Biotin, Mab anti-, AMCA
- Known as:
- Biotin, Mab (anti-) to-, AMCA
- Catalog number:
- abm152211
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Accurate
- Gene target:
- Biotin Mab anti- AMCA
Related genes to: Biotin, Mab anti-, AMCA
- Gene:
- GOLGB1 NIH gene
- Name:
- golgin B1
- Previous symbol:
- -
- Synonyms:
- GCP, GCP372, giantin, GOLIM1
- Chromosome:
- 3q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1997-11-05
- Date modifiied:
- 2016-10-05
- Gene:
- SERPINA1 NIH gene
- Name:
- serpin family A member 1
- Previous symbol:
- PI
- Synonyms:
- AAT, A1A, PI1, alpha-1-antitrypsin, A1AT, alpha1AT
- Chromosome:
- 14q32.13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- SERPINB1 NIH gene
- Name:
- serpin family B member 1
- Previous symbol:
- ELANH2
- Synonyms:
- EI, PI2, anti-elastase
- Chromosome:
- 6p25.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-27
- Date modifiied:
- 2016-04-06
Related products to: Biotin, Mab anti-, AMCA
Related articles to: Biotin, Mab anti-, AMCA
- Pulpal and periapical diseases represent a significant burden in endodontic practice, yet their molecular pathogenesis remains incompletely understood. Proteomic profiling offers unprecedented opportunities to identify disease-specific biomarkers, elucidate molecular mechanisms, and develop precision diagnostic tools. This systematic review aimed to synthesize the current evidence on proteomic profiling of pulpal and periapical diseases, focusing on key protein biomarkers, molecular pathways, and their potential clinical applications. A comprehensive literature search was conducted across PubMed, Scopus, and Web of Science from January 2009 to June 2026. Studies investigating proteomic analyses of human-derived specimens from patients with pulpal and periapical diseases were included, and data extraction and quality assessment were performed according to PRISMA guidelines. Eleven studies involving 577 participants met the inclusion criteria and analyzed diverse biological specimens, including dental pulp tissue, dentinal fluid, root canal samples, and periapical tissue biopsies. Mass spectrometry-based approaches, including LC-MS/MS, MALDI-TOF MS, and 2D-DIGE, identified 1,153 human proteins and 720 microbial proteins (cumulative counts across all included studies) across different disease states. Key biomarkers included S100 family proteins (S100-A8 and S100-A9), heat shock protein 27 (HSP27), peroxiredoxins, myeloperoxidase, serpin family member SERPINB1, hornerin, and hemoglobin subunits. Distinct proteomic signatures differentiated disease stages, symptomatic and asymptomatic presentations, and post-treatment disease states, while enriched molecular pathways involved neutrophil degranulation, oxidative stress, inflammation, pyroptosis, and bone remodeling. Overall, proteomic profiling reveals distinct molecular signatures across the spectrum of pulpal and periapical diseases, providing valuable insights into disease mechanisms and identifying promising diagnostic and prognostic biomarkers. Future studies should focus on validation in larger cohorts, standardization of sampling protocols, and translation of these findings into chairside diagnostic applications. - Source: PubMed
Publication date: 2026/08/06
Rai Ameesha SIype Aaron MBhat RakshaShetty Preethesh - Multiple sclerosis (MS) is a severe neuroinflammatory disease causing substantial long-term disability. Strong epidemiologic evidence links Epstein-Barr virus (EBV) exposure with MS risk, but genetic evidence for immune target prioritization in EBV-related phenotypes remains limited. - Source: PubMed
Publication date: 2026/08/05
Zhou YixiangHuang XindiShe XiaoHao QinMi ZhikuanYang Yanling - Chronic inflammatory lung diseases are associated with elevated levels of neutrophil elastase (NE), leading to epithelial damage and dysregulated cellular responses. However, the molecular mechanisms underlying NE-mediated disruption of epithelial anti-protease defenses, including the regulation of SERPINB1, remain poorly defined. In this study, we investigated NE-induced responses in bronchial epithelial cells cultured at air-liquid interface (ALI) focusing on epithelial cell death, inflammation, and SERPINB1 dynamics. NE exposure induced dose- and time-dependent cytotoxicity, accompanied by morphological alterations, mitochondrial membrane depolarization, and modest changes in caspase-3, -8, and -9 activity. In ALI cultures, NE was applied either apically, basolaterally or to both compartments simultaneously to evaluate exposure-side-dependent epithelial responses. NE differentially modulated apoptosis-related gene expression, including changes in BCL2, BAX, CASP3, CASP8, CASP9, PARP1, and AIF, depending on NE concentration and exposure side. Cytokine profiling revealed dose-, exposure-side-, and sampling-compartment-dependent changes in IL-6, IL-8, and GM-CSF secretion. Importantly, SERPINB1 expression was markedly reduced at both mRNA and protein levels, while domain-specific immunofluorescence suggested altered SERPINB1 localization and epitope accessibility, suggesting functional alterations beyond transcriptional loss. siRNA-mediated SERPINB1 knockdown further modified NE-associated apoptosis-related gene expression, supporting a functional link between NE exposure and epithelial SERPINB1 regulation. Collectively, these findings establish the NE-SERPINB1 axis as a critical determinant of epithelial cell fate, contributing to epithelial apoptosis, inflammatory mediator release, and protease-antiprotease imbalance. This study provides a systematic analysis of dose- and exposure-side-dependent epithelial responses to NE under ALI culture conditions. Our results highlight the NE-SERPINB1 axis as a contributor to epithelial dysfunction in chronic airway inflammation and support the exploration of SERPINB1-modulating strategies for preserving epithelial integrity and mitigating neutrophil-driven pathology in lung diseases. - Source: PubMed
Publication date: 2026/07/04
Kilic BusraAkel Bilgic HayriyeKaraaslan Cagatay - Septic shock is a life-threatening syndrome characterized by immune dysregulation, oxidative injury, and high mortality. To identify candidate regulators linking immunity and ferroptosis in septic shock, we integrated expression quantitative trait loci (eQTL)-based Mendelian randomization (MR) with transcriptomic datasets from septic shock patients and controls. Differentially expressed genes overlapping with MR-prioritized genes were further evaluated using 113 machine-learning models, among which the glmBoost plus elastic net model (alpha = 0.9) showed strong discriminatory performance, with area under the curve (AUC) values of 0.999 in GSE26378, 0.980 in GSE26440, and 0.987 in the meta-cohort. The final model retained four risk genes, SERPINB1, DDAH2, SLC22A4, and CEACAM6. Among them, SLC22A4/OCTN1, an ergothioneine transporter, was associated with neutrophil-related immune features and better survival-related outcomes, whereas CEACAM6 showed a distinct pattern associated with immune dysregulation. Protein-ligand docking predicted potential interactions between candidate compounds and selected target proteins. In neutrophil-based validation experiments, SLC22A4 perturbation altered inflammatory cytokine production, STING-associated signaling readouts, and ferroptosis-related markers. Additional transporter-related assays showed that SLC22A4 knockdown reduced intracellular ergothioneine accumulation and that ergothioneine supplementation partially rescued erastin-induced viability loss and lipid ROS accumulation. In a cecal ligation and puncture (CLP) model, D-carnitine hydrochloride, STING-IN-5, and Keap1-Nrf2-IN-9 reshaped inflammatory cytokine responses and were associated with partial attenuation of septic lung injury. These findings suggest that SLC22A4 may represent a candidate regulator connecting immune remodeling with ferroptosis-associated dysfunction in septic shock; however, independent cohort validation, direct in vivo target-engagement studies, and further mechanistic analyses are required before therapeutic translation. - Source: PubMed
Publication date: 2026/06/11
Liu LifengYao YongdongYe JingjingZhuang HangLi YimingHuang YanjingLiu Chunyu - Jalili syndrome (JS) is an autosomal recessive disorder with cone-rod dystrophy and amelogenesis imperfecta caused by CNNM4 variants. This study describes salivary proteome patterns observed in a small female JS cohort to characterize the oral molecular environment. - Source: PubMed
Publication date: 2026/03/24
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