Ask about this productRelated genes to: SFTPB antibody
- Gene:
- SFTPB NIH gene
- Name:
- surfactant protein B
- Previous symbol:
- SFTP3
- Synonyms:
- SP-B
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-07-06
- Date modifiied:
- 2016-10-05
Related products to: SFTPB antibody
Related articles to: SFTPB antibody
- Due to the global obesity crisis, increasing numbers of women enter pregnancy with overweight or obesity. Their offspring are at greater risk of respiratory complications at birth due to metabolic changes that impact lung development that may reduce capacity for surfactant production. We hypothesize that a high-fat-high-energy diet (HF-HED) negatively impacts late gestation fetal lung development. - Source: PubMed
Publication date: 2026/04/27
Lock Mitchell CHuber Hillary FLi CunOrgeig SandraNathanielsz Peter WMorrison Janna L - To explore the relationship between surfactant protein B (SFTPB) gene expression and multiple biological processes in lung adenocarcinoma (LUAD) and construct a SFTPB-related gene signature for predicting LUAD prognosis. - Source: PubMed
Publication date: 2026/03/22
Ma ShanwuXu RuiLin ChutongNing YingzeHe HuayuTang JizhengJin LiangHe WeiXiong ZhenchengQiang Guangliang - Alveolar regeneration requires coordinated alveolar type 1 (AT1)/alveolar type 2 (AT2) responses and an intact epithelial barrier. In vitro systems, however, rarely couple lineage control with high resistance. Here we establish a concise workflow in which human AT2-like progenitors are expanded in a medium containing a small-molecule cocktail (Y-27632/A-83-01/CHIR99021; YAC), followed by air-liquid interface (ALI) culture in medium without the YAC cocktail (hereafter referred to as the YAC(-) condition). Compared with submerged culture, ALI increased AT1(AQP5, AGER, and PDPN) and AT2 (SFTPB, SFTPC, and SFTPD) markers. Within ALI, β-catenin inhibition by XAV939 elevated AT1 features while retaining AT2 protein expression, but was accompanied by reduced AT2 marker expression at the transcriptional level compared with the YAC(-) condition. Transepithelial electrical resistance entered the kΩ range by ALI day 10 and remained high across ALI conditions, with hematoxylin and eosin staining confirming a continuous single-layer epithelium. Passage reduced absolute marker levels and resistance but preserved the rank order across conditions. In scratch assays, ALI monolayers closed wounds over 24-48 h, and spatial immunofluorescence staining showed surfactant protein-C enrichment at the leading edge and podoplanin predominantly behind the front. Collectively, these findings demonstrate that β-catenin modulation within ALI biases the alveolar epithelial profile toward AT1-like features, whereas the YAC(-) condition sustains a balanced AT1/AT2 state with superior epithelial barrier performance and repair capacity. This platform provides a single-monolayer system suitable for dissecting alveolar epithelial differentiation and functional maintenance. - Source: PubMed
Publication date: 2026/02/05
Lin Yu-CheIgarashi MikiSakai YasuyukiNishikawa MasakiIshikawa ShinkichiTanabe Ikuya - Lung adenocarcinoma (LUAD) is a common subtype of non-small cell lung cancer (NSCLC) with a poor prognosis. To identify novel biomarkers and understand the underlying mechanisms in LUAD, we conducted a comprehensive analysis using single-cell and bulk RNA sequencing data. Our study focused on LAD1, a basement membrane filament protein that has been implicated in tumorigenesis in various cancers. We analyzed scRNA-seq data from 10 LUAD patients and identified nine cell subgroups, with LAD1 specifically expressed in cancer cells. Further analysis revealed significant correlations between LAD1 and genes associated with LUAD progression, including SFTPB, S100A6, CEACAM6, KRT19, S100A10, ANXA2, S100A11, and CAPN2. We investigated the effects of altered LAD1 expression on differentially expressed genes (DEGs), biological processes, and signaling pathways. Furthermore, we collected cancer tissue and corresponding adjacent tissue samples from 36 LUAD patients, used immunohistochemical staining to detect LAD1 expression, and analyzed its correlation with clinicopathological characteristics. We knocked down the expression of LAD1 in A549 cells using siRNA, and detected changes in LUAD cell migration and invasion ability through scratch healing assay and Transwell assay. Our results indicated diverse effects of LAD1 at both the single-cell and whole tumor levels, with a convergence on processes associated with tumor progression. In lung adenocarcinoma tissues, LAD1 was significantly upregulated, particularly in the cancer cell subgroup within tumors. Immunohistochemical results showed that LAD1 was highly expressed in LUAD, and knocking down LAD1 could inhibit LUAD cell migration and invasion. Pan-cancer analyses demonstrated LAD1 as an independent prognostic factor for overall survival in LUAD. Moreover, we developed a nomogram model incorporating LAD1 expression and clinical parameters, which demonstrated good predictive performance. The high expression of LAD1 in cancer cells, its associations with LUAD-related genes, and its links to biological processes and pathways suggest its potential biological relevance and that it merits further investigation. Overall, this study provides insights into LUAD and supports LAD1 as a gene worthy of further investigation. - Source: PubMed
Publication date: 2025/12/21
Wang SufenQiang BanghongXu XiaoyanFang YanLiu YinhuaZhang WeiHuang Xi - The transcription factor NK2 homeobox1 (NKX2-1), associated with brain lung thyroid syndrome, regulates the transcription of surfactant proteins, thyroglobulin (TG) and thyroid peroxidase (TPO). This study explored the pathogenicity of three NKX2-1 variants (p.(Tyr214Cys), p.(Arg165Trp) and p.(Gly147Ala)) that were identified in three infants with lethal forms of childhood interstitial lung disease. - Source: PubMed
Publication date: 2025/12/19
Soreze Yohan DavidDesroziers-Louedec TifennCarré AuroreDiab FarahDaskalopoulou AphroditeStarck JulieNau ValérieLegendre MarieKarabina Sonia-AthinaHoudouin VéroniqueCoulomb-L'herminé AuroreLouvrier CamilleNathan Nadia