A5844
Monoclonal Anti-c-Abl antibody produced in mouse
clone ABL-148, ascites fluid
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Synonym(s):
Anti-ABL, Anti-BCR-ABL, Anti-CHDSKM, Anti-JTK7, Anti-bcr/abl, Anti-c-ABL, Anti-c-ABL1, Anti-p150, Anti-v-abl
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biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
ascites fluid
antibody product type
primary antibodies
clone
ABL-148, monoclonal
mol wt
antigen 145 kDa
species reactivity
monkey, rat, human, mouse, bovine
technique(s)
flow cytometry: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
microarray: suitable
western blot: 1:2,000 using human melanoma cell extract
isotype
IgG2a
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ABL1(25)
mouse ... Abl1(11350)
rat ... Abl1(311860)
Related Categories
General description
The c-Abl protein contains three high mobility group-like domains that bind to AT-rich DNA in a cooperative manner.
c-Abl is a proto-oncogene product that belongs to Tyr protein kinase family. It has a crucial role in different cellular processes like- differentiation, adhesion and regulates DNA damage-induced apoptosis.
Specificity
Mouse anti-c-Abl antibody reacts specifically with an epitope present in the SH2 domain of the c-Abl. The product has also shown reactivity for c-Abl of monkey, rat, bovine, mouse and human.
Immunogen
recombinant c-Abl, SH2 domain.
Application
Monoclonal anti-c-Abl antibody can be used in western blotting (diluted 1:2000) using melanoma cell extract from human. It can also be used in microarray and flow cytometry. Monoclonal anti-c-Abl antibody can be used for studying the mechanism of signaling pathways involving c-Abl. It may also be used for immunoprecipitation and immunocytochemistry.
Biochem/physiol Actions
Cytoplasmic c-Abl regulates SH2/SH3 adaptor protein cytoskeleton-associated adaptor protein (Crk) and the Crk-binding protein p130cas. Nuclear c-Abl has been implicated in the regulation of cell cycle-dependent and DNA damage-induced gene expression.
Target description
c-Abl is a non-receptor tyrosine kinase with both cytoplasmic and nuclear functions. The Abl oncogen has been implicated in several human leukemias including nearly all chronic myelocytic leukemias.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
WGK
nwg
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
常规特殊物品
Certificates of Analysis (COA)
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c-Abl: activation and nuclear targets
Shaul Y
Cell Death and Differentiation, 7(1), 10-10 (2000)
Cytoplasmic c-Abl provides a molecular `Rheostat?controlling carcinoma cell survival and invasion
Kain KH, et al.
Oncogene, 22(38), 6071-6071 (2003)
Lukasz Skora et al.
European journal of haematology, 96(5), 502-506 (2015-07-15)
Binding of tyrosine kinase inhibitors such as imatinib was shown to induce a novel open-inhibited conformation of BCR-ABL, in which Tyr245 is exposed and prone to phosphorylation. To evaluate whether this leads to priming of the kinase in cellular systems
Lukasz Skora et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(47), E4437-E4445 (2013-11-06)
Successful treatment of chronic myelogenous leukemia is based on inhibitors binding to the ATP site of the deregulated breakpoint cluster region (Bcr)-Abelson tyrosine kinase (Abl) fusion protein. Recently, a new type of allosteric inhibitors targeting the Abl myristoyl pocket was
Michela Restelli et al.
Human molecular genetics, 24(15), 4185-4197 (2015-04-26)
The p63 transcription factor, homolog to the p53 tumor suppressor gene, plays a crucial role in epidermal and limb development, as its mutations are associated to human congenital syndromes characterized by skin, craniofacial and limb defects. While limb and skin-specific
Articles
Quantitative and qualitative western blotting to validate knockdown by esiRNA.
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