产品: c Abl 抗体
货号: AF6038
描述: Rabbit polyclonal antibody to c Abl
反应: Human, Mouse, Rat, Monkey
预测: Pig, Zebrafish, Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量: 135kDa; 123kD(Calculated).
蛋白号: P00519
RRID: AB_2834968


   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货



WB 1:500-1:2000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

Pig(100%), Zebrafish(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(80%), Dog(100%), Chicken(100%), Xenopus(91%)
c Abl Antibody detects endogenous levels of total c Abl.
引用格式: Affinity Biosciences Cat# AF6038, RRID:AB_2834968.
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.


Abelson murine leukemia viral oncogene homolog 1; Abelson tyrosine protein kinase 1; Abl 1; ABL; ABL proto oncogene 1 non receptor tyrosine kinase; ABL1; ABL1_HUMAN; bcr/abl; bcr/c abl oncogene protein; c ABL; c abl oncogene 1 non receptor tyrosine kinase; c abl oncogene 1 receptor tyrosine kinase; c ABL1; JTK7; p150; Proto oncogene tyrosine protein kinase ABL1; Proto-oncogene c-Abl; Tyrosine-protein kinase ABL1; v abl Abelson murine leukemia viral oncogene homolog 1; v abl;


P00519 ABL1_HUMAN:

Widely expressed.

The ABL1 protooncogene encodes a cytoplasmic and nuclear protein tyrosine kinase that has been implicated in processes of cell differentiation, cell division, cell adhesion, and stress response. Activity of c-Abl protein is negatively regulated by its SH3 domain, and deletion of the SH3 domain turns ABL1 into an oncogene.




Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P00519 作为底物

Site PTM Type Enzyme
S43 Phosphorylation
S50 Phosphorylation
Y70 Phosphorylation P08631 (HCK) , P07948 (LYN) , P06241 (FYN) , P00519 (ABL1)
S75 Phosphorylation
Y93 Phosphorylation
S113 Phosphorylation
Y115 Phosphorylation P08631 (HCK) , P07948 (LYN) , P06241 (FYN)
T117 Phosphorylation
Y128 Phosphorylation P06241 (FYN) , P08631 (HCK) , P07948 (LYN)
Y139 Phosphorylation P07948 (LYN) , P08631 (HCK) , P06241 (FYN)
S142 Phosphorylation
Y167 Phosphorylation
Y172 Phosphorylation P07948 (LYN) , P08631 (HCK) , P06241 (FYN)
Y174 Phosphorylation
S180 Phosphorylation
Y185 Phosphorylation P08631 (HCK) , P07948 (LYN) , P06241 (FYN)
S187 Phosphorylation
Y215 Phosphorylation P08631 (HCK) , P07948 (LYN) , P06241 (FYN)
T224 Phosphorylation
Y226 Phosphorylation P06241 (FYN) , P08631 (HCK) , P12931 (SRC) , P07948 (LYN) , P00519 (ABL1)
S229 Phosphorylation
Y232 Phosphorylation
T243 Phosphorylation
Y253 Phosphorylation
Y257 Phosphorylation
Y264 Phosphorylation
S265 Phosphorylation
T267 Phosphorylation
K274 Acetylation
K285 Ubiquitination
T306 Phosphorylation
Y312 Phosphorylation
T315 Phosphorylation
Y320 Phosphorylation
T389 Phosphorylation
T392 Phosphorylation
Y393 Phosphorylation P08631 (HCK) , P07948 (LYN) , A0A173G4P4 (Abl fusion) , P06241 (FYN) , P12931 (SRC) , P00519 (ABL1)
T394 Phosphorylation
K400 Ubiquitination
Y413 Phosphorylation
S417 Phosphorylation
S446 Phosphorylation Q13315 (ATM)
S456 Phosphorylation
Y456 Phosphorylation
Y469 Phosphorylation
K512 Ubiquitination
T532 Phosphorylation
S535 Phosphorylation
S559 Phosphorylation
S569 Phosphorylation
T597 Phosphorylation
S601 Phosphorylation
T610 Phosphorylation
T613 Phosphorylation
S618 Phosphorylation Q13177 (PAK2)
S619 Phosphorylation Q13177 (PAK2)
S620 Phosphorylation
S642 Phosphorylation
T649 Phosphorylation
T653 Phosphorylation
S659 Phosphorylation
S676 Phosphorylation
S679 Phosphorylation
S683 Phosphorylation
K689 Methylation
S690 Phosphorylation
T692 Phosphorylation
S696 Phosphorylation
T700 Phosphorylation
S708 Phosphorylation
S709 Phosphorylation
S710 Phosphorylation
K711 Acetylation
S718 Phosphorylation
T735 Phosphorylation Q13043 (STK4) , P49759 (CLK1) , P41279 (MAP3K8) , Q9HAZ1 (CLK4) , Q13188 (STK3) , P33981 (TTK)
T751 Phosphorylation
K759 Acetylation
T781 Phosphorylation
S805 Phosphorylation
S808 Phosphorylation
S809 Phosphorylation
T814 Phosphorylation
T823 Phosphorylation
T844 Phosphorylation
T852 Phosphorylation
T854 Phosphorylation
S855 Phosphorylation
S859 Phosphorylation
S884 Phosphorylation
S915 Phosphorylation
S917 Phosphorylation
S919 Phosphorylation
T935 Phosphorylation
S936 Phosphorylation
S943 Phosphorylation
S949 Phosphorylation
T963 Phosphorylation
S977 Phosphorylation
Y1064 Phosphorylation
Y1070 Phosphorylation
S1106 Phosphorylation
T1111 Phosphorylation



Non-receptor tyrosine-protein kinase that plays a role in many key processes linked to cell growth and survival such as cytoskeleton remodeling in response to extracellular stimuli, cell motility and adhesion, receptor endocytosis, autophagy, DNA damage response and apoptosis. Coordinates actin remodeling through tyrosine phosphorylation of proteins controlling cytoskeleton dynamics like WASF3 (involved in branch formation); ANXA1 (involved in membrane anchoring); DBN1, DBNL, CTTN, RAPH1 and ENAH (involved in signaling); or MAPT and PXN (microtubule-binding proteins). Phosphorylation of WASF3 is critical for the stimulation of lamellipodia formation and cell migration. Involved in the regulation of cell adhesion and motility through phosphorylation of key regulators of these processes such as BCAR1, CRK, CRKL, DOK1, EFS or NEDD9. Phosphorylates multiple receptor tyrosine kinases and more particularly promotes endocytosis of EGFR, facilitates the formation of neuromuscular synapses through MUSK, inhibits PDGFRB-mediated chemotaxis and modulates the endocytosis of activated B-cell receptor complexes. Other substrates which are involved in endocytosis regulation are the caveolin (CAV1) and RIN1. Moreover, ABL1 regulates the CBL family of ubiquitin ligases that drive receptor down-regulation and actin remodeling. Phosphorylation of CBL leads to increased EGFR stability. Involved in late-stage autophagy by regulating positively the trafficking and function of lysosomal components. ABL1 targets to mitochondria in response to oxidative stress and thereby mediates mitochondrial dysfunction and cell death. In response to oxidative stress, phosphorylates serine/threonine kinase PRKD2 at 'Tyr-717'. ABL1 is also translocated in the nucleus where it has DNA-binding activity and is involved in DNA-damage response and apoptosis. Many substrates are known mediators of DNA repair: DDB1, DDB2, ERCC3, ERCC6, RAD9A, RAD51, RAD52 or WRN. Activates the proapoptotic pathway when the DNA damage is too severe to be repaired. Phosphorylates TP73, a primary regulator for this type of damage-induced apoptosis. Phosphorylates the caspase CASP9 on 'Tyr-153' and regulates its processing in the apoptotic response to DNA damage. Phosphorylates PSMA7 that leads to an inhibition of proteasomal activity and cell cycle transition blocks. ABL1 acts also as a regulator of multiple pathological signaling cascades during infection. Several known tyrosine-phosphorylated microbial proteins have been identified as ABL1 substrates. This is the case of A36R of Vaccinia virus, Tir (translocated intimin receptor) of pathogenic E.coli and possibly Citrobacter, CagA (cytotoxin-associated gene A) of H.pylori, or AnkA (ankyrin repeat-containing protein A) of A.phagocytophilum. Pathogens can highjack ABL1 kinase signaling to reorganize the host actin cytoskeleton for multiple purposes, like facilitating intracellular movement and host cell exit. Finally, functions as its own regulator through autocatalytic activity as well as through phosphorylation of its inhibitor, ABI1. Regulates T-cell differentiation in a TBX21-dependent manner. Phosphorylates TBX21 on tyrosine residues leading to an enhancement of its transcriptional activator activity (By similarity).


Acetylated at Lys-711 by EP300 which promotes the cytoplasmic translocation.

Phosphorylation at Tyr-70 by members of the SRC family of kinases disrupts SH3 domain-based autoinhibitory interactions and intermolecular associations, such as that with ABI1, and also enhances kinase activity. Phosphorylation at Tyr-226 and Tyr-393 correlate with increased activity. DNA damage-induced activation of ABL1 requires the function of ATM and Ser-446 phosphorylation (By similarity). Phosphorylation at Ser-569 has been attributed to a CDC2-associated kinase and is coupled to cell division (By similarity). Phosphorylation at Ser-618 and Ser-619 by PAK2 increases binding to CRK and reduces binding to ABI1. Phosphorylation on Thr-735 is required for binding 14-3-3 proteins for cytoplasmic translocation. Phosphorylated by PRKDC (By similarity).

Polyubiquitinated. Polyubiquitination of ABL1 leads to degradation.


Cytoplasm>Cytoskeleton. Nucleus. Mitochondrion.
Note: Shuttles between the nucleus and cytoplasm depending on environmental signals. Sequestered into the cytoplasm through interaction with 14-3-3 proteins. Localizes to mitochondria in response to oxidative stress (By similarity).

Nucleus membrane>Lipid-anchor.
Note: The myristoylated c-ABL protein is reported to be nuclear.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location

Widely expressed.


Interacts with SORBS1 following insulin stimulation. Found in a trimolecular complex containing CDK5 and CABLES1. Interacts with CABLES1 and PSTPIP1. Interacts with ZDHHC16, ITGB1 and HCK (By similarity). Interacts with STX17; probably phosphorylates STX17. Interacts with INPPL1/SHIP2. Interacts with the 14-3-3 proteins, YWHAB, YWHAE, YWHAG, YWHAH, SFN AND YWHAZ; the interaction with 14-3-3 proteins requires phosphorylation on Thr-735 and, sequesters ABL1 into the cytoplasm. Interacts with ABI1, ABI2, BCR, CRK, FGR, FYN, HCK, LYN, PSMA7 RAD9A, RAD51, RAD52, TP73 and WASF3. A complex made of ABL1, CTTN and MYLK regulates cortical actin-based cytoskeletal rearrangement critical to sphingosine 1-phosphate (S1P)-mediated endothelial cell (EC) barrier enhancement. Interacts (via SH3 domain) with CASP9; the interaction is direct and increases in the response of cells to genotoxic stress and ABL1/c-Abl activation. Found in a complex with ABL1, ABL2, CRK and UNC119; leading to the inhibition of CRK phosphorylation by ABL kinases. Interacts with TBX21 (By similarity).


Belongs to the protein kinase superfamily. Tyr protein kinase family. ABL subfamily.


· Cellular Processes > Cell growth and death > Cell cycle.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Pathogenic Escherichia coli infection.

· Human Diseases > Infectious diseases: Bacterial > Shigellosis.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cardiovascular diseases > Viral myocarditis.

· Organismal Systems > Development > Axon guidance.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)


1). Hippo/YAP signaling pathway protects against neomycin-induced hair cell damage in the mouse cochlea. Cellular and Molecular Life Sciences, 2022 (PubMed: 35044530) [IF=8.0]

Application: IF/ICC    Species: Mouse    Sample: HCs

Fig. 6 C-Abl expression is regulated by the Hippo/YAP signaling pathway in cochlear HCs after neomycin exposure. A The cochleae were dissected from P3 WT mice, and immunolabeled with Myosin7a (green), Sox2 (blue), and C-Abl (red). Immunofluorescence staining showed the expression and localization of C-Abl in the P3 WT mouse cochlea under a 63 × microscope, and C-Abl was expressed in the nuclei of cochlear HCs. B Schematic diagram of drug addition in tissue culture (divided into three groups). C Immunofluorescence staining with C-Abl and Myosin7a in the middle turn of the cochlear basilar membrane after different treatments. The expression of C-Abl was significantly increased in the neomycin-treated group and decreased in the XMU/neomycin-treated group. *p < 0.05, **p < 0.01, ***p < 0.001, n = 3. Scale bars = 20 µm

Application: WB    Species: Mouse    Sample: HCs

Fig. 7 YAP Overexpression inhibits C-Abl-mediated HC apoptosis in cochlear HCs after neomycin damage. A Schematic diagram of drug addition in tissue culture (divided into four groups). B The cochleae were dissected from P3 WT mice used for Western blot experiment. Western blot showed that the expression of C-Abl was significantly increased in the neomycin-treated group and decreased in the XMU/neomycin-treated group. C, D The mRNA levels of C-Abl signaling downstream genes were analyzed by qPCR in the different treatment groups. The qPCR results showed that XMU downregulated the expression of C-Abl and p73 and that VP upregulated the expression of C-Abl and p73. *p < 0.05, **p < 0.01, ***p < 0.001, n = 3. Scale bars = 20 µm

2). The enhancement of Tetrandrine to gemcitabine-resistant PANC-1 cytochemical sensitivity involves the promotion of PI3K/Akt/mTOR-mediated apoptosis and AMPK-regulated autophagy. ACTA HISTOCHEMICA, 2021 (PubMed: 34416437) [IF=2.5]

Application: WB    Species: Human    Sample: PANC-1/GEM cells

Fig. 3. Mechanisms underlying the effects of TET on the chemosensitivity of PANC-1/GEM cells to GEM. (A) Detection of Hoechst 33258-stained nuclei in PANC-1/ GEM cells treated as indicated. (B) Detection of apoptosis in PANC-1/GEM cells treated as indicated. PANC-1/GEM cells were treated with 2 μ g/mL GEM, 40 μ g/mL TET, or 5 μ M MHY1485 for 24 h. (C) Expression of PI3K/Akt/mTOR signaling-related proteins in cells treated as indicated and analyzed by immunoblotting. GAPDH was used as the loading control. Representative images of the expression profiles of all protein from three independent experiments are shown. (D) Expression profile of survivin gene in PANC-1/GEM cells treated with GEM and TET, alone or in combination. After treatment with various concentrations of GEM (0, 1, and 2 μ g/mL) and TET (0, 20, and 40 μ g/mL), alone or in combination, for 48 h, the expression profile of the survivin gene was analyzed using real-time PCR. ***P < 0.001.


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