rHu CTGF
- Known as:
- rHu CTGF
- Catalog number:
- AK8240-1000
- Product Quantity:
- 1mg
- Category:
- -
- Supplier:
- Akro
- Gene target:
- rHu CTGF
Related genes to: rHu CTGF
- Gene:
- CCN2 NIH gene
- Name:
- cellular communication network factor 2
- Previous symbol:
- CTGF
- Synonyms:
- IGFBP8
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-12-01
- Date modifiied:
- 2018-10-11
- Gene:
- CCN5 NIH gene
- Name:
- cellular communication network factor 5
- Previous symbol:
- WISP2
- Synonyms:
- CT58, CTGF-L, WISP-2
- Chromosome:
- 20q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-22
- Date modifiied:
- 2018-10-17
Related products to: rHu CTGF
Related articles to: rHu CTGF
- Liver fibrosis is a pathological process characterized by the activation of hepatic stellate cells (HSCs) and the excessive accumulation of extracellular matrix (ECM) proteins. Cellular communication network 5 (CCN5) has been recently recognized for its ability to counteract the profibrotic effects of CCN2 in fibrotic diseases. Herein, we report the discovery of a CCN5-derived peptide CDP199 that effectively suppresses HSC activation and reduces ECM protein deposition. Notably, CDP199 exhibits strong inhibitory effects on HSC proliferation and migration. The subsequent study demonstrated that peptide CDP199 significantly alleviates liver injury, enhances liver function, and mitigates liver fibrosis in a carbon tetrachloride-induced mouse model. Mechanistically, CDP199 inhibits the phosphorylation of ERK1/2 and PI3K both and . These findings highlight the therapeutic potential of CCN5-derived peptides, specifically CDP199, as a promising antifibrotic candidate for treating liver diseases through inhibition of ERK1/2 and PI3K signaling pathways. - Source: PubMed
Publication date: 2025/04/01
Fang RunminQiu ChuangnanXiao CanJiang XianxingZhou YifengDong Jiale - Smooth muscle cells (SMCs) of the proximal thoracic aorta are derived from second heart field (SHF) and cardiac neural crest (CNC) lineages. Recent studies, both in vitro and in vivo, have implied relevance of lineage-specific SMC functions in the pathophysiology of thoracic aortic diseases; however, whether 2 lineage-derived SMCs have any predisposed transcriptional differences in the control aorta remains unexplored. - Source: PubMed
Publication date: 2025/01/02
Shukla ShalabhJana SayantanSanford NicoleLee Chloe YLiu LiCheng PaulQuertermous ThomasDichek David A - The 12th international workshop on the CCN family of genes took place at the Scandic Holmenkollen Park Hotel in Oslo, Norway from June 20-23, 2024. In 2024, it was the second time, following the Nice meeting in 2022, that the scientific topics were expanded to include additional cellular signaling and communication pathways of interest to the CCN Society members, as suggested by Bernard Perbal in 2019. The 12th international CCN workshop, organized by Håvard Attramadal and Vivi T. Monsen, along with co-organizers Bernard and Annick Perbal, was given the subtitle "Cell-matrix Communication and Functions in Health and Disease" to encompass the broader scope of this meeting. The five scientific sessions covered various topics: Extracellular Matrix Proteins in Cell Communication and Signaling (Chaired by Brahim Chaqour and Vivi T. Monsen), Vascular Development and Pathophysiology (Chaired by Lester F. Lau and Håvard Attramadal), Mechanisms of Diseases (Chaired by George Bou-Gharios and Satoshi Kubota), Tissue Development and Homeostasis (Chaired by Blandine Poulet and Bernard Perbal), and Mechanisms of Disease: Cancer and the Matrix (Chaired by Stephen M. Twigg and Raymond B. Birge). The 2024 ICCNS Award was presented to Katia Scotlandi during the last session (Chaired by Bernard Perbal) before Håvard Attramadal presented the conclusion of the workshop. - Source: PubMed
Publication date: 2024/08/13
Attramadal HåvardWeiskirchen RalfPerbal Bernard - Age-related macular degeneration (AMD) is one of the major causes of blindness in the elderly worldwide. Anti-vascular endothelial growth factor (VEGF) drugs have been widely used to treat the neovascular type of AMD (nAMD). However, VEGF acts not only as a pro-angiogenic factor but also as an anti-apoptotic factor in the eyes. In this study, we found that anti-VEGF drugs, including bevacizumab (Bev), ranibizumab (Ran), and aflibercept (Afl), induced epithelial-mesenchymal transition (EMT) in ARPE-19 cells in vitro, accompanied by the induction of CCN2, a potent pro-fibrotic factor. Similarly, intravitreal injection of Afl into mouse eyes resulted in EMT in the retinal pigmented epithelium (RPE). Co-treatment with CCN5, an anti-fibrotic factor that down-regulates CCN2 expression, significantly attenuated the adverse effects of the anti-VEGF drugs both in vitro and in vivo. Inhibition of the VEGF signaling pathway with antagonists of VEGF receptors, SU5416 and ZM323881, induced EMT and up-regulated CCN2 in ARPE-19 cells. Additionally, knock-down of CCN2 with siRNA abolished the adverse effects of the anti-VEGF drugs in ARPE-19 cells. Collectively, these results suggest that anti-VEGF drugs induce EMT in RPE through the induction of CCN2 and that co-treatment with CCN5 attenuates the adverse effects of anti-VEGF drugs in mouse eyes. - Source: PubMed
Publication date: 2024/06/17
Im SoraSong Min HoElangovan MuthukumarWoo Kee MinPark Woo Jin - CCN/WISP (cellular communication network factors, or Wnt-inducted secreted proteins) family of proteins consists of six extracellular matrix (ECM)-associated proteins that regulate development, cell adhesion and proliferation, ECM remodeling, inflammation, and tumorigenesis. In the last two decades, metabolic regulation by these matricellular proteins has been studied extensively, several excellent reviews have covered the roles of CCN1, -2 and - 5. In this brief review, we will focus on those lesser-known members and more recent discoveries, together with other recent articles presenting a more complete picture of the current state of knowledge. We have found that CCN2, -4, and - 5 promote pancreatic islet function, while CCN3 plays a unique and negative role. CCN3 and - 4 are pro-adiposity leading to insulin resistance, but CCN5 and - 6 are anti-adiposity. While CCN2 and - 4 promote tissue fibrosis and inflammation, all other four members are clearly anti-fibrotic. As for cellular signaling, they are known to interact with integrins, other cell membrane proteins and ECM thereby regulate Akt/protein kinase B, myocardin-related transcription factor (MRTF), and focal adhesion kinase. Yet, a cohesive mechanism of action to comprehensively explain those major functions is still lacking. - Source: PubMed
Publication date: 2023/05/28
Xega ViktoriaAlami TaraLiu Jun-Li