Polyclonal Rabbit CST1 Antibody
- Known as:
- Polyclonal Rabbit CST1 Antibody
- Catalog number:
- KA0922
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit CST1 Antibody
Related genes to: Polyclonal Rabbit CST1 Antibody
- Gene:
- CST1 NIH gene
- Name:
- cystatin SN
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1990-02-06
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit CST1 Antibody
Related articles to: Polyclonal Rabbit CST1 Antibody
- Aging exhibits both systemic and organ-specific components, yet existing models struggle to disentangle their shared versus distinct biological determinants at the population level. We present a structural decomposition framework that partitions seven organ-based biological age gaps (BAGs) into a Common BAG (CBAG) and seven Organ-Specific BAGs (OSBAGs) in 501,388 UK Biobank participants. This dual-axis model outperforms undecomposed body/organ BAG approaches in predicting lifespan, healthspan, and organ-specific disease risk. A large-scale aging GWAS identifies 747 novel loci, complemented by integrative proteomic and metabolomic analyses that reveal causal and druggable targets, including CST1. Pathway-guided multi-omics demonstrates a modular aging architecture, with CBAG reflecting cross-tissue regulators (e.g., FOXO3) and OSBAGs capturing organ-restricted effectors (e.g., UMOD). Drug-aging profiling uncovers organ-specific pro-aging effects consistent with known toxicities that are largely missed by undecomposed models. Sex-stratified analyses further reveal divergent molecular trajectories between males and females. All findings are integrated into HONOR, the first open-access atlas for structural aging and multi-omics translation. - Source: PubMed
Publication date: 2026/05/08
Huang HeLi YiSong QinglinYuan LiyunYang YuqiZhu MinweiSun RenliangHu YueXiong ChenyihangNi TingLiu YunRuiz-Linares AndrésZhang GuoqingLiu FanPeng QianqianWang Sijia - Respiratory viral infections in early childhood are major drivers of acute morbidity and long-term airway disease, yet how distinct viruses remodel the pediatric nasal mucosa at cellular resolution remains unresolved. Here, we generated a single-cell RNA sequencing atlas of 335,174 nasal epithelial and immune cells from 132 children under five years of age with SARS-CoV-2, rhinovirus, or respiratory syncytial virus (RSV) infection, alongside uninfected controls. Mapping viral transcripts to individual cells revealed virus-specific infected epithelial states: an NF-kB-responsive ciliated subset in SARS-CoV-2 and a previously undescribed squamous-like subset in RSV. We delineated divergent mucosal response programs, including a robust interferon (IFN) response in SARS-CoV-2, an IL-13-responsive secretory program in rhinovirus, and heightened inflammatory and cytotoxic immune activation in RSV. In RSV, specific immune subsets and elevated IFN-response signatures were associated with disease severity, whereas rhinovirus-induced wheeze was marked by expansion of a + goblet cell subset. Integration of asthma genome-wide association data with our atlas revealed a hillock-like squamous epithelial subset enriched for expression of childhood-onset asthma risk loci. Finally, we demonstrate that this resource enables high-resolution annotation of independent pediatric cohorts in Kolkata, India and rural Bangladesh. Together, this atlas establishes a comprehensive view of antiviral immunity in the pediatric nasal mucosa and defines virus-specific mucosal immune programs relevant to disease severity and asthma risk in early life. - Source: PubMed
Publication date: 2026/04/24
Walsh Jaclyn M LJuttukonda Lillian JTang YingChatterjee AnkitaElosua-Bayes MarcLangan EricaFrischmann AmandaTaliaferro FaithMatthews Hannah RKimler KyleLent Chris MKeya Deb PurnaDev Preonath ChondrowMalaker Apurba RajibTanvia LubanaTanmoy Arif MohammadGhosh SupratimMaitra ArindamGhosh ApurbaBasu SurupaKane Abigail SCoomer Charles AShalek Alex Kde Silva Thushan ISesay Abdul KarimEdwards JessicaQuee Corrine SinGonzalez Wanda IYonker Lael MGlover Sarah CMajumder ParthaHooda YogeshSaha SenjutiOrdovas-Montanes JoseHorwitz Bruce H - Differentiating early-stage hepatocellular carcinoma (HCC) from hepatocellular adenoma (HCA), particularly in the context of steatosis, remains a diagnostic challenge. Accurate distinction is essential for appropriate clinical management, yet reliable ancillary assays are limited. This study focuses on hepatocellular neoplasms with steatotic change in non-cirrhotic livers, aiming to minimise confounding factors from cirrhosis and to identify genetic alterations specific to tumour biology. Using total RNA sequencing, we analysed the gene expression profiles of 12 HCA cases, ten HCC cases (including eight with steatotic change) and seven paired non-neoplastic liver samples. Transcriptomic profiles were subsequently correlated with histopathologic features and clinical outcomes. Unsupervised clustering segregated HCC from HCA and non-neoplastic liver, indicating distinct transcriptional signatures. Three histologically ambiguous hepatocellular neoplasms were also evaluated, and their clustering patterns aligned with their long-term clinical behaviour, suggesting the potential clinical utility of transcriptomic classification in diagnostically uncertain cases. Differential expression analysis identified both protein-coding and non-coding genes that may serve as candidate biomarkers for future RNA-based or immunohistochemical assays. Pathway analysis revealed distinct oncogenic and metabolic signalling cascades differentiating HCC from HCA. These findings demonstrate that transcriptomic profiling offers a promising molecular approach to distinguishing HCC from HCA and assists in the classification of indeterminate hepatocellular neoplasms. With further validation, these molecular signatures and their surrogate biomarkers have the potential to enhance diagnostic accuracy, refine histologic criteria, guide clinical management and improve our understanding of hepatocarcinogenesis. - Source: PubMed
Publication date: 2026/03/06
Zhu Lee-ChingPatil Sushant AKuhlers Peyton CMoon Andrew MRaab Jesse RPfefferle Adam DHayward Michele CWielgus AlbertDe la Cruz Gabriela EBantumilli SurekhaHoadley Katherine AMerker Jason D - Intrahepatic cholangiocarcinoma (CCA) is a highly aggressive malignancy arising from the intrahepatic biliary epithelium with insidious onset and dismal clinical outcomes. The lack of reliable early diagnostic markers and effective therapeutic targets underscores the urgent need for novel intervention strategies. Integrated evaluation of public transcriptomic datasets and local validation cohort with survival analysis were performed to assess expression pattern and prognostic significance of cystatin SN (CST1) in CCA. Functional characterization was performed via gain- and loss-of-function experiments in HuCCT1 and RBE cells, complemented by murine orthotopic liver implantation and pulmonary metastasis models. We found that CST1 was significantly upregulated in human CCA tissues. Elevated CST1 expression predicted unfavorable prognosis in CCA patients. Subsequently functional studies revealed that overexpression of CST1 suppressed cellular senescence markers, as evidenced by decreased senescence-associated β-galactosidase activity and downregulated senescence-associated secretory phenotype factors (IL-6, CCL20). Concomitantly, CST1 overexpression enhanced cell proliferation, migration, invasion, and in vivo metastatic capacity. Integrated multi-omics profiling identified CST1-mediated suppression of pyrimidine metabolism through TYMS downregulation. However, exogenous thymidine supplementation failed to rescue proliferation defects upon CST1 knockdown, indicating that CST1-promoted tumor growth is independent of pyrimidine metabolism. Mechanistically, NFATC2 transcriptionally activates CST1, which subsequently abrogates senescence through SOX4 stabilization; ectopic SOX4 expression rescues senescence induced by CST1 depletion. These findings establish CST1 as a promising therapeutic target and provide mechanistic insights for CCA intervention strategies. - Source: PubMed
Publication date: 2026/03/25
Zhao WeiZhao JingLi KunShi JianCong LiyuanYu Guangyi - Transcriptomic analysis of bronchial brushes reveals asthma-associated gene signatures but is limited by the invasiveness of bronchoscopy. Based on the "united airways" hypothesis, we evaluated whether and to what extent nasal brushes reflect asthma-associated transcriptomic changes in the lower airways. - Source: PubMed
Publication date: 2026/03/10
Wen HuiKole TessaCarpaij Orestes AKarp TatianaGuryev VictorFaiz AlenChung Kian FanBhavsar PankajAdcock Ian MSiddiqui SalmanLan AndyRaby Katie LZounemat-Kermani NazaninBrightling ChrisSingh DaveKocks JanwillemKraft MonicaBeghé BiancaRabe Klaus FPapi AlbertoHylkema Machteld NNawijn Martijn Cvan den Berge Maarten