Ask about this productRelated genes to: FCRLA Blocking Peptide
- Gene:
- FCRLA NIH gene
- Name:
- Fc receptor like A
- Previous symbol:
- FCRLM1
- Synonyms:
- MGC4595, FCRLc2, FCRLb, FCRLc1, FCRLd, FCRLe, FCRL, FCRLa, FREB, FCRLX
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-05-10
- Date modifiied:
- 2016-01-21
Related products to: FCRLA Blocking Peptide
Related articles to: FCRLA Blocking Peptide
- Chronic obstructive pulmonary disease (COPD) is a recognized risk factor for lung adenocarcinoma (LUAD), but the molecular mechanisms behind this association are still unclear. This study aims to reveal shared key genes and pathways involved in both COPD and LUAD, and identify potential biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/02/06
Li MengWang BinyuPeng QianShen WeiyunShi DanfeiLi XinminYu DaojunLi Yong - Mitochondrial dysfunction is a hallmark of chronic obstructive pulmonary disease (COPD). Nevertheless, the precise molecular mechanisms of COPD have yet to be fully elucidated. Protein-protein interaction (PPI) network construction and weighted gene co-expression network analysis (WGCNA) were conducted to identify hub genes related to mitochondrial homeostasis. A TNF receptor superfamily member 17 (TNFRSF17)-knockdown model was established in human bronchial epithelial (HBE) cells treated with cigarette smoke extract (CSE), and in mice exposed to CS and lipopolysaccharide (LPS). Cell counting kit-8, enzyme-linked immunosorbent assay, flow cytometry, JC-1 staining, senescence-associated β-galactosidase staining, western blot analysis, and hematoxylin-eosin staining were used to evaluate cellular function, inflammation, and pathology. The involvement of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway was investigated using colivelin analog 1 (C-A1). CD19, POU2AF1, FCRLA, and TNFRSF17 were identified as mitochondrial homeostasis-related hub genes, all of which were upregulated in COPD. Following TNFRSF17 knockdown, COPD mice exhibited reduced alveolar destruction, inflammatory cell infiltration, and collagen deposition. TNFRSF17 knockdown alleviated CS-induced mitochondrial membrane depolarization, calcium overload, reactive oxygen species (ROS) accumulation, ATP depletion, IL-6 and TNF-α secretion, and cellular senescence both in vitro and in vivo. TNFRSF17 knockdown suppressed the phosphorylation of JAK2 and STAT3. The protective effects mediated by TNFRSF17 knockdown were significantly abrogated by the C-A1 treatment. TNFRSF17 knockdown inhibits mitochondrial dysfunction, inflammation, and senescence in COPD by obstructing the JAK2/STAT3 pathway, offering a promising therapeutic strategy for COPD. - Source: PubMed
Yang XiaomeiHuang YuwenZheng AifangMu HaoyuCui Jiangyu - Bisphenol A (BPA) is a widely used xenoestrogen that can disrupt neuroendocrine and immune regulation through multiple hormone receptors. This study investigated BPA-induced long non-coding RNA (lncRNA)-mRNA interactions in the cerebral cortex and hypothalamic-pituitary-thyroid (HPT) axis of adult male mice. Transcriptome sequencing and comprehensive lncRNA annotation identified 14,858 novel lncRNA transcripts. Integrated network analysis using weighted gene co-expression network analysis (WGCNA) revealed four distinct tissue-specific modules: neuronal signaling alterations (, , ), RNA splicing modifications (), PI3K/Akt-mediated cellular dysfunction (, ), and immune receptor signaling disruptions (). These findings suggest that BPA reprograms transcriptional networks in a tissue-specific manner, potentially disrupting hormone-related neurotransmission, metabolic regulation, and immune signaling via lncRNA-mediated mechanisms. Such systems-level reprogramming of the immune-neuroendocrine network (INEN) provides novel mechanistic insights and biomarker candidates for assessing and mitigating the health impacts of environmental endocrine disruptors. - Source: PubMed
Publication date: 2025/10/11
Oh Seung-MiLim ByeonghwiPark Yoon-BeenJang Min-JaeLim Seok-WonLim ChiwoongKim Do-YoungPark YejeeSeo Young-JunKim Jun-Mo - The induction of mitochondrial permeability transition-driven necrosis (MPTDN) is therapeutically relevant in various cancers. However, few studies have explored the role of MPTDN-related genes (MPTDNRGs) in lung adenocarcinoma (LUAD). Therefore, this study investigated the regulatory mechanisms of MPTDNRGs in LUAD. - Source: PubMed
Publication date: 2025/08/13
Sun XiaoliCai BowenZhang ShusenCao XiaoweiWang ZhenCai Zhigang - Chronic obstructive pulmonary disease (COPD) is a leading challenge of global public health that predominantly affects developing countries. Although smoking is the main risk factor, only a fraction of smokers develop COPD. This study aimed to identify biomarkers or therapeutic targets that would effectively aid early diagnosis and treatment of smoking-induced COPD. - Source: PubMed
Publication date: 2025/08/01
Mokaram Doust Delkhah ArmanGhazvini AliArabfard Masoud