おすすめの製品
由来生物
mouse
品質水準
抗体製品の状態
purified antibody
抗体製品タイプ
primary antibodies
クローン
SD118, monoclonal
形状
liquid
含みます
≤0.1% sodium azide as preservative
化学種の反応性
human
メーカー／製品名
Calbiochem®
保管条件
do not freeze
アイソタイプ
IgG1
輸送温度
wet ice
保管温度
2-8°C
ターゲットの翻訳後修飾
unmodified
遺伝子情報
human ... BRCA1(672)
詳細
Anti-BRCA1 (Ab-4), mouse monoclonal, clone SD118, recognizes the ~220 kDa BRCA1 in HBL-100 and SK-BR3 cells. It is validated for WB, IF, IP, and for frozen sections.
Purified mouse monoclonal antibody generated by immunizing RBF/DnJ mice with the specified immunogen and fusing splenocytes with NS1 mouse myeloma cells (see application references). Recognizes the ~220 kDa BRCA1 protein.
Recognizes the ~220 kDa BRCA1 protein in HBL-100 and SK-BR3 cells. Sold under license of U.S. Patent 5,753,441 and 6,162,897.
免疫原
Human
a recombinant polypeptide corresponding to amino acids 1005-1313 in exon 11 of human BRCA1
アプリケーション
Frozen Sections (2 µg/ml)
Immunoblotting (2 µg/ml, see application references)
Immunofluorescence (2 µg/ml)
Immunoprecipitation (2 µg, see application references)
Paraffin Sections (not recommended)
Immunoblotting (2 µg/ml, see application references)
Immunofluorescence (2 µg/ml)
Immunoprecipitation (2 µg, see application references)
Paraffin Sections (not recommended)
包装
Please refer to vial label for lot-specific concentration.
警告
Toxicity: Standard Handling (A)
物理的形状
In 50 mM sodium phosphate buffer, 0.2% gelatin, pH 7.5.
アナリシスノート
Positive Control
HBL-100 or SK-BR3 cells
HBL-100 or SK-BR3 cells
その他情報
Chen, J.J., et al. 1999. Cancer Res.59, 1752s.
Cressman, V.L., et al. 1999. Cell Growth Differ.10, 1.
Irminger-Finger, I., et al. 1999. Biol. Chem.380, 117.
Xu, X., et al. 1999. Nat. Genet.22, 37.
Wilson, C.A., et al. 1999. Nat. Genet.21, 236.
Andres, J.L., et al. 1998. Oncogene16, 2229.
Chen, J., et al. 1998. Mol. Cell2, 317.
Chen, P.L., et al. 1998. Proc. Natl. Acad. Sci. USA95, 5287.
Fan, S., et al. 1998. Int. J. Cancer77, 600.
Gowen, L.C., et al. 1998. Science281, 1009.
Hsu, L.C. and R.L. White. 1998. Proc. Natl. Acad. Sci. USA95, 12983.
Shen, S.X., et al. 1998. Oncogene17, 3115.
Tulchin, N., et al. 1998. Int. J. Oncol.13, 513.
Ludwig, T., et al. 1997. Genes Dev11, 1226.
Ruffner, H. and I.M. Verma. 1997. Proc. Natl. Acad. Sci. USA94, 7138.
Scully, R., et al. 1997. Cell90, 425.
Thakur, S., et al. 1997. Mol. Cell Biol.17, 444.
Wilson, C.A., et al. 1997. Oncogene14, 1.
Cannon-Albright, L.A. and M.H. Skolnick. 1996. Semin Oncol.23, 1.
Chen, Y., et al. 1996. Cancer Res.56, 3168.
Liu, C.Y., et al. 1996. Genes Dev.10, 1835.
Gudas, J.M., et al. 1996. Cell Growth Differ.7, 717.
Scully, R., et al. 1996. Science272, 123.
Vaughn, J.P., et al. 1996. Cell Growth Differ.7, 711.
Wilson, C.A. et al. 1996. Nat. Genet.13, 264.
Thompson, M.E., et al. 1995. Nat. Genet.9, 444.
Miki, Y., et al. 1994. Science266, 66.
Cressman, V.L., et al. 1999. Cell Growth Differ.10, 1.
Irminger-Finger, I., et al. 1999. Biol. Chem.380, 117.
Xu, X., et al. 1999. Nat. Genet.22, 37.
Wilson, C.A., et al. 1999. Nat. Genet.21, 236.
Andres, J.L., et al. 1998. Oncogene16, 2229.
Chen, J., et al. 1998. Mol. Cell2, 317.
Chen, P.L., et al. 1998. Proc. Natl. Acad. Sci. USA95, 5287.
Fan, S., et al. 1998. Int. J. Cancer77, 600.
Gowen, L.C., et al. 1998. Science281, 1009.
Hsu, L.C. and R.L. White. 1998. Proc. Natl. Acad. Sci. USA95, 12983.
Shen, S.X., et al. 1998. Oncogene17, 3115.
Tulchin, N., et al. 1998. Int. J. Oncol.13, 513.
Ludwig, T., et al. 1997. Genes Dev11, 1226.
Ruffner, H. and I.M. Verma. 1997. Proc. Natl. Acad. Sci. USA94, 7138.
Scully, R., et al. 1997. Cell90, 425.
Thakur, S., et al. 1997. Mol. Cell Biol.17, 444.
Wilson, C.A., et al. 1997. Oncogene14, 1.
Cannon-Albright, L.A. and M.H. Skolnick. 1996. Semin Oncol.23, 1.
Chen, Y., et al. 1996. Cancer Res.56, 3168.
Liu, C.Y., et al. 1996. Genes Dev.10, 1835.
Gudas, J.M., et al. 1996. Cell Growth Differ.7, 717.
Scully, R., et al. 1996. Science272, 123.
Vaughn, J.P., et al. 1996. Cell Growth Differ.7, 711.
Wilson, C.A. et al. 1996. Nat. Genet.13, 264.
Thompson, M.E., et al. 1995. Nat. Genet.9, 444.
Miki, Y., et al. 1994. Science266, 66.
Maximal BRCA1 levels are observed in subconfluent cell populations after serum stimulation. Highly specific BRCA1 antibody useful for blotting and IP of full length BRCA1 protein. Antibody should be titrated for optimal results in individual systems.
法的情報
Sold under license of U.S. Patents 5,753,441 and 6,162,897.
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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保管分類コード
11 - Combustible Solids
WGK
WGK 1
引火点(°F)
Not applicable
引火点(℃)
Not applicable
適用法令
試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。
Jan Code
OP107-100UG:
OP107-MG:
OP107-ML:
試験成績書（COA）
製品のロット番号・バッチ番号を入力して、試験成績書（COA） を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。
Veronica Gomez Godinez et al.
PloS one, 15(4), e0227849-e0227849 (2020-04-29)
Understanding the mitotic DNA damage response (DDR) is critical to our comprehension of cancer, premature aging and developmental disorders which are marked by DNA repair deficiencies. In this study we use a micro-focused laser to induce DNA damage in selected
M Tanikawa et al.
British journal of cancer, 104(8), 1349-1355 (2011-03-17)
The TFII-I is a multifunctional transcriptional factor known to bind specifically to several DNA sequence elements and to mediate growth factor signalling. A microdeletion at the chromosomal location 7q11.23 encoding TFII-I and the related family of transcription factors may result
Myth T S Mok et al.
Traffic (Copenhagen, Denmark), 13(6), 800-814 (2012-03-17)
The breast cancer associated gene 1 (BRCA1)-A protein complex assembles at DNA damage-induced nuclear foci to facilitate repair of double-stranded breaks. Here, we describe the first systematic comparison of the dynamics, copy number and organization of its core components at
Amandine I Garcia et al.
EMBO molecular medicine, 3(5), 279-290 (2011-04-08)
Germ-line mutations in the BRCA1 gene strongly predispose women to breast cancer (lifetime risk up to 80%). Furthermore, the BRCA1 protein is absent or present at very low levels in about one third of sporadic breast cancers. However, the mechanisms
Maria C Villarroel et al.
Molecular cancer therapeutics, 10(1), 3-8 (2010-12-08)
Metastasis and drug resistance are the major causes of mortality in patients with pancreatic cancer. Once developed, the progression of pancreatic cancer metastasis is virtually unstoppable with current therapies. Here, we report the remarkable clinical outcome of a patient with
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