一般描述
Anti-c-Abl (Ab-3), mouse monoclonal, clone 24-21, recognizes the ~145 kDa human and ~150 kDa mouse c-Abl. It is validated for Western blotting, immunofluorescence, and immunoprecipitation.
Purified mouse monoclonal antibody generated by immunizing BALB/c mice with the specified immunogen and fusing splenocytes with p.3U1 mouse myeloma cells (see application references). Recognizes the v-Abl, the ~145-150 kDa c-Abl, the ~210 kDa Bcr-Abl (CML), and the ~190 kDa Bcr-Abl (ALL) proteins.
Recognizes the ~145 kDa human c-Abl, the ~150 kDa mouse c-Abl, v-Abl, and the Bcr/Abl translocation products in ALL (~190 kDa) and CML (~210 kDa). Does not inhibit protein tyrosine kinase activity.Antibody Target Gene Symbol: ABL1 Target Synonym: ABL, AI325092, bcr/abl, C-ABL, C-ABL 1B, CABL1, E430008G22Rik, JTK7, MGC117749, p145Abl, p150, v-abl Entrez Gene Name: c-abl oncogene 1, receptor tyrosine kinase Hu Entrez ID: 25 (Related Antibodies: PK1006PK1013OP19) Mu Entrez ID: 11350 Rat Entrez ID: 311860
免疫原
a recombinant protein consisting of the carboxyl region of v-abl protein fused to TrpE
应用
Immunoblotting (1-5 µg/ml)
Immunofluorescence (see application references)
Immunoprecipitation (1-2 µg/sample)
Neutralization Studies (not recommended)
Immunofluorescence (see application references)
Immunoprecipitation (1-2 µg/sample)
Neutralization Studies (not recommended)
包装
Please refer to vial label for lot-specific concentration.
警告
Toxicity: Standard Handling (A)
外形
In 0.05 M sodium phosphate buffer, 0.2% gelatin, pH 7.5.
分析说明
Positive Control
K562 (human bcr/abl), HL-60 (normal abl), and ANN-1 (murine abl) cells
K562 (human bcr/abl), HL-60 (normal abl), and ANN-1 (murine abl) cells
其他说明
Does not inhibit protein tyrosine kinase activity. Detects human c-Abl (145 kDa), mouse c-Abl (150 kDa), v-Abl, and the Bcr/Abl translocation products in ALL (~210 kDa) and CML (~190 kDa). HL-60 and NIH3T3 cells contain normal, non-rearranged protein. Antibody should be titrated for optimal results in individual sample types.
Wiedemann, L.M., et al. 1988. Blood71, 349.
Stam, K., et al. 1985. N. Engl. J. Med.313, 1429.
Konopka, J.B., et al. 1984. Cell37, 1035.
Prywes, R., et al. 1983. Cell34, 569.
de Klein, A., et al. 1982. Nature300, 765.
Reynolds, F.H., Jr., et al. 1980. J. Virol.36, 374.
Reynolds, F.H., Jr., et al. 1978. Proc. Natl. Acad. Sci. USA75, 3974.
Witte, O.N., et al. 1978. Proc. Natl. Acad. Sci. USA75, 2488.
Abelson, H.T. and Rabstein, L.S. 1970. Cancer Res.30, 2213.
Stam, K., et al. 1985. N. Engl. J. Med.313, 1429.
Konopka, J.B., et al. 1984. Cell37, 1035.
Prywes, R., et al. 1983. Cell34, 569.
de Klein, A., et al. 1982. Nature300, 765.
Reynolds, F.H., Jr., et al. 1980. J. Virol.36, 374.
Reynolds, F.H., Jr., et al. 1978. Proc. Natl. Acad. Sci. USA75, 3974.
Witte, O.N., et al. 1978. Proc. Natl. Acad. Sci. USA75, 2488.
Abelson, H.T. and Rabstein, L.S. 1970. Cancer Res.30, 2213.
法律信息
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
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WGK
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闪点(°F)
Not applicable
闪点(°C)
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Tamjeed Saleh et al.
Nature structural & molecular biology, 24(11), 893-901 (2017-09-26)
The activity of protein kinases is often regulated in an intramolecular fashion by signaling domains, which feature several phosphorylation or protein-docking sites. How kinases integrate such distinct binding and signaling events to regulate their activities is unclear, especially in quantitative
Shigeru Matsumura et al.
Nature communications, 7, ncomms11858-ncomms11858 (2016-06-14)
Despite theoretical and physical studies implying that cell-extracellular matrix adhesion geometry governs the orientation of the cell division axis, the molecular mechanisms that translate interphase adhesion geometry to the mitotic spindle orientation remain elusive. Here, we show that the cellular
Alexander J M Blakes et al.
European journal of human genetics : EJHG, 29(4), 593-603 (2020-11-24)
ABL1 is a proto-oncogene encoding a nonreceptor tyrosine kinase, best known in the somatic BCR-ABL fusion gene associated with chronic myeloid leukaemia. Recently, germline missense variants in ABL1 have been found to cause an autosomal dominant developmental syndrome with congenital
Cong Fang et al.
Cancer research, 70(21), 8299-8308 (2010-09-15)
Oncogenic kinase activity and the resulting aberrant growth and survival signaling are a common driving force of cancer. Accordingly, many successful molecularly targeted anticancer therapeutics are directed at inhibiting kinase activity. To assess kinase activity in minute patient samples, we
Martin Frejno et al.
Molecular systems biology, 13(11), 951-951 (2017-11-05)
Most molecular cancer therapies act on protein targets but data on the proteome status of patients and cellular models for proteome-guided pre-clinical drug sensitivity studies are only beginning to emerge. Here, we profiled the proteomes of 65 colorectal cancer (CRC)
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