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The protein encoded by SMARCA2 is a member of the SWI/SNF family of proteins and is highly similar to the brahma protein of Drosophila. Additionally we are shipping SMARCA2 Proteins (6) and many more products for this protein.
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Chicken Monoclonal SMARCA2 Primary Antibody for IF, IP - ABIN967939
Muchardt, Yaniv: A human homologue of Saccharomyces cerevisiae SNF2/SWI2 and Drosophila brm genes potentiates transcriptional activation by the glucocorticoid receptor. in The EMBO journal 1993
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Chicken Monoclonal SMARCA2 Primary Antibody for IF, IP - ABIN967938
Singh, Coe, Hong: A role for retinoblastoma protein in potentiating transcriptional activation by the glucocorticoid receptor. in Nature 1995
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Human Polyclonal SMARCA2 Primary Antibody for ICC, IF - ABIN4285267
Van Houdt, Nowakowska, Sousa, van Schaik, Seuntjens, Avonce, Sifrim, Abdul-Rahman, van den Boogaard, Bottani, Castori, Cormier-Daire, Deardorff, Filges, Fryer, Fryns, Gana, Garavelli et al.: Heterozygous missense mutations in SMARCA2 cause Nicolaides-Baraitser syndrome. ... in Nature genetics 2012
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Human Monoclonal SMARCA2 Primary Antibody for ChIP, ICC - ABIN2668505
Okada, Harada, Saiwai, Nakamura, Ohkawa: Generation of a rat monoclonal antibody specific for Brm. in Hybridoma (2005) 2009
This de novo SMARCA2 missense mutation c.3721C>G, p.Gln1241Glu is the only reported mutation on exon 26 outside the ATPase (show DNAH8 Antibodies) domain of SMARCA2 to be associated with Nicolaides-Baraitser syndrome and adds to chromatin remodeling as a pathway for epileptogenesis.
We conclude that their features better resemble Coffin-Siris syndrome, rather than Nicolaides-Baraitser syndrome and that these features likely arise from SMARCA2 over-dosage. Pure 9p duplications (not caused by unbalanced translocations) are rare. Copy number analysis in patients with features that overlap with Coffin-Siris syndrome is recommended to further determine their genetic aspects.
BRM could activate JAK2 (show JAK2 Antibodies)/STAT3 (show STAT3 Antibodies) pathway to promote pancreatic cancer growth and chemoresistance.
BRM gene mutation, chromosome 9 monosomy or BRM deletion and CpG methylation contribute collectively to the loss of BRM expression in poorly differentiated clear cell renal cell carcinoma (show MOK Antibodies)
BRM-741 and BRM-1321 insertion polymorphisms are associated with susceptibility to cancer.
BRG1 (show SMARCA4 Antibodies)/BRM and c-MYC (show MYC Antibodies) have an antagonistic relationship regulating the expression of cardiac conduction genes that maintain contractility, which is reminiscent of their antagonistic roles as a tumor suppressor and oncogene (show RAB1A Antibodies) in cancer.
Two functional promoter BRM polymorphisms were not associated with pancreatic adenocarcinoma risk, but are strongly associated with survival.
SMARCA4 (show SMARCA4 Antibodies) and SMARCA2 deficiency is observed in 5.1% and 4.8% of non-small cell lung cancer
our data suggest that concomitant loss of SMARCA2 and SMARCA4 (show SMARCA4 Antibodies) is another hallmark of small cell carcinoma of the ovary, hypercalcemic type-a finding that offers new opportunities for therapeutic interventions.
this study shows for the first time novel SMARCA4 (show SMARCA4 Antibodies)-deficient and SMARCA2-deficient variants in undifferentiated gastrointestinal tract carcinomas
SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) chromatin remodeler subunits Brg1 (show SMARCA4 Antibodies) and Brm are expressed differentially during drug-induced liver injury and regeneration in a mouse model.
these findings described a role for BRG1 (show SMARCA4 Antibodies) and BRM in mitochondrial quality control, by regulating mitochondrial number, mitophagy, and mitochondrial dynamics not previously recognized in the adult cardiomyocyte
BRM depletion enhances the proportion of cells expressing markers of osteoblast precursors at the expense of cells able to differentiate along the adipocyte lineage.
Data show that knockdown of component of chromatin remodeling complex Brm or Baf170 (show SMARCC2 Antibodies) at different stages promotes reprogramming.
Data reveal stage-specific roles of Brm during skeletal myogenesis, via formation of repressive and activatory SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) complexes.
Brm protects from UV-induced hyperplastic growth in both cutaneous and corneal keratinocytes
Data suggest that Brg1 (show SMARCA4 Antibodies) and Brm integrate various proinflammatory cues into cell adhesion molecule (show MCAM Antibodies) transactivation in endothelial injury.
A SMARCA2-containing residual SWI (show SMARCA1 Antibodies)/SNF (show SNRPA Antibodies) complex underlies the oncogenic activity of SMARCA4 (show SMARCA4 Antibodies) mutant cancers.
study identifies NO and HDAC2 (show HDAC2 Antibodies) nitrosylation as part of a signaling pathway that regulates cortical development and the expression of Brm in neurons
The protein encoded by this gene is a member of the SWI/SNF family of proteins and is highly similar to the brahma protein of Drosophila. Members of this family have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The encoded protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin. Two transcript variants encoding different isoforms have been found for this gene, which contains a trinucleotide repeat (CAG) length polymorphism.
ATP-dependent helicase SMARCA2
, BRG1-associated factor 190B
, SNF2/SWI2-like protein 2
, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin a2
, global transcription activator homologous sequence
, probable global transcription activator SNF2L2
, protein brahma homolog
, sucrose nonfermenting 2-like protein 2
, SWI/SNF-related matrix-associated actin-dependent regulator of chromatin subfamily A member 2
, subunit of the SWI/SNF chromatin remodeling complex
, phasmid Socket Absent PSA-4