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
- Allergic diseases have been linked to genetic variations in TPSAB1 and TPSB2. This study aimed to develop a Matrix-Assisted Laser Desorption/Ionization Time-of-Flight Mass Spectrometry (MALDI-TOF MS) method for simultaneous copy number detection of TPSAB1 and TPSB2. - Source: PubMed
Li YangZhao XuefengHe ShengLai YunliWei ShijieZhou Wanjun - COVID-19 does not require hospitalization in most cases, but post-acute sequelae can persist and are a public health concern. In a prospective cross-sectional study, we examine persistent ocular symptoms (POS) emerging in non-hospitalized individuals after COVID-19, with individuals without POS post-recovery as controls. Using symptom and quality of life data, clinical examinations and biofluid proteomics, we document ocular symptoms persisting from 3 months up to 3 years post-infection. POS lead to significant vision disability and are linked to clinical findings not detectable in routine exams but only with specialized tests. POS include near vision disturbances, strabismus, weakened autonomic pupillary reflexes, corneal neurodegeneration and chronic activation of ocular surface dendritic/T cells. We report a tear film proteomic profile consistent with severe COVID-19, chronic dysregulation of CD4 T cell regulatory activity, upregulation of ITGB6, NFASC, CTGF, TPSAB1 and CKMT1A-CKMT1B, pupil dysfunction correlating with elevated JUN, and dendritic/T cell dysregulation correlating with elevated ANGPTL2, SKAP2 and DAPP1 levels. Diagnostic models based on clinical examinations with or without biomarkers predict POS with 77-91% accuracy and implicate chronic T cell-mediated neuroinflammation in the pathogenesis of POS, a debilitating syndrome arising after COVID-19 recovery and characterized by strabismus, ocular dysautonomia and peripheral ocular neuropathy. - Source: PubMed
Publication date: 2026/07/08
Moustardas PetrosSetterud HelenMeijer HelenaAndersson GunnelRoth JennyDashti AvaJohansson BjörnMacedo António FilipeLagali Neil - 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