AGAP2
- Known as:
- AGAP2
- Catalog number:
- 001278A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AGAP2
Related genes to: AGAP2
- Gene:
- AGAP2 NIH gene
- Name:
- ArfGAP with GTPase domain, ankyrin repeat and PH domain 2
- Previous symbol:
- CENTG1
- Synonyms:
- -
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-29
- Date modifiied:
- 2019-03-26
Related products to: AGAP2
Related articles to: AGAP2
- This study aims to investigate the role of AGAP2 in acute myeloid leukemia (AML), particularly its involvement in lipid metabolic reprogramming and AML progression, and to explore the underlying regulatory mechanisms. - Source: PubMed
Publication date: 2026/03/16
Xin QiZhang HenanZhao ZhengXu GangZhang Jihong - Diverse haematological neoplasms are driven by tyrosine kinase (TK) fusion genes formed by recurrent or non-recurrent genomic rearrangements. The resulting chimeric proteins often present excellent targets for treatment with kinase inhibitors, and the fusion transcripts or genomic junctions can be used as specific targets for molecular monitoring. Whilst the TK genes involved are generally well characterised (e.g. ABL1, PDGFRA, FGFR1), the fusion partners are very diverse, presenting a challenge for detection and characterisation of these structural variants (SV) using current diagnostic methods. We assessed the ability of targeted nanopore sequencing using adaptive sampling to detect fusion genes in myeloid neoplasms. We sequenced genomic DNA from patients (n = 20) with a known or suspected TK gene fusion and identified rearrangements in 18 cases, including all cases with a known TK fusion, typical and atypical BCR::ABL1 rearrangements, an 843Kb deletion causing a FIP1L1::PDGFRA fusion, novel AGAP2::PDGFRB and NFIA::PDGFRB fusions, and a complex CCDC88C::PDGFRB rearrangement with multiple translocation events. The approach was fast (<72 h/sample from DNA to result), flexible with minimal hands-on laboratory time, and provided accurate, patient-specific characterisation of genomic breakpoints. - Source: PubMed
Publication date: 2025/11/18
Salmon MatthewNaumann NicoleRinke JennyMeggendorfer ManjaRadia DeeptiPomfret MarkErnst ThomasHochhaus AndreasReiter AndreasTapper William JWhite HelenCross Nicholas C P - Immune checkpoint inhibitor (ICI)-based combination therapies, such as dual ICI therapy or ICI plus vascular endothelial growth factor (VEGF) inhibitors, are recommended as first-line treatment for advanced renal cell carcinoma (aRCC). ICI-based combination therapy has improved the prognosis of patients with aRCC compared with the era of VEGF inhibitor monotherapy. Long noncoding RNAs (lncRNAs) are involved in the prognosis and metastasis of several cancers, and extracellular vesicle (EV)-derived lncRNAs play important roles in tumor progression and metastasis, serving as prognostic biomarkers. The lncRNA AGAP2-AS1 is highly expressed in RCC and is associated with poorer prognosis in patients with elevated expression levels. This study aimed to investigate the function of lncRNA AGAP2-AS1 in RCC and explore whether serum-derived EV lncRNA AGAP2-AS1 serves as a prognostic biomarker in patients with aRCC. Firstly, we examined lncRNA AGAP2-AS1 expression in RCC and normal kidney tissues with pathologically confirmed RCC at our institution. We also performed a functional analysis of lncRNA AGAP2-AS1 in RCC cell lines. Additionally, we analyzed the relationship between the EV lncRNA AGAP2-AS1 expression and the prognosis of 47 patients with aRCC treated with ICI-based combined therapy. We observed higher lncRNA AGAP2-AS1 expression in RCC tissues than in normal tissues. Furthermore, AGAP2-AS1 knockdown in RCC cells using small interfering RNA significantly decreased cell viability, invasion, and migration. Patients with progressive disease (PD) receiving ICI-based combination therapy exhibited significantly higher expression of the EV lncRNA AGAP2-AS1 than patients without PD. We then classified 47 patients into two groups by median lncRNA AGAP2-AS1 expression. Notably, the high-expression group exhibited significantly worse progression-free survival and overall survival than the low-expression group (log-rank P = 0.0193 and log-rank P = 0.0256, respectively). In multivariate analysis, high EV lncRNA AGAP2-AS1 expression was an independent risk factor for disease progression (hazard ratio = 3.6, P = 0.0287). Overall, high EV lncRNA AGAP2-AS1 expression was associated with poorer prognosis in patients with aRCC. Therefore, serum-derived EV lncRNA AGAP2-AS1 may be an effective non-invasive prognostic biomarker in patients with aRCC treated with ICI-based combination therapy. - Source: PubMed
Publication date: 2025/09/15
Fujii NakanoriHirata HiroshiBan YoshimasaTokunaga TakanoriShimizu KosukeOka ShintaroKobayashi KeitaShiraishi Koji - Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of autoimmune diseases. Our previous research demonstrated that AGAP2-AS1 in keratinocytes is involved in the pathogenesis of psoriasis, but its effect on CD4 T cell differentiation remains unclear. - Source: PubMed
Publication date: 2025/05/30
Yuan ZiqiZeng XueZhang XiweiXia ChenglaiPeng Xuebiao - Epilepsy is a multifaceted neurological disorder characterized by recurrent seizures and associated with molecular and immune alterations in key brain regions. The GASH/Sal (Genetic Audiogenic Seizure Hamster, Salamanca), a genetic model for audiogenic epilepsy, provides a powerful tool to study seizure mechanisms and resistance in predisposed individuals. This study investigates the proteomic and immune responses triggered by audiogenic kindling in the inferior colliculus, comparing non-responder animals exhibiting reduced seizure severity following repeated stimulation versus GASH/Sal naïve hamsters. To assess auditory pathway functionality, Auditory Brainstem Responses (ABRs) were recorded, revealing reduced neuronal activity in the auditory nerve of non-responders, while central auditory processing remained unaffected. Cytokine profiling demonstrated increased levels of proinflammatory markers, including IL-1 alpha (Interleukin-1 alpha), IL-10 (Interleukin-10), and TGF-beta (Transforming Growth Factor beta), alongside decreased IGF-1 (Insulin-like Growth Factor 1) levels, highlighting systemic inflammation and its interplay with neuroprotection. Building on these findings, a proteomic analysis identified 159 differentially expressed proteins (DEPs). Additionally, bioinformatic approaches, including Gene Set Enrichment Analysis (GSEA) and Weighted Gene Co-expression Network Analysis (WGCNA), revealed disrupted pathways related to metabolic and inflammatory epileptic processes and a module potentially linked to a rise in the threshold of seizures, respectively. Differentially expressed genes, identified through bioinformatic and statistical analyses, were validated by RT-qPCR. This confirmed the upregulation of six genes (-Glypican-1; -Syndecan-3; -Nerve Growth Factor Inducible; -Copine 5; -Arf-GAP with GTPase domain, ANK repeat, and PH domain-containing protein 2; and -Dipeptidyl Peptidase 8) and the downregulation of two (-RAS-like proto-oncogene B-and -S100 calcium-binding protein B), aligning with reduced seizure severity. This study may uncover key proteomic and immune mechanisms underlying seizure susceptibility, providing possible novel therapeutic targets for refractory epilepsy. - Source: PubMed
Publication date: 2025/03/05
Zeballos LauraGarcía-Peral CarlosLedesma Martín MAuzmendi JerónimoLazarowski AlbertoLópez Dolores E