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findings show elevated CD109 protein expression in esophageal squamous cell carcinoma (ESCC); CD109 expression is restricted in squamous cells of ESCCs
GRP78 binds to and acts in concert with a glycosylphosphatidylinositol-anchored protein, CD109, in blocking TGF-beta signaling by promoting the routing of the TGF-beta receptor to the caveolae, thereby disrupting its binding to and activation of Smad2.
CD109 knockdown upregulated IL-8 expression through activation of TGF-beta/Akt/NF-kappaB pathway in human umbilical vein endothelial cells
High expression of CD109 in brain tumor stem cells is involved in glioma progression.
CD109 is a putative biomarker for identifying a high-risk group among DLBCL patients.
The most common HPA genotypes among Saudis were HPA-1 a + b- (75%), HPA-2 a + b- (62%), HPA-3 a + b- (51.5%), HPA-4 a + b- (99%), HPA-5 a + b- (76.5%), HPA-6 a + b- (100%) and HPA-15 a + b + (50%). The prevalent allele among the HPA systems was (a), except in the HPA-15 system where the (b) allele was found in 52% of the subjects.
Expression levels of CD109 was reduced significantly in psoriasis. Lower expression of CD109 and TGF-beta RI was highly correlated with higher expression of Smad7 and Ki67, suggesting that CD109 may induce the pathogenesis of psoriasis through Smad7-mediated degradation of TGF-beta RI.
sCD109 can bind TGF-beta, inhibit TGF-beta binding to its receptors and decrease TGF-beta signalling and TGF-beta-induced cellular responses.
These findings indicate that CD109 is an exosomal protein and that the C-terminal region of CD109 is required for its presence in the exosome.
CD109 may be a potential pathology marker for gallbladder squamous cell/adenosquamous carcinomas.
CD109 is specifically expressed in endothelial cells of cutaneous cavernous haemangioma.
expression increased in cutaneous squamous cell carcinoma
The results suggest that circulating endothelial cells express CD109 and represent a rare population of circulating tumor endothelial cells, that play a potentially useful prognostic role in patients with glioblastoma.
CD109 overexpression was significantly associated with surgical stage, distant metastasis, and poor prognosis in myxofibrosarcoma.
Three glioblastoma cell lines, SK-MG-1, U251MG and MG178, were tested and CD109 overexpression attenuated TGF-beta1 signaling and enhanced EGF signaling in SK-MG-1, but not in U251MG or MG178.
CD109 is highly expressed in TNBC and is a potential biomarker for the initiation, progression, and differentiation of breast cancer tumors.
CD109 plays a critical role in non-small-cell lung cancer (NSCLC) progression, and is overexpressed in advanced NSCLC
High expression of CD109 antigen regulates the phenotype of cancer stem-like cells/cancer-initiating cells in a novel epithelioid sarcoma cell line ESX and is related to poor prognosis of soft tissue sarcoma.
Hematopoietic cell marker CD109 is expressed in hepatic progenitor cells.
expression of CD109 (human platelet antigen 15) mRNA is different in various human cell types
Garp deletion in mouse Tregs is not sufficient to impair their immunosuppressive activity in vivo.
Results indicate that CD109 deficiency induces a high-turnover, osteoporosis-like phenotype, which suggests that CD109 plays a role in bone metabolism in vivo.
CD109 deficiency suppresses skin tumorigenesis by enhancing TGF-beta/Smad/Nrf2 pathway activity and decreasing the mutation frequency of the H-ras gene.
platelet and endothelial GARP are not important in hemostasis and thrombosis in mice
Small-scale in vivo screening identified several genes, including Cd109, that encode novel pro-metastatic factors. We uncovered signaling mediated by Janus kinases (Jaks) and the transcription factor Stat3 as a critical, pharmacologically targetable effector of CD109-driven lung cancer metastasis
CD109 differentially regulates TGF-beta-induced ALK1-Smad1/5 versus ALK5-Smad2/3 pathways, leading to decreased extracellular matrix production in the skin; epidermal CD109 expression regulates dermal function through a paracrine mechanism
the GARP/LTGF-beta1 complex on Treg cells is a major source of TGF-beta1 needed for induction of pTreg cells during the process of oral tolerance.
GP96 serves as an essential chaperone for the cell-surface protein glycoprotein A repetitions predominant (GARP), which is a docking receptor for latent membrane-associated TGF-beta (mLTGF-beta).
CD109 decreases extracellular matrix production and fibrotic responses during hypoxic wound healing
CD109 is present in serum as a soluble form, and suggest its potential as a novel tumor marker in patients with cancers that express CD109.
CD109 might be an important regulator of osteoclastogenesis.
findings demonstrate that CD109 overexpression in the epidermis reduces inflammation and granulation tissue area and improves collagen organization in vivo.
Induction of both Th17-producing cells and Tregs is caused preferentially by Tregs expressing the latent TGF-beta1/GARP complex on their cell surface rather than by secreted latent TGF-beta1.
CD109 overexpression ameliorates skin fibrosis in a mouse model of bleomycin-induced scleroderma.
CD109 regulates differentiation of keratinocytes via a signaling pathway involving Stat3.
This gene encodes a member of the alpha2-macroglobulin/complement superfamily. The encoded GPI-linked glycoprotein is found on the cell surface of platelets, activated T-cells, and endothelial cells. The protein binds to and negatively regulates signaling of transforming growth factor beta (TGF-beta). Multiple transcript variants encoding different isoforms have been found for this gene.
150 kDa TGF-beta-1-binding protein
, C3 and PZP-like alpha-2-macroglobulin domain-containing protein 7
, CD109 antigen
, Gov platelet alloantigens
, activated T-cell marker CD109
, platelet-specific Gov antigen
, CD109 molecule
, CD109 antigen-like
, GPI-anchored alpha 2 macroglobulin-related protein
, GPI-anchored alpha-2 macroglobulin-related protein