ERp57 (Grp58) (MaP.Erp57) Mouse mAb
- Known as:
- ERp57 (Grp58) (MaP.Erp57) Mouse mAb
- Catalog number:
- ASASPA-725F
- Product Quantity:
- 200 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- ERp57 (Grp58) (MaP.Erp57) Mouse mAb
Related genes to: ERp57 (Grp58) (MaP.Erp57) Mouse mAb
- Gene:
- PDIA3 NIH gene
- Name:
- protein disulfide isomerase family A member 3
- Previous symbol:
- GRP58
- Synonyms:
- P58, ERp61, ERp57, ERp60, GRP57, PI-PLC, HsT17083
- Chromosome:
- 15q15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2016-10-05
Related products to: ERp57 (Grp58) (MaP.Erp57) Mouse mAb
Related articles to: ERp57 (Grp58) (MaP.Erp57) Mouse mAb
- Histone lactylation (Hla) represents a novel epigenetic mark priming cells toward the malignant state. Discoidin, CUB, and LCCL domain-containing type I (DCBLD1) has been reported as a carcinogenic gene so far. This project was focused on the functional role of DCBLD1 in oesophageal cancer through the lactate modification pathway. - Source: PubMed
Publication date: 2026/05/31
Yin MingWang ShanLiu HaiMinXu ChaochenLi QiushuoSun YunHao - Immune checkpoint inhibitors (ICIs) demonstrate therapeutic benefits in advanced hepatocellular carcinoma (HCC), yet most patients exhibit limited responses to anti-PD-1 therapy and the molecular basis underlying this resistance remains largely undefined. Here, we identified the circular RNA SPECC1 (circSPECC1) as a regulator of antigen presentation and a crucial factor influencing the efficacy of anti-PD-1 therapy. circSPECC1 was significantly elevated in tumor tissues of HCC patients showing resistance to anti-PD-1 therapy and correlated with diminished intratumoral CD8 T-cell infiltration. Elevated circSPECC1 levels facilitated tumor progression and impaired the therapeutic efficacy of anti-PD-1 treatment. Overexpression of circSPECC1 in cancer cells suppressed the proliferation and cytotoxic activity of CD8 T cells both in vitro and in vivo. Mechanistically, circSPECC1 bound to the peptide-loading complex (PLC) chaperone ERP57 and disrupted its interaction with TAPBP (TAP binding Protein), thereby destabilizing PLC integrity. This aberrant interaction redirected MHC-I toward ER-associated degradation (ERAD), suppressing surface antigen presentation and impairing CD8 T-cell activation. Importantly, targeted silencing of circSPECC1 using a PEG-PEI-folate nanosystem encapsulating si-circSPECC1 significantly restored sensitivity both murine and patient-derived xenograft HCC models to PD-1 blockade. In summary, these findings uncover a novel circRNA-guided ERAD of MHC-I mechanism that impairs antitumor immunity and highlight circSPECC1 as a promising therapeutic target to overcome immunotherapy resistance. - Source: PubMed
Publication date: 2026/05/05
Peng RuiZhang JiahaoZhang ChiSu BingbingFan SongsongChen YongzhiWang QianJiang GuoqingDing LiJin XinWang LipingCao JunJin ShengjieBai Dousheng - Ciguatera poisoning (CP) was traditionally associated with fish consumption, but other marine invertebrates such as gastropods and bivalves can also serve as non-traditional vectors. In this study, ciguatoxins (CTXs) accumulation, tissue distribution, depuration kinetics, and associated transcriptomic responses were studied using controlled feeding trials on green-lipped mussels (Perna canaliculus), an important seafood species, fed Gambierdiscus polynesiensis. In two experiments, mussels accumulated CTXs rapidly, peaking at concentrations of 5.14 µg kg (day 19, Experiment 1) and 4.57 µg kg (day 21, Experiment 2), with the majority of CTXs observed in the digestive system. Despite ongoing feeding for 10 more days, CTXs concentrations decreased until the end of the experiment, suggesting saturation and/or metabolic transformation. During a 35-day depuration period with CTX-free diet, mussels fully depurated CTXs (estimated initial rate of 0.90 µg kg⁻¹ day⁻¹). Parallel transcriptome analyses demonstrated that molecular responses lagged toxin accumulation: by day 19, mussels upregulated genes involved in endoplasmic reticulum stress (e.g., PDIA3), proteasomal degradation (e.g., PSMCs), autophagy (e.g., cathepsins), stress resistance (e.g., heat shock proteins) and innate immunity (e.g., MYD88). These coordinated responses suggest that transcriptional defence is activated once CTX load reaches a threshold or time. CTXs concentrations above safety thresholds and late onset of detoxification suggest that mussels may remain toxic for weeks after exposure. This study represents the first integrative assessment of CTXs accumulation, depuration and molecular stress responses, laying the groundwork for the use of molecular biomarkers to track exposure and improve harvest management in CTX-prone regions. - Source: PubMed
Publication date: 2026/04/07
Biessy LauraMurray J SamPearman John KViallon JérômeDarius H TaianaChinain MireilleSim AbigailPassfield Emillie M FRhodes Lesley LSmith Kirsty F - The recent emergence of new respiratory virus infections in humans with epidemic or pandemic potential has reiterated the urgent need for effective broad-spectrum antivirals (BSAs) as part of a strategic framework for preventing and preparing pandemics. The cellular machinery involved in the maturation of viral proteins in the endoplasmic reticulum (ER) can be considered in the search for host-targeting agents (HTAs) with potential BSA activity. In this context, human protein disulfide isomerase A3 (PDIA3) catalyzes the formation and isomerization of disulfide bonds in the ER pathway specific for folding N-glycosylated proteins. Here, we investigated the feasibility of pharmacological targeting of PDIA3 to identify BSAs against respiratory viruses. - Source: PubMed
Publication date: 2026/04/02
Sibille GiuliaMaggiora AriannaCimato GiorgiaLuganini AnnaGribaudo Giorgio - The connection between immunity and Parkinson’s disease (PD) is well-established. Myeloid immune responses influence the microenvironment of the central nervous system (CNS), which can be modulated by sargramostim, a recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF). Previous studies have demonstrated sargramostim’s neuroprotective effects, which are linked to its safety and tolerability, as well as its ability to regulate innate immunity. Changes in myeloid biomarkers correlate with clinical responses. PD symptoms were assessed using the Unified PD Rating Scale (UPDRS). Ten subjects received sargramostim through subcutaneous injections of 3 µg/kg, administered five days every week. Myeloid biomarkers were measured before treatment and at six and twelve months of treatment. Protein expression by Western blotting and gene expression by transcriptomic analysis was correlated with UPDRS III scores. Recognizing the exploratory nature of this study, patient responses were classified into potent, moderate, or no change groups based on UPDRS III score reductions of 9–13, 5–7, or none, respectively. Biomarkers from all 10 patients identified FOXP3 as a “potential” signature biomarker. The potent responders showed biomarkers linked to autophagy, inflammatory, and antioxidant proteins, including ATG7, HMOX1, RELA, and TLR8. Moderate responders displayed biomarkers associated with RELA and LRRK2. Transcriptomic analysis revealed over 2000 differentially expressed anti-inflammatory, calcium-binding, and epigenetic genes. Among these, genes such as ANXA9, CALM3, CY7B1, HDAC4, HMGB2, NR2F6, PDIA3, REST, SACS and SOX4 were identified as potential predictors of changes in UPDRS III scores. Baseline levels of ATG7, CARD9, and SACS may serve as initial biomarkers to identify subjects likely to respond to sargramostim. Female patients exhibited unique UPDRS III scores in response to sargramostim treatment. Novel cell-based biomarker signatures were identified that may predict responses to sargramostim treatment in this hypothesis-generating study. We acknowledge the inherent study limitations by limited patient numbers. This was reflected in the comparisons offered for the patient sub-groups in the year-long trial. The trial is registered on ClinicalTrials.gov under identifier NCT03790670, dated 01.30.2019. - Source: PubMed
Publication date: 2026/04/01
Sil SusmitaDu XiaoqingAkter SamiaKumar MohitOludipe Davina BSaha ArnabHu GuokuOstlund Katie RHaynatzki Gleb RSantamaria PamelaMosley R LeeGendelman Howard E