Biotin, Clone: 3D6.6; Mab anti-
- Known as:
- Biotin, Clone: 3D6.6; Mab (anti-) to-
- Catalog number:
- abm002211
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Accurate
- Gene target:
- Biotin Clone: 3D6.6; Mab anti-
Related genes to: Biotin, Clone: 3D6.6; Mab anti-
- 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, Clone: 3D6.6; Mab anti-
Related articles to: Biotin, Clone: 3D6.6; Mab anti-
- As a powerful clinical strategy for cancer treatment, immune checkpoint blockage targeting the PD-1/PD-L1 axis is frequently hampered by diverse resistance mechanisms. An in-depth elucidation of the molecular mechanisms governing PD-L1 homeostasis is crucial for improving the immunotherapy response rate. Here, we demonstrate that the PPM1L-E3s-SERPINB1 cascade plays a pivotal role in regulating PD-L1 stability. Specifically, PPM1L-modulated phosphorylation status of PD-L1 dictates its recognition by distinct E3 ubiquitin ligases, including ARIH1, RING1, and RNF2, thereby promoting its proteasomal degradation in a cancer type-dependent manner. Furthermore, we identify SERPINB1 as a driver of PD-L1 ubiquitination and degradation, which exerts the function by specifically relieving ARIH1 autoinhibition. Moreover, in mouse models, Ppm1l deficiency exhibits a synergistic antitumor effect with anti-PD-1 immunotherapy. Notably, the expression levels of both PPM1L and SERPINB1 are clinically significant. Collectively, our findings depict a regulatory landscape that governs PD-L1 homeostasis and highlights the significance of precision therapeutic strategies. - Source: PubMed
Publication date: 2026/09/07
Li PanLiu XinHu PingZhou ZhihuiChai FangniCheng WeiRen Haiyan - Carotid plaque calcification is an active multicellular process with heterogeneous clinical implications. However, endothelial cell (EC) heterogeneity and plaque-region-specific EC states associated with calcified lesions remain incompletely characterized. - Source: PubMed
Publication date: 2026/08/31
Zhou YicongLin DandanYan YanZhao MinghanWang XuelinLv XinMeng ChaoyueLiu Xiaoyun - 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