Search results for: Mouse Anti-Human CD147 Antibodies
#38166463 
2024/01/03
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CD147 Sparks Atherosclerosis by Driving M1 Phenotype and Impairing Efferocytosis.
Atherosclerosis is a globally prevalent chronic inflammatory disease with high morbidity and mortality. The development of atherosclerotic lesions is determined by macrophages. This study aimed to investigate the specific role of myeloid-derived CD147 (cluster of differentiation 147) in atherosclerosis and its translational significance.Jian-Jun Lv, Hao Wang, Cong Zhang, Tian-Jiao Zhang, Hao-Lin Wei, Ze-Kun Liu, Yi-Hui Ma, Zhi Yang, Qian He, Li-Juan Wang, Li-Li Duan, Zhi-Nan Chen, Huijie Bian
2811 related Products with: CD147 Sparks Atherosclerosis by Driving M1 Phenotype and Impairing Efferocytosis.
25 mg25 100 mg100ug2.5 mg 25 MG100ug100ug Lyophilized10 mg1000 TESTS/0.65ml
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#26849468 2016/02/05
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Protein profile of basal prostate epithelial progenitor cells--stage-specific embryonal antigen 4 expressing cells have enhanced regenerative potential in vivo.
TThomas Höfner, Corinna Klein, Christian Eisen, Teresa Rigo-Watermeier, Axel Haferkamp, Martin R Sprick
1746 related Products with: Protein profile of basal prostate epithelial progenitor cells--stage-specific embryonal antigen 4 expressing cells have enhanced regenerative potential in vivo.
0.05 mg1.00 flask0.1ml (1mg/ml)1mg1.00 flask2 ml96 wells2
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#23602236 2013/03/25
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Expression of HAb18G/CD147 and its localization correlate with the progression and poor prognosis of non-small cell lung cancer.
This study was designed to investigate the association of HAb18G/CD147 expression and localization with clinicopathological parameters and prognosis in NSCLC. Two hundred and eight (208) specimens of surgically resected NSCLC were stained by immunohistochemistry utilizing mouse anti-human HAb18G/CD147 monoclonal antibody. High levels of HAb18G/CD147 expression were associated with male gender, smoking history, tumor position, distant metastasis status, and clinical stage (p<0.05) in squamous cell carcinoma. In adenocarcinomas, HAb18G/CD147 expression was associated with male gender, tumor diameter, differentiation, lymph node status, distant metastasis status, and clinical stage (p<0.05). HAb18G/CD147 expression with higher PU was predominantly localized in the tumor cell membranes rather than in cytoplasms. In squamous cell carcinomas, membranous localization of HAb18G/CD147 was linked to distant metastasis status and TNM stage (p<0.05). Cytoplasmic localization of HAb18G/CD147 was associated with male gender and smoking history. In adenocarcinomas, membranous localization of HAb18G/CD147 correlated with tumor diameter, differentiation and distant metastasis (p<0.05). Univariate analysis indicated that patients with high HAb18G/CD147 expression and membranous localization predicted poor prognosis in both squamous cell carcinomas and adenocarcinomas. Multivariate analysis showed that lymph node status (HR=1.762, 95%CI 1.105-2.811, p=0.017), distant metastasis status (HR=3.789, 95%CI 2.196-6.539, p=0.000), expression (HR=6.632, 95%CI 2.457-17.904, p=0.000), and localization (HR=0.520, 95%CI 0.341-0.794, p=0.002) were good or excellent independent predictors of patient survival. HAb18G/CD147 is a biomarker characterizing progression and survival of NSCLC. More importantly, its cellular localizations should be considered in the analysis of clinicopathological characteristics and prognostic factors in NSCLC.Xiao-yan Xu, Ni Lin, Yu-mei Li, Cheng Zhi, Hong Shen
1751 related Products with: Expression of HAb18G/CD147 and its localization correlate with the progression and poor prognosis of non-small cell lung cancer.
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#20096685 2010/01/22
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Autocrine effects of VEGF-D on endothelial cells after transduction with AD-VEGF-D(DeltaNDeltaC).
Endothelial cells in tumor vessels display unusual characteristics in terms of survival and angiogenic properties which result from the increased expression of VEGF-D and its autocrine effect. To evaluate mechanisms by which VEGF-D leads to such abnormal phenotype, we searched for proteins with modified expression in HUVECs enriched in the recombinant mature VEGF-D (VEGFD(DeltaNDeltaC)) delivered by adenovirus. Expression of membrane proteins in endothelial cells was characterized by FACS using anti-human IT-Box-135 antibodies. HUVECs transduced with Ad-VEGF-D(DeltaNDeltaC) revealed markedly increased expression of proteins involved in adhesion and migration such as (a) integrins (alphaVbeta5, alpha2beta1, alpha5beta1, alphaMbeta2, alphaLbeta2), (b) matrix metalloproteinases (MMP-2, MMP-9, and MMP-14), (c) components of fibrinolytic system (PAI-1, u-PAR), and (d) CD45, CD98, CD147. Interestingly, there also were numerous proteins with significantly reduced expression, particularly among surface exposed membrane proteins. Thus, it can be concluded that to induce proangiogenic phenotype and facilitate migration of HUVECs, VEGF-D(DeltaNDeltaC) not only upregulates expression of proteins known to participate in the cell-matrix interactions but also silences some membrane proteins which could interfere with this process.Izabela Papiewska-Pajak, Joanna Boncela, Patrycja Przygodzka, Czeslaw S Cierniewski
1064 related Products with: Autocrine effects of VEGF-D on endothelial cells after transduction with AD-VEGF-D(DeltaNDeltaC).
2ug96T2ug2ug1.00 flask2ug1.00 flask1.00 flask1mg1.00 flask100 µg5ug
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#18616931 2008/07/09
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Blocking CD147 induces cell death in cancer cells through impairment of glycolytic energy metabolism.
CD147 is a multifunctional transmembrane protein and promotes cancer progression. We found that the anti-human CD147 mouse monoclonal antibody MEM-M6/1 strongly induces necrosis-like cell death in LoVo, HT-29, WiDr, and SW620 colon cancer cells and A2058 melanoma cells, but not in WI-38 and TIG-113 normal fibroblasts. Silencing or overexpression of CD147 in LoVo cells enhanced or decreased the MEM-M6/1 induced cell death, respectively. CD147 is known to form complex with proton-linked monocarboxylate transporters (MCTs), which is critical for lactate transport and intracellular pH (pHi) homeostasis. In LoVo cells, CD147 and MCT-1 co-localized on the cell surface, and MEM-M6/1 inhibited the association of these molecules. MEM-M6/1 inhibited lactate uptake, lactate release, and reduced pHi. Further, the induction of acidification was parallel to the decrease of the glycolytic flux and intracellular ATP levels. These effects were not found in the normal fibroblasts. As cancer cells depend on glycolysis for their energy production, CD147 inhibition might induce cell death specific to cancer cells.Miyako Baba, Masahiro Inoue, Kazuyuki Itoh, Yasuko Nishizawa