Gria1 antibody - N-terminal region (ARP37670_P050)
- Known as:
- Gria1 (anti-) - N-terminal region (ARP37670_P050)
- Catalog number:
- arp37670_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Gria1 antibody - N-terminal region (ARP37670_P050)
Related genes to: Gria1 antibody - N-terminal region (ARP37670_P050)
- Gene:
- GRIA1 NIH gene
- Name:
- glutamate ionotropic receptor AMPA type subunit 1
- Previous symbol:
- GLUR1
- Synonyms:
- GluA1, GLURA
- Chromosome:
- 5q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-13
- Date modifiied:
- 2016-10-06
Related products to: Gria1 antibody - N-terminal region (ARP37670_P050)
Related articles to: Gria1 antibody - N-terminal region (ARP37670_P050)
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Gorman Bryan RHuang Jaxon JBarr Peter BHalladay Christopher WNealon Cari LChatzinakos ChrisFrancis MichaelJiang ChenGreenberg Paul BWu Wen-ChihPyarajan SaijuChoquet HélèneBigdeli Tim BIyengar Sudha KPeachey Neal SGalor Anat - This narrative review synthesizes current evidence on incidence, the immunologic basis of hypersensitivity-including the recently clarified role of anti-PEG (rather than anti-protein) antibodies-genetic predisposition, differential diagnosis from asparaginase-associated hyperammonemia, therapeutic drug monitoring (TDM), and desensitization. Hypersensitivity to PEG-asparaginase is a frequent, clinically consequential complication of pediatric acute lymphoblastic leukemia therapy that can compromise treatment exposure and survival. Recombinant Erwinia asparaginase (crisantaspase) is now licensed in the United States (2021) and the European Union (2023) for hypersensitive patients; however, cost, reimbursement, and local availability continue to limit access in many settings. Therefore, strategies for the safe continuation of PEG-asparaginase remain clinically relevant for reasons other than supply shortages alone. Using Ponte di Legno Toxicity Working Group definitions, reactions are classified as clinical allergy, allergic-like reaction, or silent inactivation, each requiring a different response; TDM is central to making this distinction. Genetic susceptibility loci (HLA class II haplotypes, CNOT3, GRIA1) remain investigational, with moderate effect sizes and inconsistent replication, and are not yet suitable for clinical decision-making. An adapted multi-step desensitization protocol can preserve therapeutic enzyme activity in appropriately selected patients; however, tolerance is temporary and dose-specific and requires repeat TDM after every dose. Conclusion. A personalized, multidisciplinary approach-integrating TDM, realistic assessment of access to alternative formulations, and (where available) genetic data-is recommended to optimize treatment safety and antileukemic efficacy. - Source: PubMed
Publication date: 2026/09/14
Prelog TomažKavčič MarkoIvancan SimonaSalobir NežaJazbec Janez - Our previous study demonstrated that HDAC1 knockdown alleviates traumatic brain injury (TBI), although underlying mechanisms remain unclear. Given the importance of microglial polarization in brain repair and its association with protein lactylation, this study investigated whether neuroprotective effects of HDAC1 inhibition in TBI are mediated through regulation of microglial polarization. In vivo TBI models, in vitro microglial cultures, immunofluorescence, CUT&Tag-seq and RNA-seq were employed to investigate the role of HDAC1 in TBI and its effects on microglial polarization and histone lactylation. Following TBI, microglia exhibited a predominant M1 phenotype with elevated HDAC1 expression, reduced histone lactylation, and altered expression of CD86 and CD206. Pharmacological inhibition of HDAC1, particularly with suberoylanilide hydroxamic acid (SAHA), or lactate supplementation restored histone lactylation and promoted M2 polarization. CUT&Tag-seq and qRT-PCR revealed that HDAC1 inhibition increased histone lactylation at the Gria1 promoter, leading to Gria1 upregulation in microglia. Hyperlactylated genes were enriched in neuroactive ligand-receptor interaction pathway. Overexpression of Gria1 in BV2 cells promoted M2 polarization, characterized by increased CD206 and decreased CD86 expression, which was further enhanced by HDAC1 inhibition or lactate treatment. RNA-seq identified SPP1 as a key downstream effector of Gria1 involved in immune and inflammatory responses. Knockdown of SPP1 suppressed CD206 and abolished the M2 polarization induced by Gria1 overexpression and HDAC1 inhibition. In a mouse TBI model, SAHA improved neurological recovery, reduced cortical lesions, upregulated Gria1 and SPP1, increased CD206, decreased CD86, and attenuated microglial activation. Collectively, pharmacological inhibition of HDAC1-mediated histone delactylation at the Gria1 promoter enhances Gria1-dependent SPP1 expression, thereby promoting microglial M2 polarization and attenuating neuroinflammation after TBI. - Source: PubMed
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