TRYB1_HUMAN TPSB1 ELISA tesk kit
- Known as:
- TRYB1_HUMAN TPSB1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen14666
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- TRYB1_HUMAN TPSB1 ELISA tesk kit
Related genes to: TRYB1_HUMAN TPSB1 ELISA tesk kit
- Gene:
- TPSAB1 NIH gene
- Name:
- tryptase alpha/beta 1
- Previous symbol:
- TPSB1, TPS1, TPS2
- Synonyms:
- -
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-11-07
- Date modifiied:
- 2015-09-08
Related products to: TRYB1_HUMAN TPSB1 ELISA tesk kit
Related articles to: TRYB1_HUMAN TPSB1 ELISA tesk kit
- Hereditary α-tryptasemia (HαT) is a common autosomal-dominant trait caused by additional copies of the gene encoding for α-tryptase. This inheritance is the most common etiology for elevated basal serum tryptase (BST), occurring almost exclusively at BST ≥ 8 μg/L. In systemic mastocytosis (SM) and nonclonal mast cell-mediated disorders, HαT is linked to a complex constellation of symptoms. - Source: PubMed
Publication date: 2026/05/20
Koch DanielWortmann FriederikeRecke AndreasRose EllenGaffal EvelynWigger Jennifervon Bubnoff Nikolasvon Bubnoff Dagmar - Extracellular matrix (ECM) remodeling contributes to retinal vascular basement membrane thickening, an early structural hallmark of diabetic retinopathy (DR). This study aimed to identify key ECM-related genes (ECMGs) associated with DR. Transcriptomic data of DR and ECMGs from MatrixDB were integrated to identify differentially expressed ECMGs. Six machine learning (ML) models, including Extra Trees (ET), Logistic Regression, Adaptive Boosting, Random Forest, Extreme Gradient Boosting, and naive Bayes classifier, were employed to construct DR classification models, with SHapley Additive exPlanation (SHAP) used to interpret feature contributions. Functional enrichment analysis using GSEA and immune infiltration analysis using CIBERSORT were conducted to explore the potential mechanisms by which key ECMGs regulate DR. Regulatory networks were constructed using predicted miRNAs, lncRNAs, and transcription factors (TFs) via the ENCORI, miRWalk, and miRNet databases. Drug-key ECMGs-DM-related diseases interactions were further explored using the DGIdb and CTD databases. Nine candidate ECMGs were identified by overlapping 356 DM-associated DEGs, 1,626 DR-associated DEGs, and 1,023 ECMGs, including CILP2, FN1, DEFA3, COL17A1, CRISP3, TPSAB1, SFRP1, GPHA2, and ECM2. Among the six ML algorithms, the ET classifier exhibited the best overall performance, and five ECMGs (SFRP1, CILP2, FN1, TPSAB1, and ECM2) with non-zero SHAP values were retained as key genes. These genes showed distinct expression patterns across the healthy, DM, and DR groups, and were enriched in neural-related pathways, such as axon guidance, glycosphingolipid biosynthesis ganglio series, and neuroactive ligand receptor interaction. Immune profiling and correlation analysis revealed that FN1, TPSAB1, and CILP2 were correlated with memory/naive B cells, CD8 + T cells, activated memory CD4 + T cells, Tregs, monocytes, and neutrophils. Additionally, the ceRNA network contained five miRNAs, 7 lncRNAs, and two ECMGs, and further regulatory and pharmacologic analysis further linked key ECMGs to specific TFs, drugs, and diabetes-related diseases. This study identified SFRP1, CILP2, FN1, TPSAB1, and ECM2 as key ECMGs in DR, revealing their coordinated involvement in ECM remodeling, neural signaling, and immune modulation. These findings provide novel insights into DR pathogenesis and potential therapeutic targets. - Source: PubMed
Publication date: 2026/06/10
Xin WangYing WangQiang FengYan ChenWei Zhang - Patients with congenital heart disease-associated pulmonary arterial hypertension (CHD-PAH) have a reversible stage, during which shunt closure reverses PAH. However, PAH is irreversible beyond a certain time point, and the molecular mechanisms underlying the switch from reversible to irreversible PAH remain poorly understood. - Source: PubMed
Publication date: 2026/05/21
Xiao GenfaMeng YingDu ZhimingLiu ZhihuaYu HaiyangWang HaoboNie LijunLiu XiaoliLan XuemeiDuan YanyuXiong JianxianLiu Ziyou - Asthma, a complex disease, is categorized into type 2 (T2) and non-type 2 (non-T2) molecular endotypes. Growing evidence supports the overlap between endotypes and highlights a complex interplay among multiple inflammatory cell types. Combined inflammatory disease is particularly challenging to treat. Building on the background of overlapping asthma endotypes, the goal of this research was to explore common gene signatures and the underlying molecular mechanisms across different asthma subtypes. - Source: PubMed
Publication date: 2026/05/08
Jia ZaixingLiu BinCao JingHan SiqinHou ShujieChen ZixiaoChen JialunLiu ZhenweiChen WeihuaLi JingwenLi RongqinYan Xixin - Hereditary α-tryptasemia (HαT) is a genetic trait characterized by increased copy number. Identified in 2015, the HαT trait impacts approximately 4%-6% of individuals of European ancestry and manifests with core clinical features in one-third of individuals who test positive for the genetic trait. HαT represents a natural human model of α-tryptase overexpression which can be leveraged to better and more comprehensively understand tryptase and mast cell (MC) biology at the tissue level. In this review, we synthesize emerging evidence demonstrating that HαT is a clinically significant modifier of disease in the gastrointestinal (GI) tract. We summarize findings demonstrating that HαT impacts small intestinal immunopathology even in the absence of overt GI pathology. In celiac disease, coexisting HαT is associated with increased duodenal MCs and persistent GI symptoms (diarrhea, bloating, abdominal pain) despite a gluten-free diet. We also review emerging data indicating that HαT may act as a disease modifier in inflammatory bowel disease (IBD); increased α-tryptase gene dosage is associated with intestinal MC activation and increased expression of MRGPRX2. These changes may amplify MC-mediated inflammatory pathways within the intestinal mucosa and contribute to the complexity of immune signaling traditionally attributed to T-cell-driven inflammation in IBD. Taken together, emerging modern cellular and molecular biology evidence suggests that the natural overexpression of α-tryptase in HαT alters MC behavior and GI intestinal immunopathology, thereby modifying disease outcomes across a spectrum of GI illnesses. - Source: PubMed
Publication date: 2026/04/14
Simeone Ilaria MGaleas-Pena MichelleWhite KatelynSullivan BrandyMorelli AlexandraSilvester Jocelyn AKonnikova LizaTherrien AmelieGlover Sarah C