Mouse polyclonal to CTHRC1, Host Mouse
- Known as:
- Mouse pab CTHRC1, Host Mouse
- Catalog number:
- YF-PA26829
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abfron
- Gene target:
- Mouse polyclonal CTHRC1 Host
Related genes to: Mouse polyclonal to CTHRC1, Host Mouse
- Gene:
- CTHRC1 NIH gene
- Name:
- collagen triple helix repeat containing 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-07-22
- Date modifiied:
- 2008-08-07
Related products to: Mouse polyclonal to CTHRC1, Host Mouse
Related articles to: Mouse polyclonal to CTHRC1, Host Mouse
- Collagen triple helix repeat containing 1 (CTHRC1) is a secreted extracellular matrix (ECM)-associated protein involved in tissue remodeling, fibrosis, and cancer, but its functions in the nervous system remain incompletely defined. Evidence from peripheral nerve, brain tumor, neurodegeneration, and regeneration models suggests that CTHRC1 may exert context-dependent effects across neural and stromal cell populations. In Schwann cells, CTHRC1 regulates proliferation, migration, and the timing of myelination, whereas in glioma it promotes invasive behavior and treatment-resistant phenotypes. Human cortical proteomics, mouse-model studies, systems genetics, and a neuronal cell model associate CTHRC1 with Alzheimer's disease-related phenotypes, although bulk tissue does not identify the cellular source and a small cerebrospinal fluid cohort showed no significant change. Temporally resolved single-cell analysis in zebrafish identified a transient cthrc1a-expressing fibroblast state required for coordinated inflammatory dynamics during regeneration; an equivalent mammalian mechanism has not been established. Evidence connecting CTHRC1 to synaptic regulation, neuroprotection, Parkinson's disease, and cerebrovascular repair is still preliminary. Wnt, TGF-β/Smad, PI3K/AKT, and MAPK/ERK pathways provide candidate mechanisms, but many were characterized outside normal neural cells. This review critically evaluates the evidence by model and cell type and discusses biomarker and therapeutic prospects, including delivery, specificity, and safety constraints. - Source: PubMed
Publication date: 2026/10/03
Lei YingyingLuo YuxiLi Ling - Cancer-associated fibroblasts (CAFs) promote tumorigenesis and represent potential therapeutic targets, highlighting the need for precise understanding of CAF heterogeneity. In colorectal cancer (CRC), CAF subsets and nomenclature vary widely, and many studies overlook the diversity of normal colon fibroblasts that shapes tumor mesenchyme. Here, we combine large-scale single-cell RNA-sequencing analysis with spatial validation and functional assays to construct a comprehensive reference map of human normal colon fibroblasts and mesenchymal subsets, guided by the well-characterized mouse colon. We define three major fibroblast populations, subepithelial myofibroblasts (SEMFs), mucosa-associated fibroblasts (MAFs), and submucosa-associated fibroblasts (SAFs), and characterize a previously underexplored muscle-embedded interstitial fibroblast (MIF) population. This reference enabled mapping of CRC-specific changes, revealing four cancer-specific CAF subsets, including inflammatory CAFs (iCAFs), matrix CAFs (mCAFs), and two precursor populations (pre-CAFs). We also identify robust CRC CAF markers including CTHRC1, infer transcriptional regulators, and define distinct developmental trajectories driving iCAF and mCAF activation. Together, our study provides a spatially and transcriptionally resolved reference map of fibroblasts in the normal colon and CRC, enabling mechanistic studies and informing CAF-targeted therapies. - Source: PubMed
Publication date: 2026/09/23
Viitala Emma WSalminen EllaMiihkinen MitroLemmetyinen Toni TSévigny MyriamPorvari Kiisla KMalpani TanishaChalkidi NikiStavropoulou AthanasiaPäivinen Pekka JKaprio TuomasHagström JaanaHaglund CajMäkelä Tomi PKatajisto PekkaAittokallio TeroKoliaraki VasilikiOllila Saara - This study aimed to characterize plasma protein and bile acid remodeling after liver transplantation (LT) in children with biliary atresia (BA). Paired plasma samples were collected from seven BA patients before and after LT following unsuccessful Kasai portoenterostomy, and profiled using label-free quantitative proteomics and targeted metabolomics of 15 bile acids. A total of 113 proteins were significantly altered after LT, enriched in pathways governing inflammation, coagulopathy, and extracellular matrix reorganization; eight proteins were selected as signature biomarkers, including upregulated hepatocyte growth factor activator (HGFAC), insulin-like growth factor-binding protein 5 (IGFBP5), insulin-like growth factor-binding protein acid-labile subunit (IGFALS), and coagulation factor XI (F11), together with downregulated phosphatidylinositol-binding clathrin assembly protein (PICALM), S100 calcium-binding protein A11 (S100A11), polymeric immunoglobulin receptor (PIGR), and collagen triple helix repeat-containing protein 1 (CTHRC1). Four conjugated primary bile acids, glycocholic acid (GCA), taurocholic acid (TCA), glycochenodeoxycholic acid (GCDCA), and taurochenodeoxycholic acid (TCDCA), showed precipitous postoperative declines and correlated strongly with clinical liver-injury markers. Two proteins, HGFAC and PIGR, together with these four conjugated bile acids demonstrated high diagnostic accuracy (area under the curve, AUC = 0.86-1.00), supporting their potential as non-invasive biomarkers for monitoring graft function after LT. - Source: PubMed
Publication date: 2026/09/23
Jin YutingCai ZihanZhang BijunWang TingtingDong LelePan LiangxuanDu XiaoyaoGao FeiZhou YuyangFeng Jianhua - Bone metastasis is a leading cause of mortality in advanced prostate cancer (PCa), with limited therapeutic options. This study investigates the molecular mechanisms underlying PCa bone metastasis and identifies potential therapeutic targets. Using in vitro co-culture systems and in vivo mouse models, we demonstrated that tumor-derived Collagen Triple Helix Repeat Containing 1 (CTHRC1) promotes osteoclast differentiation, thereby contributing to the development of osteolytic lesions in PCa bone metastasis. Mechanistically, CTHRC1 cooperates with receptor activator of nuclear factor-κB ligand (RANKL) signaling to promote osteoblast-derived RANKL-mediated osteoclastogenesis by disrupting the RANKL/osteoprotegerin (OPG) system. Furthermore, CTHRC1 directly binds to integrin beta 3 (ITGB3) on osteoclasts to activate the FAK/MEK/ERK1/2 pathway and dissociate SRC signaling, jointly mediating osteoclast differentiation. Blocking the CTHRC1-ITGB3 axis significantly weakened CTHRC1-induced osteoclast differentiation and bone resorption. Collectively, our findings identify CTHRC1 as a novel mediator in the bone microenvironment, providing a potential therapeutic target for inhibiting the occurrence and progression of PCa bone metastasis. - Source: PubMed
Publication date: 2026/09/11
Xie TaoPeng TianmingLi QuLi MingzhaoCai MaopingLi QianyiYu Yu-ZhongZhong JiehuiWang ChongChen Ming-KunChen Zhe-ShengSong Xian-LuGu DiZhao Shan-Chao - Fibrosis, marked by excess extracellular matrix (ECM) deposition, is the end stage of many diseases. Single-cell studies have highlighted the emergence of disease-specific fibroblast populations, including a high collagen-synthesizing subpopulation. The profibrotic cytokine TGF-β1 promotes fibrogenesis via cooperation between Smad and mTORC1/4E-BP1 signaling axes. Using CRISPR-Cas9 gene editing, we report that more than one-third of TGF-β1-regulated matrisome genes are under mTORC1 control. Mapping the transcriptome of TGF-β1-stimulated fibroblasts revealed similarity to fibroblasts identified in idiopathic pulmonary fibrosis (IPF). This overlap is lost when mTORC1 is disabled. Using the selective mTORC1 inhibitor RMC-5552, we confirm a causal role for mTORC1 in promoting the acquisition of the collagen-high, phenotype in response to TGF-β1 stimulation in fibroblasts derived from patients with either IPF or lung adenocarcinoma. We conclude that mTORC1 plays a key role in shaping the transcriptional identity of these fibroblasts, with implications for therapeutic inhibition of mTORC1 in fibrosis and cancer. - Source: PubMed
Publication date: 2026/09/02
Wilson Jo-Anne AmWalters RachelContento GregRossanese MadeleineGuillotin DelphineWard Alexander IHynds Robert EJamal-Hanjani MariamKaminski NaftaliParolo SilviaPlaté ManuelaChambers Rachel C