| inhibition of migration is another crucial tumor suppressor function of hSNF5/INI1, in addition to its previously described functions in proliferation and differentiation | None |
| Loss of the epigenetic tumor suppressor SNF5 leads to cancer without genomic instability. | None |
| Imprinted CDKN1C is a tumor suppressor in rhabdoid tumor and activated by restoration of SMARCB1 and histone deacetylase inhibitors. | None |
| INI1 is the primary tumor suppressor gene involved in the development of rhabdoid tumors with no second locus identified. | None |
| Loss of the SNF5 tumor suppressor leads to elevated expression of the Polycomb gene EZH2. | None |
| Loss of the tumor suppressor Snf5 leads to aberrant activation of the Hedgehog-Gli pathway. | None |
| MYC interaction with the tumor suppressive SWI/SNF complex member INI1 regulates transcription and cellular transformation | None |
| the cytoplasmic Snr1 may play a tumor suppressive role in Drosophila imaginal tissues. | None |
| MARCB1 deficiency induced GEFs for Rac GTPase activation and augmented AML cell migration and survival. Collectively, these findings highlight tumor suppressor role of SMARCB1 and illustrate SWI/SNF(Delta) function in maintaining an oncogenic gene expression program in AML. | None |
| Modulating the Expression Strength of the Baculovirus/Insect Cell Expression System: A Toolbox Applied to the Human Tumor Suppressor SMARCB1/SNF5 | None |
| Loss of SMARCB1 tumor suppressor function is a key oncogenic event in epithelioid malignant peripheral nerve sheath tumors. | None |
| Tumor suppressor SMARCB1 suppresses super-enhancers to govern hESC lineage determination | None |
| Inhibition of MYC by the SMARCB1 tumor suppressor | None |
| Study identifies SWINGN, a lncRNA interacting with SMARCB1 exclusively in proliferating conditions, exerting a pro-oncogenic role in some tumor types. SWINGN is transcribed from an enhancer and modulates the activation of GAS6 oncogene as part of a topologically organized region, as well as a larger network of pro-oncogenic genes by favoring SMARCB1 binding. | None |