Ask about this productRelated genes to: WISP1 antibody
- Gene:
- CCN4 NIH gene
- Name:
- cellular communication network factor 4
- Previous symbol:
- WISP1-OT1, WISP1-UT1, WISP1
- Synonyms:
- WISP-1
- Chromosome:
- 8q24.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-22
- Date modifiied:
- 2018-10-11
Related products to: WISP1 antibody
Related articles to: WISP1 antibody
- Increased global lifespan is paralleled by a rise in non-communicable diseases with osteoarthritis and dementia, including Alzheimer's disease, impacting all nations with severe disability, death, and financial burden. - Source: PubMed
Publication date: 2026/05/11
Maiese Kenneth - Wooden Breast is a myopathy affecting broiler chickens, characterized by hardening of the pectoral muscle, fibrosis, adipogenesis, and deteriorated meat quality. This study investigated the pathological mechanisms underlying wooden breast development, focusing on the interplay between fibrogenesis and myogenesis. Seventy-eight broiler chickens were categorized into normal, mild, and severe wooden breast groups based on the extent of fibrosis and adipogenesis in the pectoral muscle. Histological analysis revealed immature collagen fibers within muscle fascicles in severe wooden breast, indicating concurrent fibrogenesis and muscle regeneration. Immunofluorescence staining confirmed the close spatial localization of fibro-adipogenic progenitors (FAPs) and myosatellite cells in these areas, suggesting potential interaction during wooden breast pathogenesis. RNA sequencing and qPCR revealed upregulation of and , markers of myogenesis, in the affected pectoral muscle, whereas expression remained unchanged. This pattern indicates an attempt at myogenic differentiation that is ultimately disrupted in severe wooden breast samples. Furthermore, cellular communication network (CCN) family members, particularly and , were upregulated in the wooden breast-affected pectoral muscle. expression strongly correlated with the fibro-adipogenic progenitor marker , implying that fibro-adipogenic progenitors-mediated secretion contributes to wooden breast pathogenesis. Our findings suggest that fibro-adipogenic progenitors and cellular communication network family members are associated with an imbalance between fibrogenesis and myogenesis, leading to the muscle degeneration observed in wooden breast. - Source: PubMed
Publication date: 2026/04/21
Kobayashi RyosukeHosotani MarinaSaito KarinMasuda YukitakaKawasaki TakeshiTakahashi NaokiHasegawa YasuhiroIwasaki TomohitoWatanabe Takafumi - Primary renal small cell carcinoma (PRSCC) is a rare, poorly differentiated neuroendocrine carcinoma, and its clinicopathological features and the gene mutation spectrum associated with its pathogenesis remain to be elucidated. The present study aimed to characterize the genetic mutation spectrum associated with the pathogenesis of PRSCC, identify novel driver and predisposing genes for the disease, reveal its histopathological features associated with genetic mutations and systematically summarize the clinicopathologic characteristics and prognostic factors of PRSCC patients to provide a theoretical basis for molecularly targeted therapy and prognostic assessment of PRSCC. Whole-exome sequencing (WES) was performed on PRSCC samples to characterize the spectrum of genetic mutations and the results were validated using Sanger sequencing. Immunohistochemistry (IHC) was performed to reveal the histopathological features associated with these mutations. Furthermore, based on the published literature, a population-based study was conducted by searching PubMed and EMBASE databases to systematically summarize the clinicopathologic characteristics and prognostic factors of patients with PRSCC. WES identified 113 somatic single-nucleotide variants, 26 somatic insertions and deletions and mutations in 8 predisposing genes (DST, OR10H3, PTK2B, APOBR, ZNF606, CCN4, ADCK1, and MYH2) and 10 driver genes (KRTAP10-9, HYDIN, ZNF665, KRTAP10-2, GPAM, MUC12, KRT9, CCDC168, DUSP27 and MDC1). Sanger sequencing of germline DNA identified a germline A/G variant in the HYDIN sequence, first reported in PRSCC. Furthermore, IHC analysis indicated that PRSCC was positive for CD56, Syn, insulinoma associated protein 1, CgA and neuron specific enolase. In the population-based study, the majority of patients with PRSCC were elderly (57.92±15.75 years), with a pathological tumor (T) 3/4 stage (68.3%) and presented with lymph node involvement (51.7%) and distant metastasis (51.7%). T stage was an independent prognostic factor for overall survival in patients with PRSCC (P=0.004). Driver mutations in the HYDIN gene may be a key factor in the pathogenesis of PRSCC. HYDIN may serve as a prognostic marker and a target for immunotherapy in the management of PRSCC. However, due to the extreme rarity of PRSCC, the WES analysis in the present study was based solely on individual cases. To ensure the reliability and generalizability of genetic alterations detected by WES, additional PRSCC samples, along with cell and animal experiments, are warranted to confirm the role of these genetic variants (particularly HYDIN) in PRSCC pathogenesis. The functional role of HYDIN mutations in PRSCC pathogenesis requires further validation in future research. - Source: PubMed
Publication date: 2026/03/30
Wang YangZhang LizhiXia XueyanLi Xiancheng - Rheumatoid arthritis (RA) and osteoarthritis (OA) are prevalent chronic joint diseases characterized by persistent inflammation, progressive cartilage degeneration, and impaired tissue repair mechanisms. While inflammatory pathways have been extensively studied, increasing attention has been directed toward the failure of inflammation resolution as a key contributor to chronic joint pathology. Specialized pro-resolving mediators (SPMs), including Maresin-1 (MaR1), play an active role in terminating inflammation and promoting tissue homeostasis. However, the relationship between MaR1 and cartilage-specific biomarkers such as Cartilage Oligomeric Matrix Protein (COMP) and Wnt1-inducible signaling pathway protein-1 (WISP-1) has not been sufficiently elucidated. This study investigated circulating MaR1 levels in RA and OA and examined their associations with serum COMP and WISP-1 as well as clinical inflammatory parameters. This cross-sectional, biomarker-based study included a total of 150 participants, comprising 50 patients with RA, 50 patients with OA, and 50 sex-matched healthy controls. Serum levels of MaR1, COMP, and WISP-1 were measured using enzyme-linked immunosorbent assay (ELISA). Demographic characteristics and inflammatory parameters, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and rheumatoid factor (RF), were recorded. Intergroup comparisons were performed using one-way analysis of variance (ANOVA) followed by appropriate post-hoc tests. Serum MaR1 levels were significantly reduced in both RA (44.1 ± 2.2 ng/L) and OA (42.2 ± 3.2 ng/L) compared with controls (78.5 ± 7.5 ng/L; p < 0.001). COMP levels were significantly lower in the RA group than in the OA and control groups (p < 0.05 and p < 0.001, respectively). Similarly, WISP-1 concentrations were decreased in both RA and OA compared with healthy controls (p < 0.05). The marked reduction in MaR1 levels in RA and OA is consistent with altered inflammation-resolution biology. Concurrent decreases in COMP and WISP-1 may reflect changes in cartilage remodeling dynamics. Overall, MaR1 appears to be a candidate biomarker associated with inflammation-resolution pathways in arthritic diseases. - Source: PubMed
Publication date: 2026/03/18
Esmez OmerDeniz GulnihalErcan ZubeydeYılmaz SecilDogru Meryem SedefKaratas Ahmet - Glioblastoma (GB) is a highly complex ecosystem characterized by numerous interactions between tumor cells and the surrounding tumor microenvironment (TME). Splicing factors play a pivotal role in processing nascent pre-mRNA and are important in the progression of cancer, making them promising molecular targets. In this study, we demonstrate that the DEAD-box helicase 39 A (DDX39A), a RNA helicase with several important roles in RNA metabolism and cellular processes, is significantly upregulated in GB and is primarily expressed in tumor cells, leading to an immunosuppressive macrophage polarization. Through in vitro and in vivo studies, we demonstrate that reducing DDX39A expression in GB results in reduced tumor growth and invasion. Mechanistically, through RNA-seq and RIP-seq, we identified WISP1 as a critical downstream effector of DDX39A. DDX39A stabilizes WISP1 pre-mRNA through alternative splicing regulation, thereby activating the AKT signaling pathway. We further demonstrate that WISP1, when secreted by tumor cells, functions as a paracrine signaling molecule that promotes the development of immunosuppressive tumor-associated macrophages (TAMs). Additionally, we demonstrate that Fluphenazine hydrochloride binds to and inhibits DDX39A, thereby suppressing GB growth, invasion, and the immunosuppressive function of macrophages. DDX39A thus represents a potential candidate for glioma-targeted therapy. - Source: PubMed
Publication date: 2026/03/02
Zhang YanXue ZhiweiZhang NaibinZhu YuehuaWu YanZhaoLv MeilinZhang ZhihanMu FeiyuXing WenchenTang ZiyiWang ChunjieXue ZhiyiZhou WenjingLiu XiaofeiLi XingangBjerkvig RolfHuang BinHan MingzhiWang JianWang Donghai