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Gene Review

SMARCA2  -  SWI/SNF related, matrix associated, actin...

Homo sapiens

Synonyms: ATP-dependent helicase SMARCA2, BAF190, BAF190B, BRG1-associated factor 190B, BRM, ...
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Disease relevance of SMARCA2

  • The proto-oncoprotein SYT, involved in the unique translocation t(X;18) found in synovial sarcoma, is known to interact with human BRM (hBRM), thus providing a link between chromatin remodelling factors and human cancer [1].
  • This report provides supportive evidence that BRG1 and BRM act as tumor suppressor proteins and implicates a role for their loss in the development of non-small cell lung cancers [2].
  • This effect probably results from the promotion of glucocorticoid receptor-targeted chromatin remodeling by the hBRM-containing SWI/SNF complex because the N-terminal domain of the retinoblastoma protein enhances glucocorticoid receptor-hBRM interactions [3].
  • BRG1 and/or BRM protein is absent or disrupted in approximately 17% of all human adenocarcinomas [4].
  • These results indicate that bestatin inhibits the growth of NaUCC-4 choriocarcinoma in vivo as well as in vitro not via potentiation of effector cells but rather by its direct cytostatic activity, and suggest that bestatin may have an additional therapeutic property besides as a BRM for its use in the treatment of choriocarcinoma [5].

High impact information on SMARCA2

  • BAF53b is combinatorially assembled into polymorphic complexes with ubiquitous subunits including the two ATPases BRG1 and BRM [6].
  • We show that BRG1and BRM associate with different promoters during cellular proliferation and differentiation, and in response to specific signaling pathways by preferential interaction with certain classes of transcription factors [7].
  • BRG1 binds to zinc finger proteins through a unique N-terminal domain that is not present in BRM [7].
  • BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists [8].
  • An RNA interference knockdown survey revealed that the core subunits BRM and MOR are critical for the structural integrity of both complexes [9].

Biological context of SMARCA2


Anatomical context of SMARCA2

  • In this study, we identified the first cell line negative for the BAF57 protein as well as a pancreatic carcinoma cell line negative for both the BRG-1 and hBRM proteins [14].
  • These results suggest that hSNF5 loss is not equivalent to BRG1/BRM loss in human tumor cell lines [15].
  • The expression of BRM was very low in NPCs and was induced to a high level during differentiation to neurons and astrocytes [11].
  • Small interfering RNA experiments showed that blocking the expression of BRG1 and BRM in fetal and adult hepatocytes, respectively, causes a reduction in albumin expression [16].
  • BRG1 expression was predominantly seen in cell types that constantly undergo proliferation or self-renewal; in contrast, BRM was preferentially expressed in brain, liver, fibromuscular stroma, and endothelial cell types, cell types not constantly engaged in proliferation or self-renewal [17].

Associations of SMARCA2 with chemical compounds

  • Compared with patients with a decreased Z score, those with an increased Z score had significantly higher cyclosporine and lower prednisone dosages and a greater BRM increase at six months, whereas age, sex ratio, and plasma creatinine, PTH and 25 OH vitamin D were comparable and stable from months 3 through 24 [18].
  • PMMA/ARM nanocomposites had higher thermal stability and mechanical interfacial properties than PMMA/VRM or BRM nanocomposites [19].
  • In this work, although the dispersion properties of the BRM decreased, the thermal stabilities and mechanical interfacial properties of PVC/BRM nanocomposites increased, which could be attributed to improvement in the interfacial interactions between acidic PVC and BRM [19].

Physical interactions of SMARCA2


Co-localisations of SMARCA2

  • It was also found that SYT interacts and colocalizes in the nucleus with the BRM protein, a transcriptional coactivator, and that the SSX proteins colocalize in the nucleus with polycomb group proteins, which are transcriptional corepressors [20].

Regulatory relationships of SMARCA2

  • Transcriptional co-activator activity of SYT is negatively regulated by BRM and Brg1 [21].
  • The PSA promoter was only induced by the restoration of hBRM [22].
  • Therefore, BRM may be consistently down-regulated with BRG1 during neoplastic progression because they share some redundant functions [23].

Other interactions of SMARCA2

  • We define multiple domains within hBRM and BRG1 that interact with the hOsa C terminus [24].
  • In summary, SWI/SNF function potently regulates core AR target gene promoter activation, with a preference for hBRM-containing complexes [22].
  • Instead, they appear to be transcriptional regulators whose actions are mediated primarily through protein-protein interactions, with BRM in the case of SYT, and with Polycomb group repressors in the case of SSX [25].
  • The BRG1- and hBRM-associated factor BAF57 induces apoptosis by stimulating expression of the cylindromatosis tumor suppressor gene [26].
  • By transient transfection, we found that BRM can restore RB-mediated cell cycle arrest, induce expression of CD44 protein and suppress Cyclin A expression [23].

Analytical, diagnostic and therapeutic context of SMARCA2

  • The study suggests that BRM in the natural environment such as streptococci may suppress induction and progression of autoimmunity and be useful for the immunotherapy of human IDDM [27].
  • Selective kappa opioid receptor autoradiography with [3H]bremazocine (BRM) was used to examine regional and subregional kappa receptor distribution patterns at five rostrocaudal levels through the human striatum [28].
  • Although an improvement in the results of treatment with the combined use of appropriate BRMs is anticipated in the future, when clinical trials for combined BRM and radiotherapy are planned, the subjects should be patients with satisfactory tumour regression after radiotherapy [29].
  • In addition, adoptive transfer of BRM-induced ATK effector cells resulted in prolongation of survival time even in patients with documented metastatic tumors [30].
  • We have applied the Noisy ECG to After reconstruction model (ARM) and Before reconstruction model (BRM) and is implemented and tested [31].


  1. Conserved SNH domain of the proto-oncoprotein SYT interacts with components of the human chromatin remodelling complexes, while the QPGY repeat domain forms homo-oligomers. Perani, M., Ingram, C.J., Cooper, C.S., Garrett, M.D., Goodwin, G.H. Oncogene (2003) [Pubmed]
  2. Loss of BRG1/BRM in human lung cancer cell lines and primary lung cancers: correlation with poor prognosis. Reisman, D.N., Sciarrotta, J., Wang, W., Funkhouser, W.K., Weissman, B.E. Cancer Res. (2003) [Pubmed]
  3. Retinoblastoma protein is functionally distinct from its homologues in affecting glucocorticoid receptor-mediated transcription and apoptosis. Singh, P., Chan, S.W., Hong, W. J. Biol. Chem. (2001) [Pubmed]
  4. BRG1 loss in MiaPaCa2 cells induces an altered cellular morphology and disruption in the organization of the actin cytoskeleton. Rosson, G.B., Bartlett, C., Reed, W., Weissman, B.E. J. Cell. Physiol. (2005) [Pubmed]
  5. Aminopeptidase inhibitor ubenimex (bestatin) inhibits the growth of human choriocarcinoma in nude mice through its direct cytostatic activity. Inoi, K., Goto, S., Nomura, S., Isobe, K., Nawa, A., Okamoto, T., Tomoda, Y. Anticancer Res. (1995) [Pubmed]
  6. Identification of a polymorphic, neuron-specific chromatin remodeling complex. Olave, I., Wang, W., Xue, Y., Kuo, A., Crabtree, G.R. Genes Dev. (2002) [Pubmed]
  7. Transcriptional specificity of human SWI/SNF BRG1 and BRM chromatin remodeling complexes. Kadam, S., Emerson, B.M. Mol. Cell (2003) [Pubmed]
  8. BRG1/BRM and prohibitin are required for growth suppression by estrogen antagonists. Wang, S., Zhang, B., Faller, D.V. EMBO J. (2004) [Pubmed]
  9. Functional Differentiation of SWI/SNF Remodelers in Transcription and Cell Cycle Control. Moshkin, Y.M., Mohrmann, L., van Ijcken, W.F., Verrijzer, C.P. Mol. Cell. Biol. (2007) [Pubmed]
  10. Brain-specific expression of the nuclear actin-related protein ArpNalpha and its involvement in mammalian SWI/SNF chromatin remodeling complex. Kuroda, Y., Oma, Y., Nishimori, K., Ohta, T., Harata, M. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  11. Expression of chromatin remodeling factors during neural differentiation. Machida, Y., Murai, K., Miyake, K., Iijima, S. J. Biochem. (2001) [Pubmed]
  12. SMARCA2 and THAP11: potential candidates for polyglutamine disorders as evidenced from polymorphism and protein-folding simulation studies. Pandey, N., Mittal, U., Srivastava, A.K., Mukerji, M. J. Hum. Genet. (2004) [Pubmed]
  13. Association study of the trinucleotide repeat polymorphism within SMARCA2 and schizophrenia. Sengupta, S., Xiong, L., Fathalli, F., Benkelfat, C., Tabbane, K., Danics, Z., Labelle, A., Lal, S., Krebs, M.O., Rouleau, G., Joober, R. BMC Genet. (2006) [Pubmed]
  14. Characterization of SWI/SNF protein expression in human breast cancer cell lines and other malignancies. Decristofaro, M.F., Betz, B.L., Rorie, C.J., Reisman, D.N., Wang, W., Weissman, B.E. J. Cell. Physiol. (2001) [Pubmed]
  15. Re-expression of hSNF5/INI1/BAF47 in pediatric tumor cells leads to G1 arrest associated with induction of p16ink4a and activation of RB. Betz, B.L., Strobeck, M.W., Reisman, D.N., Knudsen, E.S., Weissman, B.E. Oncogene (2002) [Pubmed]
  16. Mammalian Chromatin Remodeling Complex SWI/SNF Is Essential for Enhanced Expression of the Albumin Gene during Liver Development. Inayoshi, Y., Miyake, K., Machida, Y., Kaneoka, H., Terajima, M., Dohda, T., Takahashi, M., Iijima, S. J. Biochem. (2006) [Pubmed]
  17. The expression of the SWI/SNF ATPase subunits BRG1 and BRM in normal human tissues. Reisman, D.N., Sciarrotta, J., Bouldin, T.W., Weissman, B.E., Funkhouser, W.K. Appl. Immunohistochem. Mol. Morphol. (2005) [Pubmed]
  18. Cyclosporine bone remodeling effect prevents steroid osteopenia after kidney transplantation. Westeel, F.P., Mazouz, H., Ezaitouni, F., Hottelart, C., Ivan, C., Fardellone, P., Brazier, M., El Esper, I., Petit, J., Achard, J.M., Pruna, A., Fournier, A. Kidney Int. (2000) [Pubmed]
  19. Improvement of red mud polymer-matrix nanocomposites by red mud surface treatment. Park, S.J., Jun, B.R. Journal of colloid and interface science. (2005) [Pubmed]
  20. Molecular mechanisms underlying human synovial sarcoma development. dos Santos, N.R., de Bruijn, D.R., van Kessel, A.G. Genes Chromosomes Cancer (2001) [Pubmed]
  21. Transcriptional co-activator activity of SYT is negatively regulated by BRM and Brg1. Ishida, M., Tanaka, S., Ohki, M., Ohta, T. Genes Cells (2004) [Pubmed]
  22. Differential requirement of SWI/SNF for androgen receptor activity. Marshall, T.W., Link, K.A., Petre-Draviam, C.E., Knudsen, K.E. J. Biol. Chem. (2003) [Pubmed]
  23. Concomitant down-regulation of BRM and BRG1 in human tumor cell lines: differential effects on RB-mediated growth arrest vs CD44 expression. Reisman, D.N., Strobeck, M.W., Betz, B.L., Sciariotta, J., Funkhouser, W., Murchardt, C., Yaniv, M., Sherman, L.S., Knudsen, E.S., Weissman, B.E. Oncogene (2002) [Pubmed]
  24. Largest subunits of the human SWI/SNF chromatin-remodeling complex promote transcriptional activation by steroid hormone receptors. Inoue, H., Furukawa, T., Giannakopoulos, S., Zhou, S., King, D.S., Tanese, N. J. Biol. Chem. (2002) [Pubmed]
  25. Fusions of the SYT and SSX genes in synovial sarcoma. Ladanyi, M. Oncogene (2001) [Pubmed]
  26. The BRG1- and hBRM-associated factor BAF57 induces apoptosis by stimulating expression of the cylindromatosis tumor suppressor gene. Wang, L., Baiocchi, R.A., Pal, S., Mosialos, G., Caligiuri, M., Sif, S. Mol. Cell. Biol. (2005) [Pubmed]
  27. Mechanism of action of a streptococcal preparation (OK-432) in prevention of autoimmune diabetes in NOD mice. Suppression of generation of effector cells for pancreatic B cell destruction. Shintani, S., Satoh, J., Seino, H., Goto, Y., Toyota, T. J. Immunol. (1990) [Pubmed]
  28. Opioid receptor ligand binding in the human striatum: II. Heterogeneous distribution of kappa opioid receptor labeled with [3H]bremazocine. Vonkeman, H.E., Voorn, P., Brady, L.S., Berendse, H.W., Richfield, E.K. J. Comp. Neurol. (1996) [Pubmed]
  29. Effect of krestin (PSK) as adjuvant treatment on the prognosis after radical radiotherapy in patients with non-small cell lung cancer. Hayakawa, K., Mitsuhashi, N., Saito, Y., Takahashi, M., Katano, S., Shiojima, K., Furuta, M., Niibe, H. Anticancer Res. (1993) [Pubmed]
  30. Clinical significance of autologous tumor killing (ATK) activity and its induction therapy in human cancer. Uchida, A. Biotherapy (Dordrecht, Netherlands) (1994) [Pubmed]
  31. A wavelet coefficient smoothened RLS adaptive denoising model for ECG. Poornachandra, S., Kumaravel, N. Biomedical sciences instrumentation. (2003) [Pubmed]
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