Abl1 (Phospho_Tyr204) Antibody
- Known as:
- Abl1 (Phospho_Tyr204) Antibody
- Catalog number:
- E012053-2
- Product Quantity:
- 100ug
- Category:
- Antibodies
- Supplier:
- EnoGene
- Gene target:
- Abl1 (Phospho_Tyr204) Antibody
Related genes to: Abl1 (Phospho_Tyr204) 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_Tyr204) Antibody
Related articles to: Abl1 (Phospho_Tyr204) Antibody
- Concurrent chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL) in the same patient are rare and may be overlooked when leukocytosis is attributed to a single hematologic process. We report a case of synchronous CML and CLL identified at initial presentation, highlighting the diagnostic value of integrating morphology, immunophenotyping, cytogenetics, and molecular testing. - Source: PubMed
Publication date: 2026/05/13
Almahmood MotazAbdalla ElmustafaSaied AminSoliman DinaGanwo Ibrahim Almahdi AIbrahim FeryalFareed Shehab - Classic BCR::ABL1-negative myeloproliferative neoplasms (MPNs)-polycythaemia vera, essential thrombocythaemia, and primary myelofibrosis-are clonal haematopoietic stem cell disorders with marked heterogeneity in clinical phenotype, disease trajectory, and therapeutic response. Genomic stratification by driver and cooperating mutations only partially accounts for this variability, leaving gaps in predicting thrombotic risk, fibrotic progression, leukaemic transformation, and treatment benefit. Proteomics bridges this gap by providing function-proximal readouts of protein abundance, post-translational modifications, pathway activity, and intercellular signalling that genomics and transcriptomics cannot capture, positioning it as a theranostic platform in which the same molecular readouts simultaneously inform diagnostic stratification and therapeutic decision-making. We propose a five-stage translational framework spanning from discovery-scale mass spectrometry and affinity-based plasma profiling to targeted validation, multicentre standardisation, and machine learning-integrated clinical panels. Proteomic evidence is synthesised across the following four disease axes: clonal fitness in haematopoietic stem and progenitor cells; bone marrow microenvironmental remodelling and fibrosis; chronic inflammation and thrombosis; and leukaemic transformation. We further describe how phosphoproteomics reveals resistance mechanisms to JAK inhibitors, including AXL-MAPK bypass and PP2A-autophagy-mediated tolerance, and how protein-level biomarkers (BCL2-BCL-XL, RAS-ERK, CAMK2G, and ROCK1/2) can guide individualised therapeutic selection. Affinity-based platforms (Olink PEA and SomaScan) and spatially resolved technologies (CODEX and single-cell proteomics) complement discovery proteomics. At present, however, this evidence base is constrained by small and heterogeneous cohorts, limited cross-platform reproducibility, and a scarcity of independent external validation for candidate protein panels. Realising this vision will require multicentre standardisation, analytically validated panel assays, and prospective clinical studies that translate molecular findings into decision-grade tools for patients with MPNs. - Source: PubMed
Publication date: 2026/06/14
Zhang JingHan Yan-Qiu - Chronic myeloid leukemia (CML) is driven by the BCR-ABL1 fusion oncoprotein and is managed with tyrosine kinase inhibitors (TKIs). However, resistance and persistence of leukemic stem/progenitor cells remain major clinical challenges. Autophagy-mediated survival signaling contributes to therapeutic resistance in CML. We hypothesized that histone deacetylase 6 (HDAC6), a key regulator of protein homeostasis and autophagic flux, is a therapeutic target in this context. Transcriptomic analysis of CML bone marrow datasets revealed enrichment of HDAC6-associated autophagy and stress-response gene programs. The selective HDAC6 inhibitor 7b induced sustained α-tubulin acetylation at lower concentrations than ricolinostat or nexturastat A. 7b reduced primary CML PBMC viability while sparing healthy PBMCs and was active in vivo. Combining 7b with the allosteric BCR-ABL1 inhibitor asciminib synergistically suppressed cell viability and clonogenic growth. A tandem mCherry-GFP-LC3 reporter showed that 7b blocks autophagosome maturation, thereby decreasing autophagic degradation. Cotreatment engaged a maladaptive integrated stress response (ISR), characterized by eIF2α phosphorylation, ATF4 and CHOP induction, MCL-1 suppression, PUMA and NOXA upregulation, and BCL-xL-dependent mitochondrial apoptosis, accompanied by caspase-2 activation. ISR activation occurred downstream of the autophagy disruption: rapamycin attenuated ISR activation, whereas ATG7 silencing intensified ISR signaling and apoptosis. CHOP knockdown blunted the BCL-xL/PUMA/NOXA shift and caspase-3 cleavage, establishing CHOP as required. Caspase-10 acted upstream of caspases-9, -7, and -3. The combination elicited immunogenic cell death markers: calreticulin exposure, ATP and HMGB1 release, elevated TNF-α, and reduced IL-8. These findings identify HDAC6-driven autophagy as a therapeutically exploitable vulnerability in CML that, when combined with asciminib, triggers ISR-dependent immunogenic apoptosis. - Source: PubMed
Publication date: 2026/06/12
Paik Ji YeonGajulapalli Sruthi ReddyLi VladimirPark SujungLee YejinOrlikova-Boyer BarboraLorant AnneChristov ChristoKirsch GilbertKang Hyoung JinSchnekenburger MichaelCerella ClaudiaDiederich Marc - Early diagnosis of hematologic malignancies can be challenging when initial diagnostic studies are discordant, particularly because flow cytometry, although central to evaluation, may be non-diagnostic in evolving disease. We report the case of a 33-year-old female who presented with leukocytosis, systemic symptoms, and progressive hematologic abnormalities, including circulating blasts identified on peripheral blood analysis. Initial diagnostic evaluation included laboratory studies, peripheral smear review, and flow cytometry, followed by cross-sectional imaging that demonstrated an anterior mediastinal mass, lymphadenopathy, and hepatosplenomegaly concerning for lymphoproliferative malignancy. Despite strong clinical suspicion, early flow cytometric findings were insufficient for definitive classification, prompting escalation to bone marrow biopsy with comprehensive immunophenotypic and cytogenetic analysis. Bone marrow examination ultimately demonstrated T-lymphoblastic leukemia/lymphoma with an abnormal immature T-cell population and isolated copy number gain in the absence of fusion. The hospital course was further complicated by catheter-associated upper extremity thrombosis. This case highlights the limitations of isolated diagnostic modalities in early hematologic malignancy and underscores the importance of integrating clinical, laboratory, morphologic, immunophenotypic, and imaging findings. Persistent clinical suspicion should prompt timely tissue-based evaluation despite initially inconclusive studies to avoid delays in definitive diagnosis and management. - Source: PubMed
Publication date: 2026/05/11
Izadian Bidgoli AlirezaGomez Veliz AlbertoVermejo Blumen MariaNoriega-Toledo Daina - : Chronic myeloid leukemia (CML), essential thrombocythemia (ET), primary myelofibrosis (PMF), and polycythemia vera (PV) are myeloproliferative neoplasms (MPNs) that require precise molecular characterization. Although driver mutations such as BCR-ABL1 and JAK2 are diagnostically important, they do not fully explain disease heterogeneity. The NanoString nCounter system enables direct multiplex gene expression analysis without RNA amplification and is suitable for degraded bone marrow specimens. This study aimed to analyze cytokine gene expression in bone marrow mononuclear cells of patients with MPNs and controls using NanoString technology, identify differentially expressed genes (DEGs) among MPN subtypes, and investigate their biological significance. : Bone marrow aspirates were collected from 19 patients with MPNs (CML, ET, PMF, and PV) and 6 control patients. Mononuclear cells were isolated, and RNA expression of a 40-gene cytokine panel was analyzed using the NanoString nCounter system with strict quality control and normalization. DEGs were identified for each MPN subtype, followed by Gene Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway analyses. : CML and PV demonstrated 20 and 12 DEGs, respectively. In contrast, ET showed only one DEG (IRAK2), and PMF showed none. Functional analyses revealed enrichment of cytokine signaling, Toll-like receptor (TLR), and JAK-STAT pathways in CML, indicating immune and inflammatory dysregulation. PV DEGs were associated with TLR signaling, IL-17 pathways, and cytokine-cytokine receptor interactions, suggesting active cytokine-mediated inflammation. CML and PV exhibited distinct cytokine-driven transcriptional signatures, whereas ET and PMF exhibited minimal alterations. These findings support the clinical utility of NanoString technology for bone marrow specimens and highlight disease-specific immune pathways as potential diagnostic biomarkers in MPNs. - Source: PubMed
Publication date: 2026/06/03
Bae Jun-HyungBae Kyung-JinCho Chi-Hyun