15. Paresis of a bone morphogenetic protein-antagonist response in a genetic disorder of heterotopic skeletogenesis. Ahn, J., Serrano de la Pena, L., Shore, E.M., Kaplan, F.S. The Journal of bone and joint surgery. American volume. (2003) [Pubmed]
  16. Human disease-causing NOG missense mutations: effects on noggin secretion, dimer formation, and bone morphogenetic protein binding. Marcelino, J., Sciortino, C.M., Romero, M.F., Ulatowski, L.M., Ballock, R.T., Economides, A.N., Eimon, P.M., Harland, R.M., Warman, M.L. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  17. Differential gene expression and regulation of the bone morphogenetic protein antagonists follistatin and gremlin in normal and osteoarthritic human chondrocytes and synovial fibroblasts. Tardif, G., Hum, D., Pelletier, J.P., Boileau, C., Ranger, P., Martel-Pelletier, J. Arthritis Rheum. (2004) [Pubmed]
  18. Myricetin induces human osteoblast differentiation through bone morphogenetic protein-2/p38 mitogen-activated protein kinase pathway. Hsu, Y.L., Chang, J.K., Tsai, C.H., Chien, T.T., Kuo, P.L. Biochem. Pharmacol. (2007) [Pubmed]
  19. Adenovirally expressed noggin and brain-derived neurotrophic factor cooperate to induce new medium spiny neurons from resident progenitor cells in the adult striatal ventricular zone. Chmielnicki, E., Benraiss, A., Economides, A.N., Goldman, S.A. J. Neurosci. (2004) [Pubmed]
  20. A new mutation of the noggin gene in a French Fibrodysplasia ossificans progressiva (FOP) family. Fontaine, K., Sémonin, O., Legarde, J.P., Lenoir, G., Lucotte, G. Genetic counseling (Geneva, Switzerland) (2005) [Pubmed]
  21. RhoA GTPase inactivation by statins induces osteosarcoma cell apoptosis by inhibiting p42/p44-MAPKs-Bcl-2 signaling independently of BMP-2 and cell differentiation. Fromigu??, O., Ha??, E., Modrowski, D., Bouvet, S., Jacquel, A., Auberger, P., Marie, P.J. Cell Death Differ. (2006) [Pubmed]
  22. Bone morphogenetic proteins induce gremlin, a protein that limits their activity in osteoblasts. Pereira, R.C., Economides, A.N., Canalis, E. Endocrinology (2000) [Pubmed]
  23. Regulation of BMP-induced transcription in cultured human bone marrow stromal cells. Diefenderfer, D.L., Osyczka, A.M., Garino, J.P., Leboy, P.S. The Journal of bone and joint surgery. American volume. (2003) [Pubmed]
  24. Induction of osteogenic differentiation of human mesenchymal stem cells by histone deacetylase inhibitors. Cho, H.H., Park, H.T., Kim, Y.J., Bae, Y.C., Suh, K.T., Jung, J.S. J. Cell. Biochem. (2005) [Pubmed]
  25. Glia induce dendritic growth in cultured sympathetic neurons by modulating the balance between bone morphogenetic proteins (BMPs) and BMP antagonists. Lein, P.J., Beck, H.N., Chandrasekaran, V., Gallagher, P.J., Chen, H.L., Lin, Y., Guo, X., Kaplan, P.L., Tiedge, H., Higgins, D. J. Neurosci. (2002) [Pubmed]
  26. Vascular endothelial growth factor contributes to the prostate cancer-induced osteoblast differentiation mediated by bone morphogenetic protein. Dai, J., Kitagawa, Y., Zhang, J., Yao, Z., Mizokami, A., Cheng, S., Nör, J., McCauley, L.K., Taichman, R.S., Keller, E.T. Cancer Res. (2004) [Pubmed]
  27. A novel R486Q mutation in BMPR1B resulting in either a brachydactyly type C/symphalangism-like phenotype or brachydactyly type A2. Lehmann, K., Seemann, P., Boergermann, J., Morin, G., Reif, S., Knaus, P., Mundlos, S. Eur. J. Hum. Genet. (2006) [Pubmed]
  28. Noggin upregulates Fos expression by a calcium-mediated pathway in amphibian embryos. Leclerc, C., Duprat, A.M., Moreau, M. Dev. Growth Differ. (1999) [Pubmed]
  29. The mechanisms of uremic serum-induced expression of bone matrix proteins in bovine vascular smooth muscle cells. Chen, N.X., Duan, D., O'Neill, K.D., Wolisi, G.O., Koczman, J.J., Laclair, R., Moe, S.M. Kidney Int. (2006) [Pubmed]
  30. Noggin is a negative regulator of neuronal differentiation in developing neocortex. Li, W., LoTurco, J.J. Dev. Neurosci. (2000) [Pubmed]
  31. Transplacental RNAi: Deciphering Gene Function in the Postimplantation-Staged Embryo. O'shea, K.S., De Boer, L.S., Slawny, N.A., Gratsch, T.E. J. Biomed. Biotechnol. (2006) [Pubmed]
  32. Current concepts in periodontal bioengineering. Taba, M., Jin, Q., Sugai, J.V., Giannobile, W.V. Orthodontics & craniofacial research. (2005) [Pubmed]
  33. Functional CD5+ B cells develop predominantly in the spleen of NOD/SCID/gammac(null) (NOG) mice transplanted either with human umbilical cord blood, bone marrow, or mobilized peripheral blood CD34+ cells. Matsumura, T., Kametani, Y., Ando, K., Hirano, Y., Katano, I., Ito, R., Shiina, M., Tsukamoto, H., Saito, Y., Tokuda, Y., Kato, S., Ito, M., Motoyoshi, K., Habu, S. Exp. Hematol. (2003) [Pubmed]
 
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