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A5844

Sigma-Aldrich

Monoclonal Anti-c-Abl antibody produced in mouse

clone ABL-148, ascites fluid

Synonyme(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

Numéro MDL:
MFCD00239646
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.44

Source biologique

mouse

Conjugué

unconjugated

Forme d'anticorps

ascites fluid

Type de produit anticorps

primary antibodies

Clone

ABL-148, monoclonal

Poids mol.

antigen 145 kDa

Espèces réactives

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

Numéro d'accès UniProt

P00519

Conditions d'expédition

dry ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... ABL1(25)
mouse ... Abl1(11350)
rat ... Abl1(311860)

Catégories apparentées

Description générale

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.

Spécificité

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.

Immunogène

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.

Actions biochimiques/physiologiques

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.

Description de la cible

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.

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

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
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
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