Key features and details
- Rabbit polyclonal to ABL1 (phospho Y412)
- Suitable for: WB
- Reacts with: Human
- Isotype: IgG
Product nameAnti-ABL1 (phospho Y412) antibody
See all ABL1 primary antibodies
DescriptionRabbit polyclonal to ABL1 (phospho Y412)
Tested applicationsSuitable for: WBmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse
The antiserum was produced against a chemically synthesized phosphopeptide derived from a region of human c-Abl 1b that contains tyrosine 412. Note: there are two widely expressed forms of c-Abl produced by alternative splicing, designated 1b (the more common form) and 1a. The corresponding phosphorylation site from 1a is tyrosine 393.
- Fibroblasts transfected with oncogenic ∆SH3-Abl.
c-Abl is a 140-150 kDa non-receptor protein tyrosine kinase whose precise functions are not known, but roles for Abl in growth factor and integrin signaling, cell cycle regulation, cytoskeletal reorganization, neurogenesis, and responses to DNA damage and oxidative stress have been suggested. c-Abl kinase activity is increased in vivo by diverse physiological stimuli including ionizing radiation, entry into S phase, integrin activation, and platelet-derived growth factor (PDGF) stimulation. c-Abl contains various protein binding domains that appear to enable it to regulate the functions of many proteins by forming complexes, most notably three isoforms of the oncogenic protein Bcr/Abl. c-Abl becomes fully activated by sequential phosphorylation of tyrosines 412 and 245.
Previously labelled as c Abl.
Storage instructionsShipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Storage bufferpH: 7.30
Preservative: 0.05% Sodium azide
Constituents: PBS, 0.1% BSA
PBS is without Mg2+ and Ca2+ and BSA is IgG and protease free.
Concentration information loading...
PurityImmunogen affinity purified
Purification notesPurified from rabbit serum by sequential epitope-specific chromatography. The antibody has been negatively pre-adsorbed using a non-phosphopeptide corresponding to the site of phosphorylation to remove antibody that is reactive with non-phosphorylated c-Abl. The final product is generated by affinity chromatography using a c-Abl derived peptide that is phosphorylated at tyrosine 245.
Primary antibody notesc-Abl is a 140-150 kDa non-receptor protein tyrosine kinase whose precise functions are not known, but roles for Abl in growth factor and integrin signaling, cell cycle regulation, cytoskeletal reorganization, neurogenesis, and responses to DNA damage and oxidative stress have been suggested. c-Abl kinase activity is increased in vivo by diverse physiological stimuli including ionizing radiation, entry into S phase, integrin activation, and platelet-derived growth factor (PDGF) stimulation. c-Abl contains various protein binding domains that appear to enable it to regulate the functions of many proteins by forming complexes, most notably three isoforms of the oncogenic protein Bcr/Abl. c-Abl becomes fully activated by sequential phosphorylation of tyrosines 412 and 245.
Our Abpromise guarantee covers the use of ab4717 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.1 - 1 µg/ml. Detects a band of approximately 140 kDa.|
FunctionProtein kinase that regulates key processes linked to cell growth and survival. Regulates cytoskeleton remodeling during cell differentiation, cell division and cell adhesion. Localizes to dynamic actin structures, and phosphorylates CRK and CRKL, DOK1, and other proteins controlling cytoskeleton dynamics. Regulates DNA repair potentially by activating the proapoptotic pathway when the DNA damage is too severe to be repaired. Phosphorylates PSMA7 that leads to an inhibition of proteasomal activity and cell cycle transition blocks.
Tissue specificityWidely expressed.
Involvement in diseaseNote=A chromosomal aberration involving ABL1 is a cause of chronic myeloid leukemia. Translocation t(9;22)(q34;q11) with BCR. The translocation produces a BCR-ABL found also in acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL).
Sequence similaritiesBelongs to the protein kinase superfamily. Tyr protein kinase family. ABL subfamily.
Contains 1 protein kinase domain.
Contains 1 SH2 domain.
Contains 1 SH3 domain.
modificationsPhosphorylated by PRKDC (By similarity). DNA damage-induced activation of c-Abl requires the function of ATM and Ser-446 phosphorylation (By similarity). Phosphorylation on Thr-735 is required for binding 14-3-3 proteins for cytoplasmic translocation.
Isoform IB is myristoylated on Gly-2.
Cellular localizationCytoplasm > cytoskeleton. Nucleus. Sequestered into the cytoplasm through interaction with 14-3-3 proteins and Nucleus membrane. The myristoylated c-ABL protein is reported to be nuclear.
- Information by UniProt
- Abelson murine leukemia viral oncogene homolog 1 antibody
- Abelson tyrosine protein kinase 1 antibody
- Abl 1 antibody
Peptide Competition:Peptide Competition: Fibroblasts transfected with oncogenic ?SH3-Abl were resolved by SDS-PAGE on a 10%
Fibroblasts transfected with oncogenic ∆SH3-Abl were resolved by SDS-PAGE on a 10% polyacrylamide gel and transferred to PVDF. Membranes were blocked with a 5% BSA-TBST buffer overnight at 4°C, then were incubated with 0.50
µg/mL phospho c-Abl (Tyr 412) antibody for two hours at room temperature in a 3% BSA-TBST buffer, following prior incubation with: no peptide (1), the non-phosphopeptide corresponding to the immunogen (2), a generic phosphotyrosine containing peptide (3), or, the phosphopeptide immunogen (4). After washing, membranes were incubated with goat F(ab’)2 anti-rabbit IgG alkaline phosphatase and signals were detected using the Tropix WesternStar method. The data show that only the peptide corresponding to phospho c-Abl (Tyr 412) blocks the antibody signal, thereby demonstrating the specificity of the antibody.
ab4717 has been referenced in 4 publications.
- Latella L et al. DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation. Genes Dev 31:648-659 (2017). PubMed: 28446595
- Kim SY et al. Rescue of platinum-damaged oocytes from programmed cell death through inactivation of the p53 family signaling network. Cell Death Differ 20:987-97 (2013). PubMed: 23598363
- Furlan A et al. Abl interconnects oncogenic Met and p53 core pathways in cancer cells. Cell Death Differ 18:1608-16 (2011). PubMed: 21455220
- Stevens TL et al. Using bcr-abl to examine mechanisms by which abl kinase regulates morphogenesis in Drosophila. Mol Biol Cell 19:378-93 (2008). WB . PubMed: 17959833