ABL1 pThr735 antibody Ab
- Known as:
- ABL1 pThr735 (anti-) Antibody
- Catalog number:
- 1488120
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- ABL1 pThr735 antibody
Related genes to: ABL1 pThr735 antibody Ab
- 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 pThr735 antibody Ab
Related articles to: ABL1 pThr735 antibody Ab
- Aflatoxin B1 (AFB1) is a widespread foodborne mycotoxin with well-established hepatotoxic and carcinogenic effects; however, its potential role in neuropsychiatric disorders remains unclear. Emerging evidence suggests that AFB1 can cross the blood-brain barrier, inducing oxidative stress and neuronal dysfunction. Whether these alterations contribute to anxiety-related molecular changes in the human brain remains poorly understood. An integrative approach combining network toxicology, brain-region-specific two-sample Mendelian randomization (MR), molecular docking, and experimental validation was employed. AFB1-associated targets were identified via STITCH, ChEMBL, and SwissTargetPrediction, and intersected with anxiety-related genes from GeneCards and GSEA. Protein-protein interaction (PPI) analysis, topological screening, and functional enrichment were used to identify hub genes and key pathways. MR analysis utilized cortex and cerebellum expression quantitative trait loci (eQTL) data from GTEx v8. Molecular docking evaluated binding interactions between AFB1 and key proteins. SH-SY5Y cells were used to validate alterations in oxidative stress and signaling. A total of 196 shared targets were identified, and 24 hub genes were screened based on the intersection of the top 40 genes ranked by degree, betweenness, and closeness centrality analyses. Enrichment analysis highlighted oxidative stress, apoptosis, MAPK, PI3K-Akt signaling, and monoaminergic synaptic pathways. MR analysis revealed region-specific associations: cortical EGFR expression positively correlated with anxiety risk, while cerebellar PPARG expression exhibited a protective effect. Additional genes (AKT1, KRAS, ABL1, PRKACB) showed positive cerebellar associations. Docking analysis indicated stable binding between AFB1 and key proteins. Experimental validation confirmed increased EGFR and AKT1 expression, reduced PPARG expression, and elevated ROS levels in SH-SY5Y cells. AFB1 promotes anxiety-related neurotoxicity in a brain-region-specific manner, supported by Mendelian randomization evidence, by inducing oxidative stress, disrupting EGFR/AKT signaling, and suppressing PPARG-mediated neuroprotection. These findings elucidate a mechanistic link between AFB1 exposure and neuropsychiatric risk, and highlight the need for stricter food safety regulation and incorporation of mycotoxin exposure into anxiety risk assessment and prevention strategies. - Source: PubMed
Publication date: 2026/07/24
Chen TingtingDu JiangBu LipingJiao Long - CD19-directed therapy remains the mainstay treatment for relapsed/refractory B-cell acute lymphoblastic leukemia (ALL). However, treatment patterns and outcomes following CD19-negative (CD19-) relapse remain poorly defined. We retrospectively analyzed 65 adult patients with ALL who developed CD19-relapse after CD19-directed therapy. TP53 mutations and BCR::ABL1-like ALL were each identified in 27.7% (n = 18) of patients. Forty-six patients (70.8%) received one CD19-targeted therapy, whereas 19 patients (29.2%) received ≥ 2 prior to CD19-relapse. Overall, 60 patients (92.3%) received blinatumomab, and 23 (35.4%) received CAR T-cell therapy. The median time from the initiation of the most recent CD19-targeted therapy to CD19-relapse was 155 days (range, 13-1946). The median follow-up of the entire cohort was 32.7 months (IQR, 15.1-90.3). The median event-free and overall survival (EFS and OS) was 3.1 months (95% CI, 2.5-4.5) and 9.9 months (95% CI, 6.8-24.7), respectively. In multivariate analysis, receipt of ≥ 2 CD19-directed therapies was associated with both inferior EFS and OS, HR 2.17 (95% CI, 1.10-4.29; p = 0.03) and HR 3.05 (95% CI, 1.40-6.62; p = 0.005). The complete remission rate following first salvage therapy was 47.5% and 72.1% any time following CD19-relapse. Sixteen (34.8%) of 46 patients evaluated had subsequent CD19 re-expression, 5 of whom subsequently received CD19-directed therapy, and all 5 patients responded. Patients with ALL who develop CD19-relapse after CD19-directed therapy have poor outcomes and limited therapeutic options. However, since this study lacked a comparator cohort of patients with CD19-positive relapse, the independent prognostic impact of CD19 negativity could not be determined. - Source: PubMed
Publication date: 2026/07/23
Othman TamerAgrawal VaibhavSong Joo YGu ZhaohuiKoller PaulPourhassan HodaSamara YazeedThiebaud Julio AlvarengaTinajero JoseNgo DatLin RickSandhu KaramjeetAlMalki MonzrAribi AhmedOtoukesh SalmanBall BrianArtz AndrewSalhotra AmandeepKhaled SamerBlackmon AmandaAmanam IdoroenyiAli HarisPark SunminBecker PamelaNakamura RyotaroMarcucci GuidoStein AnthonyForman StephenPullarkat VinodAldoss Ibrahim - Quizartinib, a second-generation FLT3 inhibitor, has shown clinical efficacy in FLT3 mutated Acute Myeloid Leukemia (AML). However, emerging evidence suggests its pharmacological profile extends beyond FLT3 inhibition, contributing to both therapeutic efficacy and off-target effects. This study employs a computational framework to comprehensively characterize the multi-target interactome of Quizartinib in AML. - Source: PubMed
Publication date: 2026/07/18
Hebballi Akshata PHampannavar Girish AGatibyali IrannaMishra Manas - ABL-rearranged (ABLr) acute lymphoblastic leukemia (ALL) is associated with treatment failure and relapse and novel treatments are required. We investigated asciminib efficacy against NUP214::ABL1 ALL, the second most common ABL1 rearrangement associated with aggressive disease. Asciminib activity was established in three patient derived xenograft models of NUP214::ABL1 ALL with different ABL1 breakpoints (e31a2, e32a3, e34a3). In all models, treatment with asciminib reduced NUP214::ABL1 leukemic burden and increased survival outcomes compared with control mice. These results contrast with recent in vitro studies in the setting of BCR::ABL1 leukemia, where ABL1 exon 3 breakpoints (e13a3, e14a3) result in asciminib resistance due to incomplete SH3 domain. Conversely, in silico modeling of NUP214::ABL1 e32a3 predicted NUP214 exon 32 mimics the missing ABL1 exon 2, forming a chimeric SH3 domain that rescues asciminib sensitivity. This prediction was supported by viability assays of Ba/F3 cells expressing NUP214::ABL1 with exon 32 present and absent. Additional viability assays and structural modeling of NUP214::ABL1 Ba/F3 cells expressing various ABL1 deletions defined a region of the SH3 domain critical for asciminib efficacy and necessary for allosteric inhibition. Our findings establish asciminib as a potential treatment for NUP214::ABL1 ALL and reveal a critical role for the fusion partner gene. Asciminib efficacy in ABLr leukemia cannot be predicted by evaluating ABL1 exon 2 inclusion/exclusion in isolation. This is of clinical importance as first-line use of STAMP inhibitors such as asciminib becomes more common. - Source: PubMed
Publication date: 2026/07/22
Eadie Laura NMcDougal Daniel PLagonik EliasSchutz Caitlin EPage Elyse CConlin Tace SRehn JacquelineBruning John BMoore Andrew SYeung David THughes Timothy PWhite Deborah L - Philadelphia chromosome (Ph)-positive T-lymphoblastic leukemia (T-ALL) is exceptionally rare. Distinguishing Ph-positive T-ALL from T-lymphoid blast-phase chronic myeloid leukemia (BP-CML) can be highly challenging, yet this distinction has important therapeutic and prognostic implications. We report a pediatric patient initially diagnosed with Ph-positive T-ALL who subsequently developed CML following treatment discontinuation. - Source: PubMed
Publication date: 2026/07/07
Dong RongrongDai XinyingFeng Yuan