Phospho-ABL1 (T735) Antibody

Datasheet
Code CSB-PA008492
Size US$167
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Product Details

Uniprot No. P00519
Target Names ABL1
Alternative Names Abelson murine leukemia viral oncogene homolog 1 antibody; Abelson tyrosine protein kinase 1 antibody; Abl 1 antibody; ABL antibody; ABL proto oncogene 1 non receptor tyrosine kinase antibody; ABL1 antibody; ABL1_HUMAN antibody; bcr/abl antibody; bcr/c abl oncogene protein antibody; c ABL antibody; c abl oncogene 1 non receptor tyrosine kinase antibody; c abl oncogene 1 receptor tyrosine kinase antibody; c ABL1 antibody; JTK7 antibody; p150 antibody; Proto oncogene tyrosine protein kinase ABL1 antibody; Proto-oncogene c-Abl antibody; Tyrosine-protein kinase ABL1 antibody; v abl Abelson murine leukemia viral oncogene homolog 1 antibody; v abl antibody
Raised in Rabbit
Species Reactivity Human,Mouse,Rat,Monkey
Immunogen Synthesized peptide derived from Human Abl1 around the phosphorylation site of T735.
Immunogen Species Homo sapiens (Human)
Conjugate Non-conjugated
Isotype IgG
Purification Method The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen.
Concentration It differs from different batches. Please contact us to confirm it.
Buffer Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Form Liquid
Tested Applications WB, IHC, ELISA
Recommended Dilution
Application Recommended Dilution
WB 1:500-1:2000
IHC 1:100-1:300
ELISA 1:5000
Protocols Western Blotting(WB) Protocol
Immunohistochemistry (IHC) Protocol
ELISA Protocol
Troubleshooting and FAQs Antibody FAQs
Storage Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.
Lead Time Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

Target Data

Function 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'
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
  51. demonstrated that depletion of endogenous MAPK15 expression inhibited BCR-ABL1-dependent cell proliferation PMID: 26291129
  52. By visually examining the dynamics behavior, structural basis and energetic property of few typical Abl-drug complex cases, a significantly different pattern of non-bonded interactions between the binding of drug ligands to Abl receptor was revealed. PMID: 25418123
  53. Identify a novel BCR-ABL/IkappaBalpha/p53 network, whereby BCR-ABL functionally inactivates a key tumor suppressor in chronic myeloid leukemia. PMID: 26295305
  54. Blockade of the interaction between Bcr-Abl and PTB1B by small molecule SBF-1 to overcomes imatinib-resistance of K562 cells. PMID: 26721204
  55. BCR-ABL1 transcript types found in Syria were similar to that of Indian Far-Eastern, African or European populations. The M-BCR rearrangement types were not dependent on white blood count, platelet count, hemoglobin level or gender of the patients. PMID: 27273956
  56. Data suggest elevated interleukin-1beta secretion from tyrosine kinase inhibitor- (TKI-)resistant chronic myeloid leukemia (CML) cells contributes to TKI/imatinib resistance via promotion of cell viability/migration; cells used lack BCR-ABL mutation. PMID: 26831735
  57. Our results link FGF8, c-Abl and p300 in a regulatory pathway that controls DeltaNp63alpha protein stability and transcriptional activity. PMID: 25911675
  58. Suggest that AIC-47 in combination with imatinib strengthened the attack on cancer energy metabolism in BCR-ABL-harboring leukemic cells. PMID: 26607903
  59. Molecular rearrangements and the minimal residual disease follow-up for 5 chronic myeloid leukaemia patients; 3 resulted from new rearrangements between the BCR and ABL1 sequences (the breakpoints being located within BCR exon 13 in 2 cases and within BCR exon 18 in one case). The other 2 cases revealed a complex e8-[ins]-a2 fusion transcript involving a 3rd partner gene. PMID: 26252834
  60. analysis of WT1 and M-BCR-ABL expressions in chronic myeloid leukemia reveals that high WT1 expression in CML patients is detected especially in the advanced stages of the disease PMID: 26429162
  61. loss of expression or even the down-regulation of c-abl, but not WYHAZ, is a fundamental event that leads to genesis and progression of tumors PMID: 26429164
  62. Separase protein levels decrease and Separase proteolytic activity increases exclusively in b3a2 p210BCR-ABL-positive cell lines under Imatinib treatment. PMID: 26087013
  63. single oncogenic lesion triggers DNA methylation changes PMID: 25997600
  64. our results confirm that not obtaining a BCR-ABL/ABL ratio of PMID: 25756742
  65. Deleterious c-Cbl Exon Skipping Contributes to Glioma. PMID: 26152360
  66. These results reveal a new pathway in the DNA damage response wherein ABL-dependent tyrosine phosphorylation of DGCR8 stimulates the processing of selective primary miRNAs. PMID: 26126715
  67. we describe a regulatory pathway modulating BCR and BCR/ABL1 expression, showing that the BCR promoter is under the transcriptional control of the MYC/MAX heterodimer. PMID: 26179066
  68. High cABL expression is associated with triple-negative breast cancer. PMID: 25883211
  69. BCR- ABL1 mutations are associated with the clinical resistance, but may not be considered the only cause of resistance to imatinib. PMID: 25740611
  70. Expression profiling of adult acute lymphoblastic leukemia identifies a BCR-ABL1-like subgroup characterized by high non-response and relapse rates. PMID: 25769542
  71. expression of the BCR-ABL gene were confirmed by FISH, which revealed a high concordance (100%) rate. We found that real-time RT-qPCR is more reliable and should be used in Moroccan biomedical analysis laboratories to monitor CML progression PMID: 25730044
  72. c-Abl regulates proteasome abundance by controlling the ubiquitin-proteasomal degradation of PSMA7 subunit PMID: 25620702
  73. Findings suggest that proto-oncogene protein c-abl promotes hepatitis C virus (HCV) paoticle assembly by phosphorylating nonstructural protein 5A (NS5A) at Tyr(330). PMID: 26203192
  74. Expression of the ETS transcription factor GABPalpha is positively correlated to the BCR-ABL1/ABL1 ratio in CML patients and affects imatinib sensitivity in vitro. PMID: 26072332
  75. JunB is likely to be a key target of c-Abl in expression of p21 in Adriamycin-induced DDR. PMID: 26217035
  76. c-Abl induces HDAC1 stabilization possibly through phosphorylation of a cytoplasmic target that is involved in proteasomal degradation of HDAC1. PMID: 25561363
  77. ABL phosphorylates tyrosine 137 of H-, K-, and NRAS. PMID: 25999467
  78. In conclusion, specific c-Abl gene silencing using siRNA effectively reduced fibrosis-related gene expression. Inhibition of c-Abl by siRNA may be a potential therapeutic approach for fibrotic diseases such as systemic sclerosis. PMID: 25527259
  79. c-Abl was required for endogenous HIPK2 accumulation and phosphorylation of p53 at Ser46 in response to DNA damage by gamma- and UV radiation. PMID: 25944899
  80. Data sugget that the acquisition of additional BCR-ABL1 fusion genes in chronic myeloid leukemia (CML) in the blast phase (BP) through mitotic recombination between the derivative chromosome and the normal homologue. PMID: 26186983
  81. Lack of response to tyrosine kinase inhibitors associated with mutation in the BCR-ABL gene was significantly higher in imatinib-treated patients, and all mutations arose after treatment. T315I was a common treatment-emergent mutation PMID: 25615000
  82. ATRA treatment decreased DNA damage repair and suppressed acquisition of BCR-ABL mutations PMID: 24967705
  83. LPS-induced paxillin phosphorylation at Y31 and Y118 was mediated by c-Abl tyrosine kinase PMID: 25795725
  84. AIC-47, acting through the PPARgamma/beta-catenin pathway, induced down-regulation of c-Myc, leading to the disruption of the bcr-abl/mTOR/hnRNP signaling pathway, and switching of the expression of PKM2 to PKM1 in acute myeloid leukemia. PMID: 25644089
  85. Taken together, NS1 proteins of avian influenza A viruses interfere with the kinase activity of c-Abl, a major cellular signalling integrator that controls multiple signalling processes and cell fate regulations apparently including virus infections. PMID: 25052580
  86. Data (including data from mouse mutant strains) suggest that neuropilin-1 in vascular endothelium contributes to angiogenesis via VEGFA-independent mechanism involving ABL1 signaling in the extracellular matrix in VEGFA-independent mechanism. [REVIEW] PMID: 25233427
  87. The epigenetic silencing of miR-23a led to derepression of BCR/ABL expression, and consequently contributes to CML development and progression. PMID: 25213664
  88. Combined treatment with bortezomib and As2O3 downregulates Bcr/Abl mRNA and protein expression. PMID: 24939418
  89. STAT3 is a critical signaling node in BCR-ABL1 tyrosine kinase-independent leukemia resistance that is reversed by a discovered BP-5-087. PMID: 25134459
  90. C817 is a promising compound for treatment of CML patients with Bcr-Abl kinase domain mutations that confer imatinib resistance. PMID: 24487968
  91. PPARgamma2 physically associated with c-Abl and was phosphorylated on 2 Tyr residues in its regulatory activation function 1 domain. This positively regulates PPARgamma2 stability and adipogenesis. c-Abl binding to PPARgamma2 required the Pro12 residue. PMID: 25368164
  92. Clinical outcome under imatinib treatment was comparable and no risk prediction can be made according to e13a2 versus e14a2 BCR-ABL1 transcript type at diagnosis. PMID: 24837466
  93. Altered protein distribution in chronic myeloid leukemia dendritic cells was associated with defective generation of ABL1-dependent maturation signals and a dislocation of ABL1 from the F-actin cytoskeleton. PMID: 24617663
  94. Leptin levels were increased in BCR-ABL p210 positive chronic myeloid leukemia patients. PMID: 25648025
  95. BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene. PMID: 25293778
  96. Although BCR-ABL induces STAT5-tyrosine phosphorylation independent of JAK2-kinase activity, BCR-ABL is less efficient in inducing active STAT5A:STAT5B-heterodimerization than IL-3. PMID: 24836440
  97. c-Abl-mediated phosphorylation of Y39 play a role in regulating alpha-syn clearance and contribute to the pathogenesis of Parkinson's disease. PMID: 24412932
  98. The c-Abl/HDAC2 signaling pathway participates in the epigenetic blockade of gene expression in Alzheimer's disease pathology. PMID: 25219501
  99. BCR-ABL1 compound mutants confer different levels of tyrosine kinase inhibitor resistance, necessitating rational treatment selection to optimize clinical outcome. PMID: 25132497
  100. the functional relationship between Abl and CLASP2 is conserved and provides a means to control the CLASP2 association with the cytoskeleton. PMID: 24520051

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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, 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), SUBCELLULAR LOCATION: Isoform IB: Nucleus membrane, Lipid-anchor
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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