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BRMS1 reduces the metastatic potential, but not the tumorogenicity, of human breast cancer and melanoma cell lines. Additionally we are shipping BRMS1 Antibodies (61) and BRMS1 Proteins (9) and many more products for this protein.
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Phosphorylation of BRMS1 by CDK2 (show CDK2 ELISA Kits) regulates the migration of tumor cells.
Data show that Cullin3 exerts its function through promoting breast-cancer metastasis suppressor 1 (BRMS1) protein degradation, which was associated with epithelial-mesenchymal transition (EMT (show ITK ELISA Kits)), migration and invasion.
The studies reviewed here with respect to BRMS1 structure, cellular effects, intracellular signaling, and clinical value consolidate the importance of BRMS1 in the development of metastasis.
Aberrant methylation of BRMS1 frequently occurs in the down-regulation of BRMS1 in triple negative breast cancer and that it may play a role in the metastasis of breast cancer.
the present study demonstrates a mechanical cascade of BRMS1 suppressing cancer cell invasion through downregulating HIF-1alpha (show HIF1A ELISA Kits) transcript and consequently reducing Snail (show SNAI1 ELISA Kits) and TWIST1 (show TWIST1 ELISA Kits) expression.
MRTF-A (show MKL1 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) synergistically recruited DNMT1 (show DNMT1 ELISA Kits) to hypermethylate the promoter of BRMS1 and affect the expression of BRMS1.MRTF-A (show MKL1 ELISA Kits) and STAT3 (show STAT3 ELISA Kits) promote breast cancer cell migration via hypermethylating BRSM1.
BRMS1 expression in human breast cancer is negatively correlated with JARID1C (show KDM5C ELISA Kits) expression. Our results, for the first time, portray a pivotal role of JARID1C (show KDM5C ELISA Kits) in regulating metastatic behaviors of breast cancer cells
loss of BRMS1 promotes malignant phenotypes that are dependent on NF-kappaB (show NFKB1 ELISA Kits)-dependent regulation of Twist1 (show TWIST1 ELISA Kits)
BRMS1 is a key regulator required to maintain a cellular morphology and cytoskeletal architecture consistent with an epithelial phenotype.
BRMS1 overexpression inhibited glioma cell invasion.
findings indicate the expression of Brms1L (show BRMS1L ELISA Kits) depends on beta-catenin (show CTNNB1 ELISA Kits) activity and contributes to follicle stimulating hormone beta (show FSHB ELISA Kits) induction by Gonadotropin-Releasing Hormone.
The Brms1 suppressed pulmonary metastasis and promoted apoptosis of tumor cells located in the lungs but not in the mammary glands.
BRMS1 may participate in transcriptional regulation via interaction with the mSin3.HDAC (show HDAC3 ELISA Kits) complex
results show for the first time that BRMS1 contains both nuclear import and export signals enabling its nucleo-cytoplasmic shuttling
This gene reduces the metastatic potential, but not the tumorogenicity, of human breast cancer and melanoma cell lines. The protein encoded by this gene localizes primarily to the nucleus and is a component of the mSin3a family of histone deacetylase complexes (HDAC). The protein contains two coiled-coil motifs and several imperfect leucine zipper motifs. Alternative splicing results in two transcript variants encoding different isoforms.
breast cancer metastasis suppressor 1
, breast cancer metastasis-suppressor 1
, breast cancer metastasis-suppressor 1 homolog
, breast cancer metastasis-suppressor 1-like protein