ABL1 (phospho-Tyr412) Antibody
- Known as:
- ABL1 (phosphorilated-Tyr412) Antibody
- Catalog number:
- abx000351
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- ABL1 (phospho-Tyr412) Antibody
Ask about this productRelated 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
- Chronic myeloid leukemia (CML) is driven by constitutive BCR-ABL1 activity and remains clinically challenging due to disease persistence and resistance to tyrosine kinase inhibitors (TKIs). SIRT1, a NAD-dependent deacetylase, has been implicated in leukemic cell survival and chemoresistance through negative regulation of p53. In this study, we evaluated the antileukemic effects of the hybrid H387 extract and its impact on the SIRT1-p53 signaling axis in K562 CML cells. Cell proliferation was assessed using a crystal violet assay, while gene and protein expression were analyzed by RT-qPCR, immunofluorescence, and flow cytometry. Apoptosis was determined by Annexin V/7-AAD staining. The extract significantly inhibited K562 cell proliferation and downregulated SIRT1 expression, reducing its nuclear localization. These effects were associated with increased p53 acetylation at lysine 382 (Ac-K382-p53) and enhanced apoptosis. Notably, a higher percentage of apoptotic cells was observed following extract treatment than with imatinib under the experimental conditions used, although the two agents have distinct mechanisms of action. These findings suggest that the antileukemic activity of hybrid H387 extract is associated with modulation of the SIRT1-p53 axis and induction of apoptosis in K562 cells. - Source: PubMed
Publication date: 2026/08/27
Aguiñiga-Sánchez ItzenRomero-Trejo DanielMiranda-Duarte KarenRomero-López ErnestoCadena-Iñiguez JorgeShira LorenaRosado-Pérez JuanaMendoza-Núñez Víctor ManuelMacías Zaragoza Víctor ManuelWeiss-Steider BennySantiago-Osorio Edelmiro - : Evidence regarding long-term outcomes among offspring following maternal or paternal exposure to BCR::ABL1 tyrosine kinase inhibitors (TKIs) is limited. We described pregnancy outcomes and offspring health through adolescence and early adulthood in a single-centre cohort of patients with chronic myeloid leukemia (CML). : This retrospective, descriptive cohort study included patients with chronic-phase CML who experienced a pregnancy, or whose partner experienced a pregnancy, in association with TKI exposure and for whom longitudinal offspring follow-up was available. Long-term offspring outcomes were ascertained from detailed obstetric and pediatric medical records supplemented by parental reports. Fourteen patients (nine women and five men) contributed 21 pregnancy events and 23 live-born offspring, including two twin pregnancies in the paternal-exposure group. : In the maternal-exposure group, median gestational age at delivery was 38.0 weeks (range, 35-40), and four of 15 deliveries were preterm. In the paternal-exposure group, median gestational age was 39.0 weeks (range, 38-41), with no preterm deliveries. Median offspring follow-up was 252 months (range, 212-295), extending through adolescence and into early adulthood. One offspring had a primum atrial septal defect that was surgically corrected. No additional clinically documented major abnormalities in growth or developmental progress were identified during available follow-up. Given the small cohort, these observations were interpreted descriptively and were not considered evidence of equivalence with population-level rates. : This small retrospective cohort provides unusually long observational follow-up of offspring after selected maternal or paternal TKI exposures. The findings are clinically informative but cannot establish reproductive safety or exclude rare adverse outcomes. Larger multicentre registries using standardized long-term developmental, neurocognitive, and endocrine assessments are needed. - Source: PubMed
Publication date: 2026/09/06
Pál SándorSolymár MargitAlizadeh Hussain - New -(4-(chlorodifluoromethoxy)phenyl)-1-pyrrolo[2,3-]pyridine-5-carboxamide derivatives were designed, synthesised, and evaluated as potential anticancer agents. Among the synthesised derivatives, compound 9c showed the highest potency against BCR-ABL1-positive K562 leukemia cells, with an IC of 0.26 ± 0.029 µM, followed by 9a (0.50 ± 0.005 µM), 9k (0.64 ± 0.075 µM) and 9l (0.69 ± 0.11 µM). Importantly, compounds 9a, 9c and 9k showed selectivity for leukemia cells and low toxicity to normal fibroblasts (IC > 50 µM), with selectivity indices of 100-192. Docking analysis showed that the designed analogues preserved the key pharmacophoric interactions of Asciminib, with compound 9k showing the best docking score (-42.07 kcal mol), followed by 9a (-40.44 kcal mol), compared with Asciminib (-40.13 kcal mol). Taken together, these results suggest that the -(4-(chlorodifluoromethoxy)phenyl)-1-pyrrolo[2,3-]pyridine-5-carboxamide scaffold is a useful template for designing selective BCR-ABL1-directed anticancer agents, with compound 9c as an encouraging lead for further optimisation and mechanistic studies. - Source: PubMed
Publication date: 2026/09/11
Bhise Pradeep BBhise Sandeep BDasgupta SomnathNandy AshisGundla RambabuGurska SonaDzubak PetrHajdúch MarianDas ViswanathThopate Shankar RBadadhe Pravin V - The development of BCR::ABL1 tyrosine kinase inhibitors (TKIs) has transformed chronic myeloid leukemia into a chronic disease with near-normal life expectancy. More recently, treatment-free remission (TFR), defined as sustained molecular remission even after TKI discontinuation, has emerged as a realistic therapeutic goal and a type of functional cure. Landmark studies, including STIM1, A-STIM, EURO-SKI, ENESTfreedom, DADI, and J-SKI, have established the feasibility and safety of TFR. Their results showed that approximately half of eligible patients can successfully discontinue therapy. However, the reliable prediction of TFR success remains a major challenge. Accumulating evidence indicates that durable TFR reflects a dynamic equilibrium between residual leukemic stem cells (LSCs) and host immune surveillance. Natural killer cells and T-cell immunity contribute to maintaining remission after TKI discontinuation. Conversely, immune exhaustion and the persistence of LSCs are associated with molecular relapse. Emerging biomarkers, including immune profiling, immunogenetic markers, and minimal residual disease kinetics, may improve relapse-risk stratification. To increase the proportion of patients who achieve durable TFR, future efforts should focus on the development of risk-adapted consolidation strategies incorporating optimized TKI therapy, immune modulation, and LSC-targeted approaches. - Source: PubMed
Publication date: 2026/09/11
Ureshino Hiroshi - Cancer treatment is difficult, there are many issues regarding cancer treatment because Protein Kinase Inhibitors (PKIs) are unable to control tumors that are resistant to them. Resistance to drugs starts with changes in genetic code and continues with fresh changes, routes and alterations in the tumour. When treating cancer with imatinib or osimertinib, PKIs can correct faulty signals, yet patients generally become resistant swiftly and this resistance can include unpleasant side effects. Reviewing Epidermal Growth Factor Receptor (EGFR) T790M and BCR::ABL1 T315I mutations reveals that the important interactions and binding sites are removed or obstructed with the drug. This is how researchers design second- and third-generation drug inhibitors. In addition, the use of single-cell sequencing, CRISPR screens and liquid biopsies helps researchers and doctors to accurately fight resistance in cancer patients. For cancer treatments to succeed, systems to reduce drug costs and make them available, fresh ideas, global experts and equitable healthcare laws should be implemented. - Source: PubMed
Publication date: 2026/09/10
Sengar Mridul SinghPaliwal AjitaKaushik NiranjanSingh ShristiKashyap PushpPaliwal DeepikaNegi Sweta