BCAS2 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC-P, IF, E |
---|---|
Primary Accession | O75934 |
Other Accession | CAG46834, 49457027 |
Reactivity | Human, Mouse, Rat |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | IgG |
Calculated MW | 26131 Da |
Application Notes | BCAS2 antibody can be used for detection of BCAS2 by Western blot at 0.5 - 1 µg/mL. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
Gene ID | 10286 |
---|---|
Target/Specificity | BCAS2; |
Reconstitution & Storage | BCAS2 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. |
Precautions | BCAS2 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BCAS2 |
---|---|
Synonyms | DAM1 {ECO:0000303|PubMed:10403562} |
Function | Required for pre-mRNA splicing as component of the activated spliceosome (PubMed:28076346, PubMed:28502770, PubMed:29301961, PubMed:29360106, PubMed:30705154). Component of the PRP19-CDC5L complex that forms an integral part of the spliceosome and is required for activating pre-mRNA splicing. May have a scaffolding role in the spliceosome assembly as it contacts all other components of the core complex. The PRP19-CDC5L complex may also play a role in the response to DNA damage (DDR). |
Cellular Location | Nucleus. Nucleus, nucleolus |
Tissue Location | Ubiquitously expressed. |

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Background
BCAS2 Antibody: BCAS2 was identified through differential display analysis as an mRNA species that was overexpressed in MCF7 and BT-20 breast cancer cell lines. The chromosomal region containing this gene, 1p13.3021, is amplified in these cells lines. BCAS2 is a transcriptional cofactor that enhances estrogen receptor-mediated gene expression, and directly interacts with the tumor suppressor p53 to reduce p53 transcriptional activity by reducing p53 protein level in the absence of DNA damage. Deprivation of BCAS2 through RNA inhibition induces apoptosis in p53-wild type cells, but causes G2-M arrest in p53-null or -mutant cells; this effect was reversed with the expression of ectopic BCAS2. BCAS2 may thus be potentially useful as a therapeutic target in the treatment of cancer.
References
Nagasaki K, Maass N, Manabe T, et al. Identification of a novel gene, DAM1, amplified at chromosome 1p13.3-21 region in human breast cancer cell lines. Cancer Lett.1999; 140:219-26.
Qi C, Zhu YT, Chang J, et al. Potentiation of estrogen receptor transcriptional activity by breast cancer amplified sequence Biochem. Biophys. Res. Commun.2005; 328:393-8.
Huo PC, Tsao YP, Chang HW, et al. Breast cancer amplified sequence 2, a novel negative regulator of the p53 tumor suppressor. Cancer Res.2009; 69:8877-85.

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