Ask about this productRelated genes to: PTPN4 antibody
- Gene:
- PTPN4 NIH gene
- Name:
- protein tyrosine phosphatase non-receptor type 4
- Previous symbol:
- -
- Synonyms:
- PTPMEG
- Chromosome:
- 2q14.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-12
- Date modifiied:
- 2019-02-14
Related products to: PTPN4 antibody
Related articles to: PTPN4 antibody
- Osteoarthritis (OA) is a degenerative joint disease with high global prevalence, and YKL-40 is an important factor related to the pathological process of OA. Increased levels of YKL-40 exert a protective influence against TNF-α-induced apoptosis in chondrocytes, thereby enhancing chondrocyte survival and activation, while counteracting TNF-α-driven expression of specific inflammatory mediators such as S100A8/A9.This study aims to evaluate the role and molecular mechanism of YKL-40 on chondrocytes in OA and provide a potential therapeutic avenue requiring further validation. A meta-analysis compared serum YKL-40 and TNF-α levels between OA patients and healthy controls. In vitro experiments examined the effects of YKL-40 on TNF-α-induced OA chondrocytes, assessing proliferation, differentiation, apoptosis, and inflammatory pathways. Meta-analysis revealed significantly elevated serum levels of YKL-40 and TNF-α in osteoarthritis (OA) patients compared to healthy controls. In vitro, TNF-α (10 ng/mL) induced extracellular matrix (ECM) degradation in chondrocytes, significantly reducing glycosaminoglycan (GAG) and type II collagen content. This degradation was effectively rescued by YKL-40 (100 ng/mL). RNA sequencing identified differentially expressed genes in TNF-α-treated chondrocytes, enriched in pathways like IL-17 and NF-κB signaling. YKL-40 treatment reversed the expression of key genes altered by TNF-α. Crucially, these differentially expressed genes (including S100A8/A9, ISG15, CDSN, BAAT, PTPN4, NPTX1, SMARCA1) were validated in independent OA cartilage and synovium GEO datasets. Protein-protein interaction (PPI) networks highlighted central genes within treatment groups. Western blotting confirmed YKL-40 counteracted TNF-α-induced NF-κB pathway activation (reduced p65 and IκBα phosphorylation) and modulated key targets (S100A8/A9, ASB7, ZFPM2), consistent with qRT-PCR data. YKL-40 is a promising biomarker and therapeutic target for OA. Its interplay with TNF-α provides a molecular basis for novel therapies targeting chondrocyte dysfunction, guiding future translational research. - Source: PubMed
Publication date: 2026/04/27
Li ZhuozhengSun XueXie YongfangHong ZexinDou ZeminYan ShichaoZhang YulongQin HeLiu DanFeng TingtingWang Guohui - Protein tyrosine phosphatase, non-receptor type 4 (PTPN4) is a gene involved in glutamate downstream signaling contributing to cerebral maturation. Loss-of-function of this gene has been reported in patients showing various neurodevelopmental disorders, although the PTPN4 gene is not clearly considered a disease-causing gene in the Online Mendelian Inheritance in Man catalogue. - Source: PubMed
Publication date: 2026/03/03
Tasu CorentinOppetit AliceGalbert ChantalOuaki SéverineZammouri IngridGazzano OdileMourao JorgeMignot CyrilCohen DavidBenarous Xavier - Circular RNAs (circRNAs) are crucial regulators of gene expression, exhibiting dynamic expression patterns during both normal brain development and diverse pathological states. This study reports the elevated expression of CircPTPN4 in the brain tissue and plasma during early epileptogenesis in a murine temporal lobe epilepsy model. Overexpression of CircPTPN4 disrupts the tight junctions of brain microvascular endothelial cells (BMECs), compromising blood-brain barrier (BBB) integrity. Mechanistically, CircPTPN4 functions as a competitive endogenous RNA by sequestering miR-145a-5p, thereby upregulating endothelin-converting enzyme-1 (ECE-1). Subsequent ECE-1-mediated endothelin-1 (ET-1) production activates the p38/MAPK pathway, downregulating tight junction protein expression. Knockdown of CircPTPN4 attenuated tight junction disruption and BBB impairment during acute epileptogenesis while reducing spontaneous seizure frequency in chronic epilepsy. These findings establish the CircPTPN4/miR-145a-5p/ECE-1 axis as both a diagnostic biomarker and therapeutic target for BBB preservation in early-stage epilepsy. - Source: PubMed
Publication date: 2025/12/14
Yang JiurongHu YangWang FeiyuPeng XintaoQi HonggangYao YuanyuanZhang CanyuZhou LijieLiang XuemeiXu KangZhang CongZhang AifengChen ChenZeng YuZhang ChenchenGan GuangmingZhu Xinjian - During animal growth and development, the reproductive system is tightly controlled by the central nervous system through a highly conserved, self-feedback loop-the hypothalamic-pituitary-gonadal (HPG) axis. Gonadotropin-releasing hormone (GnRH), which is produced in the hypothalamus and secreted into the hypophyseal portal circulation, serves as a master regulator of pituitary follicle-stimulating hormone (FSH) and luteinizing hormone (LH) synthesis and secretion, thereby orchestrating growth and reproductive functions. We identified circ-ptpn4 as a GnRH-responsive circular RNA (circRNA) that sequesters let-7b-5p, thereby attenuating its suppression of ELK1. This decrease in let-7b-5p availability thus allows enhanced ELK1 expression, which ultimately stimulates FSH production. In summary, we revealed a novel competing endogenous RNA (ceRNA)-dependent pathway (circ-ptpn4/let-7b-5p/ELK1) underlying GnRH-induced FSH regulation. - Source: PubMed
Publication date: 2025/10/26
Zhang Yu-XinQiu Ling-LingZhang ZheGuo Hai-XiangZheng YiWang Bing-BingChen Cheng-ZhenJiang HaoZhang Jia-BaoGao FeiYuan Bao - This systematic review investigates the role of noncoding RNAs (ncRNAs), including miRNAs, long noncoding RNAs (lncRNAs), circular RNAs (circRNAs), and transfer RNAs, in regulating mitochondrial biogenesis, dynamics, oxidative phosphorylation, and mitophagy in skeletal muscle and the potential applications of these ncRNAs in exercise molecular physiology. We conducted a comprehensive search in PubMed, Scopus, and Web of Science databases, identifying 45 relevant studies out of 2,378 records. The main findings indicate that miRNAs such as miR-128, miR-133a, miR-696, and miR-499 are critical regulators of mitochondrial function. Moreover, lncRNAs (lncEDCH1 and lncRNA-H19) and circRNA (circ-PTPN4) significantly influence mitochondrial biogenesis and function. Exercise interventions were shown to modulate the expression of these ncRNAs, particularly miR-133a and miR-696, leading to enhanced mitochondrial biogenesis and function. The review highlights the potential of these ncRNAs as biomarkers and therapeutic targets for improving mitochondrial function and treating metabolic and mitochondrial disorders. Further research is needed to explore the muscle-specific and exercise-modality-specific effects of ncRNAs to develop personalized interventions. Understanding the complex regulatory mechanisms of ncRNAs in mitochondrial adaptations can pave the way for innovative therapeutic strategies in exercise molecular physiology and metabolic health. - Source: PubMed
Publication date: 2025/11/25
Chavez-Guevara Isaac AVázquez-Lorente HéctorHerrera-Quintana LourdesRubio-Valles MariazelLópez Luis CPlaza-Díaz JulioAmaro-Gahete Francisco J