ABL1 (phospho-Tyr412) Antibody
- Known as:
- ABL1 (phosphorilated-Tyr412) Antibody
- Catalog number:
- abx000092
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- ABL1 (phospho-Tyr412) Antibody
Related genes to: ABL1 (phospho-Tyr412) Antibody
- Gene:
- ABL1 NIH gene
- Name:
- ABL proto-oncogene 1, non-receptor tyrosine kinase
- Previous symbol:
- ABL
- Synonyms:
- JTK7, c-ABL, p150
- Chromosome:
- 9q34.12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ABL1 (phospho-Tyr412) Antibody
Related articles to: ABL1 (phospho-Tyr412) Antibody
- Tauopathies arise when normal functions of the tau protein in axonal transport and neuronal maintenance are disrupted by an imbalance between kinases and phosphatases. Dysregulation of key kinases such as dual-specificity Tyrosine-Regulated Kinase 1A (DYRK1A), Tau Tubulin Kinase 1 (TTBK1), and ABL Proto-Oncogene 1, and Non-Receptor Tyrosine Kinase (ABL1) drives excessive tau phosphorylation and neurofibrillary tangle accumulation. DYRK1A regulates MAPT exon 10 splicing and phosphorylates tau at multiple Ser/Thr residues, priming it for further phosphorylation by other kinases. TTBK1 phosphorylates tau at disease-associated epitopes within the microtubule-binding domain, promoting detachment from microtubules and aggregation. ABL1 phosphorylates tau at tyrosine residues, linking tau modification with Aβ-induced synaptic dysfunction. These events collectively drive tau hyperphosphorylation, misfolding, and neurofibrillary pathology characteristic of tauopathies. To identify natural product-derived multitarget inhibitors for these kinases, we developed a comprehensive machine learning (ML) workflow trained on bioactivity data from ChEMBL and BindingDB. We implemented five distinct classifiers: CatBoost, Support Vector Machine (SVM), k-Nearest Neighbors (KNN), Naive Bayes, and XGBoost. Stratified sampling and SMOTE were employed to address class imbalance for DYRK1A and ABL1, while Bemis-Murcko scaffold splitting was used to ensure rigorous evaluation of the data-scarce TTBK1 data set. A soft-voting ensemble model, integrating optimized CatBoost, XGBoost, and SVM, demonstrated superior performance. This robust ensemble was deployed to screen ∼695,000 natural compounds from the COCONUT 2.0 database. The resulting hits were refined through consensus molecular docking and deep learning-based rescoring (GNINA), leading to the identification of two high-potential lead molecules, CNP0591834.1 and CNP0484145.0. Validation using 1 μs molecular dynamics simulations confirmed their conformational stability and strong binding affinities. Steered MD further demonstrated their superior mechanical resistance to unbinding, particularly in DYRK1A and ABL1 complexes. Overall, this integrative computational framework highlights these two natural compounds as potent multitarget leads with strong potential to mitigate tau-hyperphosphorylation-driven neurodegeneration. - Source: PubMed
Publication date: 2026/04/17
Choudhury ArunabhSaeed Mohammad UmarPrabha SnehHassan Md Imtaiyaz - Pediatric Chronic Myeloid Leukemia (CML), a rare hematologic malignancy, accounts for only 2-3% of cases of leukemia in pediatric patients. The case presented here is of a previously healthy 13-year-old male, who came to the emergency department with increasing fatigue, abdominal distention, and discomfort. On examination, he was pale with significant splenomegaly. His investigation findings included marked leukocytosis (WBC > 600 × 10/L), severe anemia (Hb 5 g/dL), along with thrombocytosis (Platelets > 1,530 × 10/L). The diagnosis was made by peripheral smear and bone marrow biopsy, showing Chronic Phase CML with less than 3% blasts along with intense granulocytic hyperplasia. Molecular studies by PCR identified the BCR:ABL1 fusion transcript. The initial treatment approach emphasized cytoreduction therapy with hydroxyurea, intravenous fluid administration, and preventive medication with allopurinol to protect against the risk of tumor lysis syndrome. After the patient became stabilized, imatinib, a first-line tyrosine kinase inhibitor, was started. The supportive care consisted of transfusion support and gastrointestinal protection. The patient responded quite well to therapy and was therefore discharged with instructions for further follow-up care. As highlighted by this case, the importance of prompt diagnosis, the initiation of cytoreduction therapy, and the use of molecular therapy in treating CML in children cannot be neglected. CML in children is an uncommon but curable form of leukemia. - Source: PubMed
Publication date: 2026/04/01
Asees MohammadAbdalhaq ToleenAmer Johnny - Chronic myeloid leukemia (CML) is a myeloproliferative disorder caused by the translocation and usually presents with leukocytosis. While somatic mutations can occasionally occur within CML, co-mutations in have rarely been reported. We describe a case of concurrent CML and MDS with mutated , presenting with macrocytic anemia without leukocytosis. Whole-genome sequencing using Nanopore technology was performed to identify the t(9;22) breakpoint. Probes were designed to target the translocation and the mutation. Single-cell DNA sequencing suggested that the mutation likely preceded and blunted the expected granulopoiesis, thereby explaining the myelodysplastic syndrome phenotype without leukocytosis. This case illustrates how single-cell analysis can reveal meaningful clonal interactions that would not be evident with traditional bulk sequencing. - Source: PubMed
Publication date: 2026/04/15
Brailovski EugeneVahedi AmiraliLisi VéroniqueDmitrienko SvetlanaMercier François ELavallée Vincent-PhilippeAssouline Sarit - Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL), the most common subtype of adult ALL, has undergone dramatic transformation in prognosis over the past two decades. Introduction of tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 fusion protein has revolutionized frontline therapy, with successive generations of TKIs-from imatinib to dasatinib and most recently ponatinib-achieving progressively deeper and more durable molecular responses. Concurrently, the integration of immunotherapy, particularly blinatumomab, has enabled chemotherapy-sparing approaches further improving tolerability and efficacy. These advances have fundamentally challenged the historical paradigm that allogeneic hematopoietic cell transplantation (HCT) is indispensable for all Ph+ ALL patients in first complete remission. The role of allogeneic HCT is often debated and increasingly individualized, guided by measurable residual disease (MRD) assessment, TKI generation, depth and duration of molecular response, and patient-specific factors. Emerging data suggest that a subset of patients achieving early, deep MRD negativity with TKIs and immunotherapy may achieve durable remissions without transplant, though long-term follow-up remains limited. For patients proceeding to allogeneic HCT, optimization of transplant strategy-including donor selection, conditioning intensity, graft-versus-host disease prophylaxis, and posttransplant TKI maintenance-is critical to maximize graft-versus-leukemia effects while minimizing toxicity. Treatment-free remission strategies following prolonged TKI maintenance in non-transplant patients, and the integration of chimeric antigen receptor (CAR) T-cell therapy as bridge, consolidation, or salvage, represent emerging frontiers. This review critically examines the contemporary role of allogeneic HCT in Ph+ ALL and provides a framework for transplant decision-making in the contemporary era of targeted and cellular immunotherapy. - Source: PubMed
Publication date: 2026/04/15
Pasic IvanLipton Jeffrey H - Chronic myeloid leukemia (CML) often presents with hematologic findings that overlap with reactive leukocytosis and other myeloproliferative neoplasms (MPNs), creating diagnostic uncertainty that may delay targeted therapy or prompt unnecessary molecular testing. Harlequin cells-abnormal eosinophils containing basophilic granules-are well described in acute myeloid leukemia (AML) with fusion, but their diagnostic relevance in CML has not been systematically assessed. - Source: PubMed
Publication date: 2026/04/06
Cai JenniferYue ChangjunTomassetti Sarah