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Adamts1  -  a disintegrin-like and metallopeptidase...

Mus musculus

Synonyms: A disintegrin and metalloproteinase with thrombospondin motifs 1, ADAM-TS 1, ADAM-TS1, ADAMTS, ADAMTS-1, ...
 
 
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Disease relevance of Adamts1

 

Psychiatry related information on Adamts1

  • In spontaneous activity studies, doses of BNMPA ranging from 1 mg/kg to 50mg/kg failed to alter locomotor activity significantly from controls though 5 mg/kg METH alone significantly increased spontaneous activity [6].
 

High impact information on Adamts1

  • Vaccination of mice with heat shock protein 70 (hsp70) preparations derived from the Meth A sarcoma, but not from normal tissues, renders the mice immune to a substantial challenge with Meth A sarcoma [7].
  • In this report, we demonstrate that infusion of low concentrations of TNF (3 micrograms/animal) into mice bearing meth A fibrosarcomas leads to localized fibrin deposition with formation of occlusive intravascular thrombi in close association with the endothelial cell surface [8].
  • The results of this study show that during growth of the immunogenic Meth A fibrosarcoma, two different types of suppressor T lymphocytes are generated in sequence [9].
  • These results show that failure of intravenously-infused, tumor-sensitized T cells to cause regression of the Meth A fibrosarcoma growing in its syngeneic or semi-syngeneic host is caused by the presence of a tumor-induced population of cyclophosphamide-sensitive suppressor T cells [10].
  • Chromosome and serologic analysis of microcell hybrids between Meth A sarcoma cells and Chinese hamster cells shows a clear correlation of Meth A antigen expression with the presence of the distal region of chromosome 12 (bands F1 and F2) [5].
 

Chemical compound and disease context of Adamts1

 

Biological context of Adamts1

 

Anatomical context of Adamts1

 

Associations of Adamts1 with chemical compounds

  • Coordinate transcription of the ADAMTS-1 gene by luteinizing hormone and progesterone receptor [16].
  • Forskolin plus phorbol myristate acetate also increased promoter activity and, when added to cells cotransfected with PRA, ADAMTS-1 promoter activity increased further [16].
  • ADAMTS-5, but not ADAMTS-1, -4, or -9, was up-regulated 8-fold by retinoic acid and 17-fold by IL-1alpha treatment [20].
  • The growth of Meth 1, another syngeneic tumor of BALB/c origin, inoculated on day 10 as a rechallenge tumor was unaffected by the treatment with RP and/or FUra [12].
  • Winn assay revealed that the suppressive effect on tumor growth of immune lymph node cells obtained from Meth A-inoculated beta-carotene-treated mice on day 12 was enhanced dose dependently [13].
 

Enzymatic interactions of Adamts1

 

Other interactions of Adamts1

 

Analytical, diagnostic and therapeutic context of Adamts1

  • Immunohistochemistry was used to assess the localization of type IV collagen, TGF-beta and F4/80-positive macrophages in the kidneys of Adamts-1 null mice compared to wild-type control animals [3].
  • Because the presence of suppressor T cells generated in response to the Meth A did not suppress the capacity of Meth A-bearing mice to generate and express immunity against a tumor allograft, it is obvious that they were not in a state of generalized immunosuppression [23].
  • The results of this paper are consistent with the hypothesis that progressive growth of the Meth A fibrosarcoma evokes the generation of a T-cell-mediated mechanism of immunosuppression that prevents this highly immunogenic tumor from being rejected by its immunocompetent host [23].
  • On the basis of preceding studies showing that tumor-induced, T cell-mediated immunosuppression serves as an obstacle to adoptive immunotherapy of the Meth A fibrosarcoma, it was predicted that cyclophosphamide treatment of tumor bearers would remove this obstacle and allow passively transferred immune T cells to cause tumor regression [10].
  • It was shown that it is possible to cause the regression of large, established Meth A tumors by intravenous infusion of tumor-sensitized T cells from immune donors, but only if the tumors are growing in T-cell-deficient recipients [23].

References

  1. Expression of ADAMTS1 during murine development. Thai, S.N., Iruela-Arispe, M.L. Mech. Dev. (2002) [Pubmed]
  2. The carboxyl-terminal half region of ADAMTS-1 suppresses both tumorigenicity and experimental tumor metastatic potential. Kuno, K., Bannai, K., Hakozaki, M., Matsushima, K., Hirose, K. Biochem. Biophys. Res. Commun. (2004) [Pubmed]
  3. Neonatal calyceal dilation and renal fibrosis resulting from loss of Adamts-1 in mouse kidney is due to a developmental dysgenesis. Mittaz, L., Ricardo, S., Martinez, G., Kola, I., Kelly, D.J., Little, M.H., Hertzog, P.J., Pritchard, M.A. Nephrol. Dial. Transplant. (2005) [Pubmed]
  4. Enhanced in vivo growth and resistance to rejection of tumor cells expressing dominant negative IFN gamma receptors. Dighe, A.S., Richards, E., Old, L.J., Schreiber, R.D. Immunity (1994) [Pubmed]
  5. Chromosome assignment of the tumor-specific antigen of a 3-methylcholanthrene-induced mouse sarcoma. Pravtcheva, D.D., DeLeo, A.B., Ruddle, F.H., Old, L.J. J. Exp. Med. (1981) [Pubmed]
  6. alpha-Benzyl-N-methylphenethylamine (BNMPA), an impurity of illicit methamphetamine synthesis: pharmacological evaluation and interaction with methamphetamine. Moore, K.A., Lichtman, A.H., Poklis, A., Borzelleca, J.F. Drug and alcohol dependence. (1995) [Pubmed]
  7. Heat shock protein 70-associated peptides elicit specific cancer immunity. Udono, H., Srivastava, P.K. J. Exp. Med. (1993) [Pubmed]
  8. Tumor necrosis factor/cachectin-induced intravascular fibrin formation in meth A fibrosarcomas. Nawroth, P., Handley, D., Matsueda, G., De Waal, R., Gerlach, H., Blohm, D., Stern, D. J. Exp. Med. (1988) [Pubmed]
  9. T cell suppressors of antitumor immunity. The production of Ly-1-,2+ suppressors of delayed sensitivity precedes the production of suppressors of protective immunity. DiGiacomo, A., North, R.J. J. Exp. Med. (1986) [Pubmed]
  10. Cyclophosphamide-facilitated adoptive immunotherapy of an established tumor depends on elimination of tumor-induced suppressor T cells. North, R.J. J. Exp. Med. (1982) [Pubmed]
  11. Potentiation of anticancer agents by new synthetic isoprenoids. II. Inhibition of the growth of transplantable murine tumors. Yamaguchi, T., Ikezaki, K., Kishiye, T., Tahara, Y., Koyama, H., Takahasi, T., Fukawa, H., Komiyama, S., Akiyama, S., Kuwano, M. J. Natl. Cancer Inst. (1984) [Pubmed]
  12. Combined treatments with vitamin A and 5-fluorouracil and the growth of allotransplantable and syngeneic tumors in mice. Tomita, Y., Himeno, K., Nomoto, K., Endo, H., Hirohata, T. J. Natl. Cancer Inst. (1982) [Pubmed]
  13. Augmentation of tumor immunity against syngeneic tumors in mice by beta-carotene. Tomita, Y., Himeno, K., Nomoto, K., Endo, H., Hirohata, T. J. Natl. Cancer Inst. (1987) [Pubmed]
  14. Tumor rejection antigens of chemically induced sarcomas of inbred mice. Srivastava, P.K., DeLeo, A.B., Old, L.J. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  15. ADAM-TS5, ADAM-TS6, and ADAM-TS7, novel members of a new family of zinc metalloproteases. General features and genomic distribution of the ADAM-TS family. Hurskainen, T.L., Hirohata, S., Seldin, M.F., Apte, S.S. J. Biol. Chem. (1999) [Pubmed]
  16. Coordinate transcription of the ADAMTS-1 gene by luteinizing hormone and progesterone receptor. Doyle, K.M., Russell, D.L., Sriraman, V., Richards, J.S. Mol. Endocrinol. (2004) [Pubmed]
  17. Progesterone-regulated genes in the ovulation process: ADAMTS-1 and cathepsin L proteases. Robker, R.L., Russell, D.L., Espey, L.L., Lydon, J.P., O'Malley, B.W., Richards, J.S. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  18. ADAMTS1 proteinase is up-regulated in wounded skin and regulates migration of fibroblasts and endothelial cells. Krampert, M., Kuenzle, S., Thai, S.N., Lee, N., Iruela-Arispe, M.L., Werner, S. J. Biol. Chem. (2005) [Pubmed]
  19. ADAMTS-1 is involved in normal follicular development, ovulatory process and organization of the medullary vascular network in the ovary. Shozu, M., Minami, N., Yokoyama, H., Inoue, M., Kurihara, H., Matsushima, K., Kuno, K. J. Mol. Endocrinol. (2005) [Pubmed]
  20. ADAMTS-5 Deficiency Does Not Block Aggrecanolysis at Preferred Cleavage Sites in the Chondroitin Sulfate-rich Region of Aggrecan. East, C.J., Stanton, H., Golub, S.B., Rogerson, F.M., Fosang, A.J. J. Biol. Chem. (2007) [Pubmed]
  21. Evidence for proteolytic cleavage of brevican by the ADAMTSs in the dentate gyrus after excitotoxic lesion of the mouse entorhinal cortex. Mayer, J., Hamel, M.G., Gottschall, P.E. BMC neuroscience [electronic resource]. (2005) [Pubmed]
  22. Adamts-1 is essential for the development and function of the urogenital system. Mittaz, L., Russell, D.L., Wilson, T., Brasted, M., Tkalcevic, J., Salamonsen, L.A., Hertzog, P.J., Pritchard, M.A. Biol. Reprod. (2004) [Pubmed]
  23. T-cell-mediated suppression of anti-tumor immunity. An explanation for progressive growth of an immunogenic tumor. Berendt, M.J., North, R.J. J. Exp. Med. (1980) [Pubmed]
 
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