ANTI-BRM Chemische Eigenschaften,Einsatz,Produktion Methoden
Verwenden
All Prestige Antibodies Powered by Atlas Antibodies are developed and validated by the Human Protein Atlas (HPA) project
(www.proteinatlas.org)and as a result, are supported by the most extensive characterization in the industry.
The Human Protein Atlas project can be subdivided into three efforts: Human Tissue Atlas, Cancer Atlas, and Human Cell Atlas. The antibodies that have been generated in support of the Tissue and Cancer Atlas projects have been tested by immunohistochemistry against hundreds of normal and disease tissues and through the recent efforts of the Human Cell Atlas project, many have been characterized by immunofluorescence to map the human proteome not only at the tissue level but now at the subcellular level. These images and the collection of this vast data set can be viewed on the Human Protein Atlas (HPA) site by clicking on the Image Gallery link. To view these
protocols and other useful information about Prestige Antibodies and the HPA, visit .
Allgemeine Beschreibung
SMARCA2 (SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily a, member 2) gene is mapped in human chromosome 9p24.3. SMARCA2 is also known as BRM(Brahma) and is an important catalytic component of the SWI/SNF (switch sucrose nonfermentable) chromatin remodeling complex.
Biochem/physiol Actions
The components of SWI/SNF (switch sucrose nonfermentable) chromatin remodeling complex is often regarded as tumor suppressors. SMARCA2 along with SMARCA4 is an ATPase of the complex. SMARCA2 might be post-translationally silenced in many cancers. The loss of this gene expression might be as a result of epigenetic or post-translational modifications and may not be due to gene mutation in pancreatic and lung cancer cell lines. The expression of SMARCA2 is regulated by histone deacetylases HDAC3 (Histone deacetylases) and HDAC9 (Histone deacetylases), along with transcription factors MEF2D (myocyte enhancer factor 2D) and GATA3 (GATA binding protein 3). Loss of both SMARCA2 and SMARCA4 is specifically observed in small cell carcinoma of the ovary hypercalcaemic type.. The expression of SMARCA2 is retained by histone deacetylase inhibitor trichostatin A. Nicolaides-Baraitser syndrome involves SMARCA2 mutation.
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