Recombinant Human Tyrosine-protein kinase ABL1 (ABL1), partial

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Code CSB-RP043554h
Size $224
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.
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Product Details

Greater than 90% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Alternative Names
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
Homo sapiens (Human)
Expression Region
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
Protein Length
Tag Info
N-terminal GST-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

To produce recombinant Human ABL1 protein, a well-established recombinant DNA technology is the key. A DNA template of ABL1 was constructed with N-terminal GST tag using the technique. Once the template was made, the recombinant Human ABL1 protein could be produced with it efficiently. CUSABIO has built a strict QC system to ensure quality. The expression region is 4-194aa of the Human ABL1. The purity of this recombinant is 90% determined by SDS-PAGE.

ABL1 is a protein coding gene that encodes Tyrosine-protein kinase ABL1. According to some studies, ABL1 may have the following features.
BCR-ABL1 lymphocytic leukemia is characterized by deletion of Ikaros. Genetic and epigenetic silencing of microRNA-203 enhances oncogene expression of ABL1 and BCR-ABL1. The xenobiotic inhibitor ABL001 can achieve dual targeting of BCR-ABL1. BCR-ABL1 composite mutations in combination with key kinase domain locations confer clinical resistance to ponatine in Ph-chromosome-positive leukemia patients. Combining BCR-ABL1 kinase inhibition and protein degradation may represent a strategy to address BCR-ABL1-dependent resistance.

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Target Background

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.
Gene References into Functions
  1. Findings demonstrate an important role of c-Abl kinase in Runx1-mediated megakaryocytes maturation and platelets formation and provide a potential mechanism of Abl kinase-regulated hematopoiesis. PMID: 29730354
  2. Data indicate that c-Abl kinase interacts with and phosphorylates YY1 protein regulation its transcriptional activity. PMID: 29807053
  3. The significant role of c-Abl kinase in barrier altering agonists-mediated cytoskeletal biomechanics has been demonstrated. PMID: 29343719
  4. We did not find the AIF1L-ETV6 and ABL1-AIF1L fusions in other ETV6-ABL1-positive ALL. Nevertheless, functional studies would be needed to establish the biological role of AIF1L-ETV6 and ABL1-AIF1L and to determine whether they contribute to leukemogenesis and/or to the final leukemia phenotype. PMID: 29726059
  5. Once activated, c-Abl kinase regulated the activity of Vav1, which further affected Rac1/PAK1/LIMK1/cofilin signaling pathway. PMID: 29058761
  6. The combination of BCR-ABL1 transcript type and spleen size at diagnosis is significantly predictive for achieving an overall MMR and FFS. Incorporating these predictors could be important when making clinical decisions regarding changing therapy for CML patients treated initially with IM. PMID: 28540759
  7. Patients with its E255K/V mutation have a poor prognosis, regardless of the stage of the disease at detection. PMID: 29464484
  8. Therefore EphA4 is an emerging AbetaOs receptor and the activation of the EphA4/c-Abl axis would explain the synaptic spine alterations found in Alzheimer's disease. PMID: 29378302
  9. expression of WASP inversely correlates with BCR-ABL1 levels and the progression of the disease in Chronic myeloid leukemia patients. BCR-ABL1 downregulates WASP in part by epigenetic modification of its proximal promoter. PMID: 29022901
  10. The imaging method achieved ultrasensitive detection of BCR/ABL fusion gene with a low detection limit down to 23 fM. And this method exhibited wide linear ranges over seven orders of magnitude and excellent discrimination ability toward target PMID: 27577607
  11. This study combines a chemical rescue approach with quantitative phosphoproteomics to identify targets of Abl and their phosphorylation sites with enhanced temporal resolution. Both known and novel putative substrates are identified, presenting opportunities for studying unanticipated functions of Abl under physiological and pathological conditions. PMID: 29341593
  12. This is the first report evaluating the role of SOD2 in native and T351-mutated BCR-ABL-expressing cells and in a large cohort of chronic myeloid leukemia patients. In leukemic cells silenced for SOD2 expression a specific down-regulation of the expression of PRDX2 gene was found. PMID: 29550484
  13. we identified a novel mutant p53:c-Abl cytoplasmic signaling complex that promotes MDA-MB-231 cell growth and highlights the contextual cues that confer oncogenic activity to c-Abl in breast cancer PMID: 28661474
  14. c-Abl/Arg are oncogenic kinases that regulate differential gene expression PMID: 28555614
  15. The compound missense mutations in BCR-ABL kinase domain responsible to elicit disease progression, drug resistance or disease relapse in chronic myeloid leukemia. PMID: 28278078
  16. JNJ-26854165, an inhibitor of MDM2, inhibits proliferation and triggers cell death in a p53-independent manner in various BCR/ABL-expressing cells, which include primary leukemic cells from patients with CML blast crisis and cells expressing the Imatinib-resistant T315I BCR/ABL mutant. PMID: 27999193
  17. we identified a novel c-Abl:p53:p21 signaling axis that functions as a powerful suppressor of mammary tumorigenesis and metastatic progression. PMID: 27626309
  18. Double inhibition of the N- and C-terminal termini can disrupt Hsp90 chaperone function synergistically, but not antagonistically, in Bcr-Abl-positive human leukemia cells. PMID: 28036294
  19. this study identifies different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction PMID: 27852045
  20. BGB324 does not inhibit BCR-ABL1 and consequently inhibits chronic myeloid leukemia (CML)independent of BCR-ABL1 mutational status. Our data show that Axl inhibition has therapeutic potential in BCR-ABL TKI-sensitive as well as -resistant CML and support the need for clinical trials PMID: 27856601
  21. BCR-ABL1-positive microvesicles from chronic myeloid leukemias malignantly transform human bone marrow mesenchymal stem cells. PMID: 28836580
  22. Data indicate the Sp1 oncogene functions as a positive regulator for BCR/ABL expression. PMID: 27144331
  23. dehydrocostus lactone significantly inhibits the phosphorylation expression of Bcr/Abl, STAT5, JAK2, and STAT3 and downstream molecules including p-CrkL, Mcl-1, Bcl-XL, and Bcl-2 proteins in K562 cells. PMID: 28300289
  24. H19 overexpression, a frequent event in chronic myeloid leukemia, was associated with higher BCR-ABL transcript and disease progression. H19 DMR/ICR hypomethylation in CML may be one of the mechanisms mediating H19 overexpression. PMID: 28776669
  25. These findings show that drug-resistance mutations in the Abl RM exert their allosteric effect by promoting the activated state of Abl and not by decreasing the drug affinity for the kinase. PMID: 28945248
  26. Germline variants in ABL1 cause a syndrome characterized by congenital heart disease, skeletal abnormalities, and failure to thrive. PMID: 28288113
  27. c-Abl has a critical role in alpha-synuclein-induced neurodegeneration; selective inhibition of c-Abl may be neuroprotective PMID: 27348587
  28. We demonstrate that nanopore technology is suitable for employment in the hematology laboratory for detecting BCR-ABL1 kinase domain mutation in Philadelphia-positive leukemias. PMID: 28663031
  29. Frequent molecular monitoring and intervention are required for patients who do not show a reduction in BCR-ABL1 transcripts to these levels after stem cell transplantation. PMID: 27334764
  30. c-Abl promotes TGF-beta-induced SKIP/Smad3 interaction. PMID: 28666867
  31. Data indicate the feasibility of detecting ABL1 mutations in cerebrospinal fluid (CSF) by next-generation sequencing (NGS) in patients with central nervous system relapse in BCR-ABL1-positive acute lymphoblastic leukemia. PMID: 28451802
  32. the e13a2 BCR-ABL1 fusion transcript affects the rate, the depth, and the speed of the response to treatment with imatinib firstline, and that including the transcript type in the calculation of the baseline risk scores may improve prognostic stratification and may help the choice of the best treatment policy. PMID: 28466557
  33. Normal ABL1 is a tumor suppressor in BCR-ABL1-induced leukemia. Allosteric stimulation of the normal ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors. PMID: 26864341
  34. the ABL family of tyrosine kinases rheostatically enhances IRE1alpha's enzymatic activities, thereby potentiating endoplasmic reticulum stress-induced apoptosis. PMID: 28380378
  35. 6 overexpression may contribute to the high proliferation and low apoptosis in chronic myeloid leukemia cells and can be regulated by BCR/ABL signal transduction through downstream phosphoinositide 3-kinase/Akt and Janus kinase/signal transducer and activator of transcription pathways, suggesting cell division cycle protein 6 as a potential therapeutic target in chronic myeloid leukemia. PMID: 28639894
  36. ETV6-ABL1 fusion occurs in both lymphoid and myeloid leukemias; the genomic profile and clinical behavior resemble BCR-ABL1-positive malignancies, including the unfavorable prognosis, particularly of acute leukemias. The poor outcome suggests that treatment with tyrosine kinase inhibitors should be considered for patients with this fusion. PMID: 27229714
  37. the c-Abl non-receptor kinase phosphorylates DDB1 at residue Tyr-316 to recruit a small regulatory protein, DDA1, leading to increased substrate ubiquitination PMID: 28087699
  38. drug sensitivity profiles of a set of compound mutations in ABL kinase were also presented in this study. Thus, our large scale computational study provides comprehensive sensitivity/resistance profiles of ABL mutations toward specific kinase inhibitors. PMID: 28475010
  39. though our data support the previous findings that co-expression of BCR-ABL transcripts is due to the occurrence of exonic and intronic polymorphisms in the BCR gene, it also shows that the intronic polymorphism can arise without the linked exonic polymorphism. The occurrence of ABL kinase domain mutation is less frequent in Indian population. PMID: 27748288
  40. In silico three-dimensional modeling of apoptin, molecular docking experiments between apoptin model and the known structure of Bcr-Abl, and the 3D structures of SH2 domains of CrkL and Bcr-Abl, were performed. PMID: 22253690
  41. The present study screened for the presence of bcr-abl transcripts in the blood of a group of healthy individuals. PMID: 24535287
  42. inhibition of c-Abl minimizes receptor recycling pathways and results in chaperone-dependent trafficking of the TfR1 to the lysosome for degradation. PMID: 27226592
  43. Data indicate that the biosensor showed excellent analytical performance for the detection of the BCR/ABL oncogene in clinical samples of patients with leukemia. PMID: 27693719
  44. In this review, we examine the evidence to illuminate the molecular mechanism of ABL1 in the progression of gastric cancer (GC) patients with depression and identify out new and effective methods for the initial and longterm treatment of GC. PMID: 27666407
  45. Studies indicate that the prognosis of BCR-ABL-positive acute myeloid leukemia (BCR-ABL+ AML) seems to depend on the cytogenetic and/or molecular background rather than on BCR-ABL itself. PMID: 27297971
  46. Results indicate that eIF4B integrates the signals from Pim and PI3K/Akt/mTOR pathways in Abl-expressing leukemic cells. PMID: 26848623
  47. The notion that regular and close monitoring of MSI2 mRNA levels in chronic myeloid leukemia patients might identify patients at risk of progressing to blast crisis was not supported by this study; an increase in MSI2 transcripts does not precede an increase in BCR-ABL1 mRNA levels. PMID: 27160312
  48. Collective results lead us to conclude that GADD45alpha modulates curcumin sensitivity through activation of c-Abl > JNK signaling in a mismatch repair-dependent manner PMID: 26833194
  49. ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling. PMID: 26838548
  50. mammalian c-Abl plays an important role in steroid hormone receptor-mediated transcription by regulating RBM39 PMID: 27018250

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Involvement in disease
Leukemia, chronic myeloid (CML); Congenital heart defects and skeletal malformations syndrome (CHDSKM)
Subcellular Location
Cytoplasm, cytoskeleton. Nucleus. Mitochondrion.; [Isoform IB]: Nucleus membrane; Lipid-anchor. Note=The myristoylated c-ABL protein is reported to be nuclear.
Protein Families
Protein kinase superfamily, Tyr protein kinase family, ABL subfamily
Tissue Specificity
Widely expressed.
Database Links

HGNC: 76

OMIM: 189980

KEGG: hsa:25

STRING: 9606.ENSP00000361423

UniGene: Hs.431048

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