ABL1 Forward PCR Primer (390bp position)
- Known as:
- ABL1 Forward PCR test kit Primer (390bp position)
- Catalog number:
- MP1105
- Product Quantity:
- ea
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- ABL1 Forward PCR Primer (390bp position)
Related genes to: ABL1 Forward PCR Primer (390bp position)
- 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 Forward PCR Primer (390bp position)
Related articles to: ABL1 Forward PCR Primer (390bp position)
- Lipid modifications are critical for membrane anchoring and signal transduction. N-myristoylation, catalyzed by NMT1/2, irreversibly attaches myristic acid to N-terminal glycine residues, enabling stable membrane localization and crosstalk with other post-translational modifications. This review traces NMT research from structural characterization to substrate profiling, highlighting the ordered double-substitution catalytic mechanism and variations in substrate recognition. While prior reviews have covered NMT biochemistry and innate immunity, we emphasize underappreciated roles of N-myristoylation in metabolic vulnerability, immune evasion, and acquired resistance to targeted therapies and immunotherapies. We discuss how exogenous myristic acid from dietary sources fuels oncogenic signaling, and how N-myristoylation regulates key signaling pathways (PI3K/AKT, MAPK, ferroptosis) and targets (Src, AMPK, EZH2) to drive immunosuppressive and pro-tumor phenotypes. Antitumor potential of NMT inhibitors (e.g., B-13, Zelenirstat) and allosteric ABL1 inhibitors (asciminib) is evaluated. Recent methodological advances (including metabolic labeling, click chemistry, spatial proteomics, and computational simulations) are reviewed. However, translational challenges such as biomarker absence, blood-brain barrier limitations, and functional redundancy remain. Addressing these will require combination therapies tailored to specific mutational, metabolic, and immune profiles. In summary, N-myristoylation integrates signaling, metabolism, and immunity, offering a rationale for future precision oncology. - Source: PubMed
Publication date: 2026/09/07
Xie DeqianLiu DequanZheng ZunwenYang YingLi XiaoruiYuan QihangSun TaoWu Guangzhen - Treatment-free remission (TFR), defined as the maintenance of molecular remission without resumption of therapy after tyrosine kinase inhibitor (TKI) discontinuation, represents the clinical manifestation of functional cure in chronic-phase chronic myeloid leukemia (CML-CP), in which durable disease control is maintained without ongoing therapy despite the potential persistence of residual leukemic stem cells (LSCs). Emerging evidence supports a model in which outcomes after TKI discontinuation are determined by the balance between residual LSC persistence and coordinated host immune surveillance. Natural killer (NK)-cell abundance and maturation have shown the most consistent associations with TFR, while killer immunoglobulin-like receptor (KIR)-human leukocyte antigen (HLA) immunogenetics may further influence NK-cell education and antileukemic activity. Adaptive and regulatory mechanisms-including leukemia-associated antigen-specific cytotoxic T lymphocytes, T-cell receptor repertoire dynamics, T-cell exhaustion, plasmacytoid dendritic cells, and regulatory T cells-are increasingly implicated in residual disease control. Neutrophil abundance and maturation have also emerged as readily accessible candidate biomarkers. In parallel, persistent LSCs exploit BCR::ABL1-independent survival programs, immune-evasion mechanisms, and the protective bone marrow niche, providing a reservoir for molecular relapse. These observations argue against reliance on any single biomarker and instead support integrated models incorporating clinical variables, molecular residual disease, immune competence, immunogenetics, and LSC biology. Most candidate biomarkers remain exploratory and require independent prospective validation. Such multidimensional approaches may enable a transition from empiric TKI discontinuation toward precision, biomarker-guided TFR and extend durable functional cure to a broader population of patients with CML. Trail Registration: N/A. - Source: PubMed
Publication date: 2026/09/06
Ureshino HiroshiKimura Shinya - ATP-site resistance mutations, exemplified by T315I in BCR::ABL1, limit the durability of kinase inhibitor therapy in hematological malignancies. Allosteric sites outside the catalytic cleft offer an alternative: ligands that bind regulatory pockets can stabilize inactive conformations and retain activity against mutations that defeat ATP-site drugs. Several reviews have addressed this principle across the kinome, but none has applied a hematology-focused druggability appraisal anchored in the BCR::ABL1/asciminib precedent. This review fills that gap with two contributions: mechanistic evidence that crizotinib engages BCR::ABL1 through a putative dual ATP-site/myristoyl-pocket mechanism, supported by indirect evidence and pending direct structural confirmation; and a hypothesis linking recurrent synonymous mutations in non-receptor tyrosine kinases to transiently structured regulatory regions, as a strategy for identifying latent allosteric sites Asciminib is the proof of concept. It binds the MBP of ABL1, locking the kinase in an autoinhibited-like state without competing for ATP. In the ASCEMBL trial, it achieved a major molecular response rate of 25.5% at 24 weeks versus 13.2% for bosutinib in heavily pretreated CML, with better tolerability-the first regulatory-site inhibitor approved for a hematological malignancy. The question is whether this can extends further. Dual-site strategies may raise the barrier to resistance, but the structural and biochemical validation remains incomplete for FLT3, JAK2, and BTK. Asciminib resistance is already real: A337V and P465S mutations reduce binding, and bypass signaling adds another layer. Each approved allosteric agent-asciminib, trametinib, and ivosidenib-required extensive structural and functional validation before reaching the clinic; structural prediction alone is not enough. - Source: PubMed
Publication date: 2026/09/06
Marx AilieCohen MaorRuthardt MartinMahajna Jamal - Concurrent atypical BCR::ABL1 transcripts and SET::NUP214 fusions are rare in chronic myeloid leukemia (CML) and may complicate disease classification and treatment decisions. - Source: PubMed
Publication date: 2026/08/30
Manoharan MeenakkshyAlnoor FnuYang PingAmador-Ortiz CatalinaBeitinjaneh AmerVenugopal SangeethaWang XiaoqiongZhou YiRuiz-Cordero RobertoChapman JenniferNovoa FelipeMadarang EllenWatts JustinTaylor Justin - Collision hematologic malignancies, characterized by the concurrent presence of clonally independent myeloid and lymphoid neoplasms within a single patient, are exceptionally uncommon. Diagnosing these malignancies is particularly challenging when they occur in the context of chronic inflammatory diseases, where distinguishing between reactive and neoplastic processes is complex. - Source: PubMed
Publication date: 2026/08/21
Zhang LiangZhang Mei YingZhou Chang ShengCi Xing YuanZhu Long YingHu Qi LeiQi Zhi RongFu ShuiLi Zuo Jie