Ask about this productRelated genes to: SCGB1A1 Blocking Peptide
- Gene:
- SCGB1A1 NIH gene
- Name:
- secretoglobin family 1A member 1
- Previous symbol:
- UGB
- Synonyms:
- CC10, CCSP, CC16
- Chromosome:
- 11q12.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-03
- Date modifiied:
- 2016-01-05
Related products to: SCGB1A1 Blocking Peptide
Related articles to: SCGB1A1 Blocking Peptide
- To elucidate the molecular mechanisms underlying Benzo[a]pyrene (BaP)-induced lung carcinogenesis, we constructed lung organoid and BaP-induced malignant transformation cell model (16HBE-T). Single-cell sequencing analysis confirmed that organoids were primarily composed of basal cells and secretory cells. Following BaP exposure, the lung organoids exhibited G1-phase cell cycle arrest. The expression of CYP1A1 (Log2FC = 10.24) and CYP1B1 (Log2FC = 6.27) were significantly upregulated, while that of SCGB1A1 (Log2FC = -0.26) was downregulated, indicating early-stage lung epithelial injury. Mfuzz soft clustering analysis and FindMarker function were employed to characterize gene expression patterns and identify differentially expressed genes (DEGs). GO, KEGG, GSEA and WikiPathway enrichment analyses revealed that these DEGs were enriched in redox-related metabolic processes (including cysteine/glutamate metabolism and glutathione biosynthesis), NRF2 signaling pathways, and carcinogenesis-associated pathways. Among the DEGs, 9 DEGs were associated with oxidative stress and amino acid metabolism, with SLC7A11 showing the most prominent upregulation (Log2FC = 3.40). The AddModuleScore function indicated that NRF2 exhibited the most significant transcriptional activity. In 16HBE-T cells, the protein expression of SLC7A11 and NRF2 increased by 35.74% and 82.85%, respectively. Knockdown of SLC7A11 significantly inhibited the migration, invasion, and colony-forming abilities of 16HBE-T cells. Meanwhile, intracellular glutamate and cysteine levels decreased, whereas glutamine levels increased. ChIP-PCR verified that NRF2 could directly bind to two specific regions (460-565 bp and 1488-1623 bp) within the SLC7A11 promoter to regulate amino acid metabolism. Collectively, our findings demonstrate that NRF2-regulated SLC7A11-mediated amino acid metabolic reprogramming plays a pivotal role in BaP-induced cellular malignant transformation. - Source: PubMed
Publication date: 2026/04/03
Wang YongKong HongyueZhang YuSu JiawenWei JiajunGuo YingYu XiaoNie JishengYang Jin - Acupuncture has emerged as a promising complementary therapy for allergic asthma, but the molecular mechanisms underlying its therapeutic effects remain unclear. This study aimed to investigate whether Clara cell 10-kDa protein (CC10), an airway epithelial immunoregulatory protein, mediates the anti-inflammatory actions of acupuncture through the modulation of pulmonary dendritic cells (DCs). - Source: PubMed
Long JieCheng MiWu Quan-LongZhang Ya-YaWang YuChen Yan-JiaoYin Lei-MiaoYang Yong-QingXu Yu-Dong - Respiratory syncytial virus (RSV), a member of the genus , is an etiological agent in infant lower respiratory tract infections (LRTIs) producing substantial global morbidity. Here, secretoglobin ()-derived progenitors play a primary role in triggering innate, inflammatory, and cell state transitions in response to RSV LRTIs. Whether RSV activation of innate signaling in this epithelial sentinel population leads to chronic airway disease is unknown. To understand the role of innate signaling in -derived progenitors, a model of RSV post-viral disease (PVLD) was developed and studied in the presence or absence of RelA conditional knockout (CKO). Single-cell RNA sequencing (scRNA-seq) studies showed that RSV-PVLD induced a transition of atypical, differentiation-intermediate, alveolar type 2 (aAT2) cells characterized by tumor protein 63 (TRP63), aquaporin 3 (AQP3), and Itgβ4 expression, as well as changes in PDGFRβ mesenchyme. A single-cell trajectory analysis and lineage-tracing experiments using CreER X mTmG mice demonstrated that the populations were precursors to the aAT2 population. Mechanistically, we found that the formation of the aAT2 population was prevented by RelA CKO. A differential gene expression analysis revealed that RSV-PVLD coordinately upregulates nuclear receptor subfamily 1 group D (), clock and basic helix-loop-helix ARNT-like 1 () genes both in the aAT2 cell and in its + mesenchymal niche in a RelA-dependent manner. A systematic analysis of intercellular epithelial-mesenchymal communication in the scRNA-seq data showed that the clock-dysregulated epithelial-mesenchymal niche produces aberrant expression. ANGPTL4 upregulation was confirmed by the measurement of both its mRNA and protein. Moreover, ANGPTL4 is biologically active in the BALF of RSV-PVLD mice, inhibiting lipoprotein lipase activity. We conclude that RSV-PVLD is mediated, at least in part, by RelA signaling in -derived epithelial progenitors, dysregulating ANGPTL4 signaling in an epithelial-mesenchymal niche, resulting in persistence of atypical alveolar epithelial cells with dysregulated of clock gene expression. - Source: PubMed
Publication date: 2026/03/21
Skibba MelissaBrasier Allan R - Osteogenesis imperfecta (OI), or brittle bone disease, is a rare congenital disorder characterized by bone fragility and increased fracture incidence mainly due to mutations in type I collagen or genes associated with collagen synthesis. Genetic and allelic heterogeneity underlie the phenotypic spectrum of OI yet all forms commonly feature early mortality stemming from pulmonary complications, the molecular cause for which has not been resolved. Using single-cell RNA sequencing (scRNAseq), we identified novel molecular and cellular mechanisms underlying the lung abnormalities observed in our () mouse, which recapitulates a moderate form of OI. Pulmonary tissues in OI models have consistently displayed a histological emphysematous phenotype, however the origin of this and the effect on lung cell development and function remains unknown. Using scRNAseq data derived from young and adult lungs, we found significantly increased AT2 to AT1 cell transition (cells necessary for alveolar structure and gas exchange) in young mice but decreased AT2 cell differentiation in adults. Further, adult lungs show increased fibroblast activation and differentiation. Finally, our scRNAseq analysis revealed a chronic inflammation phenotype in the Aga2 lung with increased neutrophil and monocyte numbers, IL1B and TNF pathway activation, NOD-like receptor signaling activation, and expression of the NLRP3 inflammasome. Most importantly, we saw a significant decrease in the expression of Scgb1a1 in immune, epithelial, and fibroblast cells. Decreased expression of Scgb1a1 is associated with multiple lung diseases such as emphysema, chronic obstructive pulmonary disease (COPD), and asthma and has become an important therapeutic target for chronic lung inflammation. Clinical treatments specific to pulmonary complications in OI are non-existent and our results reveal that chronic inflammation could be a target to prevent the pulmonary insufficiency and early mortality observed in OI patients. - Source: PubMed
Publication date: 2026/02/26
Zieba JenniferBagheri RoyaKot AlexMartin Jorge HWachtell DavisWong SereenMungovan MaeveWight CarolineKrakow Deborah - No specific follow-up strategy has shown to improve overall survival (OS) after surgical resection of non-small cell lung cancer (NSCLC). Club cell secretory protein (CCSP) is produced by bronchiolar club cells and shows promise as a survival biomarker as its concentration depends on degree of lung inflammation. Our objective was to evaluate prognostic impact of postoperative serum CCSP concentration on OS after resection of stage I to IIIA NSCLC in a post hoc ancillary analysis of the IFCT-0302 trial. - Source: PubMed
Publication date: 2026/02/24
Brosseau SolennEtienne HarryPeoc'h KatellLanglais AlexandraBlanché HélèneFoucher PascalBarlesi FabriceDomas JeanGirard PhilippeScherpereel ArnaudDumont PatrickDerollez MarcQuoix ElisabethDebieuvre DidierDeleuze Jean-FrançoisLeçon-Malas VéroniqueZalcman GérardWesteel VirginieMordant Pierre