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A5844

Sigma-Aldrich

Monoclonal Anti-c-Abl antibody produced in mouse

clone ABL-148, ascites fluid

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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About This Item

MDL number:
MFCD00239646
UNSPSC Code:
12352203
NACRES:
NA.44

biological source

mouse

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.

P00519

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.

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Storage Class Code

10 - Combustible liquids

WGK

nwg

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Cytoplasmic c-Abl provides a molecular `Rheostat?controlling carcinoma cell survival and invasion
Kain KH, et al.
Oncogene, 22(38), 6071-6071 (2003)
c-Abl: activation and nuclear targets
Shaul Y
Cell Death and Differentiation, 7(1), 10-10 (2000)
Z M Yuan et al.
Proceedings of the National Academy of Sciences of the United States of America, 94(4), 1437-1440 (1997-02-18)
Activation of the c-Abl protein tyrosine kinase by certain DNA-damaging agents contributes to downregulation of Cdk2 and G1 arrest by a p53-dependent mechanism. The present work investigates the potential role of c-Abl in apoptosis induced by DNA damage. Transient transfection
Qianyi Bao et al.
Cell communication and signaling : CCS, 22(1), 247-247 (2024-05-01)
Renal fibrosis is a prevalent manifestation of chronic kidney disease (CKD), and effective treatments for this disease are currently lacking. Myofibroblasts, which originate from interstitial fibroblasts, aggregate in the renal interstitium, leading to significant accumulation of extracellular matrix and impairment
Daniela A Gutierrez et al.
Frontiers in cellular neuroscience, 13, 526-526 (2019-12-19)
Spine pathology has been implicated in the early onset of Alzheimer's disease (AD), where Aβ-Oligomers (AβOs) cause synaptic dysfunction and loss. Previously, we described that pharmacological inhibition of c-Abl prevents AβOs-induced synaptic alterations. Hence, this kinase seems to be a
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