CYR61 ELISA
- Known as:
- CYR61 Enzyme-linked immunosorbent assay test
- Catalog number:
- ELI-6973
- Product Quantity:
- 96 Wells
- Category:
- -
- Supplier:
- Nal Von Minden
- Gene target:
- CYR61 ELISA
Ask about this productRelated genes to: CYR61 ELISA
- Gene:
- CCN1 NIH gene
- Name:
- cellular communication network factor 1
- Previous symbol:
- IGFBP10, CYR61
- Synonyms:
- GIG1
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-02
- Date modifiied:
- 2018-10-11
Related products to: CYR61 ELISA
Related articles to: CYR61 ELISA
- The transcriptional co-activators YAP and TAZ are key regulators of cell proliferation, apoptosis, and differentiation, thereby maintaining tissue homeostasis and controlling organ size. While their roles in epithelial cancers and fibrosis are well established, their involvement in the physiological regulation of the dermal extracellular matrix (ECM) by fibroblasts is less understood. Here, we investigated the role of Yap/Taz during postnatal development of the dermal ECM. During postnatal growth, mouse skin steadily undergoes significant surface expansion. Postnatal deletion of Yap/Taz in dermal fibroblasts, the primary cells responsible for dermal ECM homeostasis, significantly impaired dermal ECM maturation, as evidenced by marked deficiencies in collagen expression, deposition, and organization. Isolated fibroblasts from Yap/Taz knockout mice showed reduced expression of Yap/Taz target genes (Ccn1, Ccn2, Col1a1), which were rescued by reintroduction of active Yap/Taz. RNA-seq, spatial transcriptomics, and proteomics of Yap/Taz knockout skin revealed substantial downregulation of ECM-related genes, including type I (Col1a1, Col1a2) and type III (Col1a3) collagens, which together constitute more than 90% of the skin's collagen content. Mechanistically, deletion of Yap/Taz impaired mouse dermal maturation, at least in part through suppression of TGF-β/Smad signaling, the primary pathway governing fibroblast collagen synthesis. These findings demonstrate that YAP/TAZ are essential for postnatal dermal ECM homeostasis. - Source: PubMed
Publication date: 2026/06/18
Ermilov Alexandre NKim Ava JHansen Kirk CMcCabe MaxwellKim Jun YoungQin ZhaopingZhang ZhaolinHe TianyuanGuo ChunfangVoorhees John JFisher Gary JQuan Taihao - CCN1, also called Cyr61, is a secreted protein involved in diverse biological processes including senescence. While elevated in brains of Alzheimer's disease (AD) models and patients, CCN1/Cyr61 levels in cerebrospinal fluid (CSF) remain unclear. Using a high-sensitive quantification method, we analyzed CSF samples from 79 subjects (age: 77.7 ± 5.4 years [63-94], MMSE: 20.1 ± 5.9 [0-30]) who underwent CSF tap test. CCN1/Cyr61 showed strong associations with Aβ40 (r = 0.67), Aβ42 (r = 0.48), Aβ42/40 ratio (r = -0.53), and phospho-tau levels (r = 0.53) (all; < 0.0001). CCN1/Cyr61 also moderately associated with glial markers, YKL-40, sTREM2, CD163, and a lymphatic endothelial marker, LYVE-1 (r ≈ 0.4). While these cellular markers also associated with Aβ and phospho-tau, effects were much weaker. Collectively, CCN1/Cyr61 is associated with Aβ species and p-tau in CSF. These associations are considerably stronger than those observed with typical glial or other cellular markers, providing a clue to understanding the link between senescence and AD pathology at the levels of fluid biomarkers. - Source: PubMed
Publication date: 2026/06/05
Shinohara MitsuruMomota HiroyukiSaito TsuyoshiTakenobu ChisakoKasuga KensakuGheni GhupurjanKawai KaoriMorishima MahoSaito YukoShindo AkihiroYasuno FumihikoIkeuchi TakeshiFukumori AkioSato Naoyuki - Cellular communication network (CCN) proteins are key matricellular regulators of cartilage development, yet their species-specific roles and network-level context remain unclear. This study integrated bulk RNA sequencing from chicken and mouse embryonic limb bud micromass cultures and human mesenchymal stem cell chondrogenesis with co-expression, protein-protein interaction, and ortholog analyses to construct CCN-centered regulatory networks across models. CCN1 and CCN2 emerged as dominant, conserved hubs enriched in collagen-containing extracellular matrix, cartilage development, and growth factor signaling modules, whereas CCN3-CCN6 showed lower context-dependent expression and connectivity. Functional and ortholog analyses revealed moderate pathway conservation, with high conservation of IGF, EGFR, and HIF-1 signaling, but reduced overlap in hypoxia and mechanosensing/Hippo categories, indicating species-specific tuning of environmental sensing. A focused ortholog screen identified multifunctional conserved hubs, including , , , , , , , and . Single-cell RNA-seq meta-analysis of human iPSC-derived chondrogenesis and embryonic limb datasets showed CCN1/2 expression and homologous network activity peaking in mesenchymal and early chondrocyte populations, consistent with model-dependent persistence into hypertrophic and ossification stages in vivo. Overall, this work defines a conserved CCN1/2-centered axis integrating extracellular matrix formation with growth factor and mechanical cues, providing a framework for model selection and CCN-targeted cartilage regeneration strategies. - Source: PubMed
Publication date: 2026/06/02
Wang ZhangzhengVágó JuditTakács RolandPóliska SzilárdKim Ee HyunJin Eun-JungKubota SatoshiKleer Celina GPerbal BernardMatta Csaba - This study investigated the impact of a high-carbohydrate diet (HC: 25% carbohydrate) on skin wound healing in turbot vs. a control diet (CC: 16% carbohydrate). Following 10 weeks of triple replicates of fish (n=40), standardized 8 mm skin wounds were created and healing assessed macroscopically and molecularly at baseline, 1, 3, and 7 days post-wounding (dpw). While growth performance remained unaffected, HC-fed fish exhibited persistent hyperglycemia and hyperinsulinemia, indicative of systemic insulin resistance. Macroscopic analysis showed significantly impaired wound contraction in the HC group at 3 and 7 dpw compared to CC controls. Histological assessment revealed defective re-epithelialization characterized by aberrant keratinocyte migration, suppressed provisional matrix formation, ill-defined epidermal stratification, and persistent goblet cell aggregation in HC fish. Molecular analyses demonstrated HC-mediated suppression of re-epithelialization markers (suppressed MMP9, EGF, FGF2, and KRT2 gene expression; reduced MMP9 protein distribution), dysregulated inflammation (reduced myeloperoxidase and NAG activity; lower IL1B, IL6, IL8, TGFB1, and TNF expression; elevated IL10 expression), and impaired tissue formation and remodeling (downregulated FN1, VEGF, CCN1, LAMB2, and COL1A mRNA; reduced collagen deposition; attenuated CD31-based angiogenesis). Importantly, HC feeding promoted skin advanced glycation end-products (AGEs) accumulation, which was accompanied by reduced mechanistic target of rapamycin kinase (MTOR) phosphorylation, decreased hypoxia inducible factor 1 subunit alpha (HIF1A) protein levels, and blunted post-wounding induction of glycolytic genes, including PFK, HK2, and PK. Collectively, these findings indicate that HC feeding compromises multiple phases of skin wound healing in turbot and suggest that AGE-associated suppression of MTOR-HIF1A-mediated glycolytic adaptation is an important metabolic mechanism associated with delayed healing. - Source: PubMed
Publication date: 2026/06/04
Chen ZhichuLi YuantingFang YuanyuanHuang DongÁngeles Esteban MariaChen XinhuaZhang Yanjiao - One of the hallmarks of skin aging is the accumulation of senescent cells, which drives the process of inflammaging. The senescence-associated secretory phenotype (SASP), which characterizes senescent cells, can induce dysfunction in both neighboring skin cells and cells of distant organs. In this study, distant negative effects of senescent dermal fibroblasts on target cells (B-lymphocytes, hepatocytes, and alveolar epithelial cells) were demonstrated. The expression of Klotho, Parkin, SIRT6, VDR, Ki-67, CCN1, p16, and p65 proteins was assessed. The effects of an extract from a plant native to Russia, Hippophae rhamnoides (Sea buckthorn, S), extracts from plants of the African ecosystem Aspalathus linearis (Rooibos, R), Moringa oleifera (Moringa, M), Kigelia Africana (Kigelia, Kg), and an injectable hyaluronic acid gel (HA-gel) on the formation of the senescent phenotype in dermal fibroblasts were evaluated. The studied extracts and HA-gel protected cells from the negative processes induced by genotoxic stress. Moreover, extracts R, S, and HA-gel suppressed the adverse distant effects of damaged fibroblasts, normalizing marker expression in recipient cells, suggesting an influence on signaling pathways involved in the senescent transformation of distant cells. These results suggest considering cosmetic products based on the studied extracts and the injectable preparation as potential agents capable of delaying the aging of not only the skin but also the whole organism, which may be a component of the healthy aging concept. - Source: PubMed
Prokopov A YDrobintseva A OLiubiakina P NKvetnoy I M