Phospho-ABL1 (T735) Antibody

1. Findings demonstrate a significant role of c-Abl kinase in Runx1-mediated megakaryocytes maturation and platelets formation, providing a potential mechanism for Abl kinase-regulated hematopoiesis. PMID: 29730354
2. Data indicate that c-Abl kinase interacts with and phosphorylates YY1 protein, regulating its transcriptional activity. PMID: 29807053
3. The substantial role of c-Abl kinase in barrier-altering agonists-mediated cytoskeletal biomechanics has been demonstrated. PMID: 29343719
4. Although we did not find the AIF1L-ETV6 and ABL1-AIF1L fusions in other ETV6-ABL1-positive ALL, functional studies are needed to establish the biological role of AIF1L-ETV6 and ABL1-AIF1L and to determine if they contribute to leukemogenesis and/or the final leukemia phenotype. PMID: 29726059
5. Upon activation, c-Abl kinase regulated the activity of Vav1, further affecting the 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 crucial when making clinical decisions regarding therapy adjustments for CML patients initially treated with IM. PMID: 28540759
7. Patients with the E255K/V mutation have a poor prognosis, regardless of the disease stage at detection. PMID: 29464484
8. EphA4 is an emerging AbetaOs receptor, and the activation of the EphA4/c-Abl axis could explain the synaptic spine alterations found in Alzheimer's disease. PMID: 29378302
9. WASP expression inversely correlates with BCR-ABL1 levels and disease progression 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 the BCR/ABL fusion gene with a low detection limit down to 23 fM. This method exhibited wide linear ranges over seven orders of magnitude and excellent discrimination ability toward the target. PMID: 27577607
11. This study combined 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 were 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 the 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. Compound missense mutations in the BCR-ABL kinase domain are responsible for eliciting 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, including 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 demonstrate 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 that 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, not by decreasing 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 plays 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, depth, and speed of the response to treatment with imatinib firstline, and including the transcript type in the calculation of the baseline risk scores may improve prognostic stratification and assist in choosing the best treatment policy. PMID: 28466557
33. Normal ABL1 is a tumor suppressor in BCR-ABL1-induced leukemia. Allosteric stimulation of normal ABL1 kinase activity enhances 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. Although 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 the Indian population. PMID: 27748288
40. In silico three-dimensional modeling of apoptin, molecular docking experiments between the 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 demonstrated excellent analytical performance for detecting 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 new and effective methods for the initial and long-term treatment of GC. PMID: 27666407
45. Studies indicate that the prognosis of BCR-ABL-positive acute myeloid leukemia (BCR-ABL+ AML) appears to depend on the cytogenetic and/or molecular background rather than 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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HGNC: 76

OMIM: 189980

KEGG: hsa:25

STRING: 9606.ENSP00000361423

UniGene: Hs.431048