Ask about this productRelated genes to: SFTPC antibody
- Gene:
- SFTPC NIH gene
- Name:
- surfactant protein C
- Previous symbol:
- SFTP2
- Synonyms:
- SP-C, PSP-C, SMDP2, BRICD6
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-10-05
Related products to: SFTPC antibody
Related articles to: SFTPC antibody
- This study retrospectively analyzed the clinical data of a female child with primary ciliary dyskinesia (PCD) caused by variants in the CFTR (NM_000492.3) and SFTPC (NM_003018.3). All variant descriptions in this report follow the HGVS standardized nomenclature guidelines. These two variants are considered to be potentially associated with pediatric PCD. - Source: PubMed
Publication date: 2026/08/24
Yuan XinhuiShao DanLi YumeiLing JizuGong Yigu - The progressive lung function decline in severe asthma is poorly explained by traditional inflammation‑centered paradigms. Calcium (Ca²⁺) dysregulation and transforming growth factor‑β (TGF‑β) signaling have been implicated, but the molecular link between them and their upstream regulators remain elusive. - Source: PubMed
Publication date: 2026/08/14
Zhu ZhiqinXiao QingaoCai RunjinQi EnyuGong XiaoxiaoTang JialeLi XiaozhaoFeng Juntao - To determine whether radiation directly compromises AT2 cell stemness through oxidative and DNA damage, and to evaluate whether Compound Kushen Injection (CKI) protects AT2 cells, restores alveolar regeneration, and mitigates radiation-induced pulmonary fibrosis. - Source: PubMed
Publication date: 2026/08/15
Liu Yan-LiXu Cheng-YanWang YongLiang Xiao-YanChen Yun - Lung cancer is the second most commonly diagnosed malignancy worldwide and remains the leading cause of cancer-related death. Non-small cell lung cancer (NSCLC) accounts for approximately 80-85% of lung cancers. Given the low rate of early detection and substantial interpatient heterogeneity, management of NSCLC, particularly locally advanced disease, remains challenging. This study aimed to characterize clinical heterogeneity and progression-associated molecular features of locally advanced NSCLC and to identify candidate biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/24
Tian YuanhuiDeng YanLiao XiaoliYuan ShutaoLi Ke - Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible fibrosing interstitial lung disease characterized by excessive extracellular matrix (ECM) accumulation, disruption of lung architecture, and progressive loss of pulmonary function. IPF is frequently accompanied by comorbid conditions that exacerbate disease progression and negatively impact prognosis. To address the biological complexity of IPF, this study presents a comprehensive molecular systems architecture that enables a system-level understanding of biomolecular interactions within the fibrotic lung microenvironment in response to external and physiological triggers. A literature search is conducted using the Medical Subject Headings (MeSH) keywords in PubMed and MEDLINE to identify relevant peer-reviewed articles published from April 2008 to June 2025, with Google Scholar used solely to retrieve full-text versions of articles identified through this search. The systems biology tool CytoSolve was used to perform the systematic review and to support the curation and development of the molecular systems architecture of IPF pathogenesis. Full-length articles that contained Medical Subject Headings keywords relevant to IPF pathogenesis were selected for a comprehensive review. A total of 150 studies published between April 2008 and June 2025 met the inclusion criteria and were included in the systematic analysis. This systematic review was not registered. Findings were synthesized qualitatively into a multilayered molecular interactome rather than through statistical meta-analysis. The architecture integrates interactions across sixteen lung-associated cell types, including epithelial, endothelial, mesenchymal, immune, and stromal populations. Key external triggers-such as bleomycin (BLM), asbestos, silica, radiation, cigarette smoke, Herpes virus, and genetic mutations (SFTPC I73T), along with hypoxia associated with comorbidities-initiate coordinated cellular responses that converge on three fundamental pathological processes: inflammation, myofibroblast differentiation, and tissue remodeling. These interconnected processes collectively drive the initiation and progression of IPF. This molecular systems architecture unifies triggers, cellular components, molecular pathways, and biological processes into a multilayered framework for identifying therapeutic targets, biomarkers, and rational single- and combination-treatment strategies in IPF. - Source: PubMed
Publication date: 2026/07/29
Ayyadurai V A ShivaManoharan YamunaDeonikar Prabhakar