Search results for: Brain Specific Angiogenesis Inhibitor 1 (BAI1), Human
#28259299 2017/03/05 Save this To Up
Regulatory roles of brain-specific angiogenesis inhibitor 1(BAI1) protein in inflammation, tumorigenesis and phagocytosis: A brief review.Brain-specific angiogenesis inhibitor (BAI) family of proteins are basically putative G-protein-coupled receptors with wide spectrum of cellular activities. These BAIs exhibit intricate and complex nature of modulatory activities that researchers are only now beginning to understand. Here we mainly focus on the regulatory activities of a prominent member of BAI family, BAI1, with respect to its role in inflammation, tumorigenesis and phagocytosis. The emerging knowledge on cell- and site-specific function of BAI1 makes it both versatile and promising candidate for studies relating to cancer and host immune response. This review collectively specifies and comprehends important findings of BAI1 from several studies and provides latest insight to explore its properties for possible biomedical therapeutics.
2403 related Products with: Regulatory roles of brain-specific angiogenesis inhibitor 1(BAI1) protein in inflammation, tumorigenesis and phagocytosis: A brief review.Brain-Specific Angiogenes Brain Specific Angiogenes Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 9 (P Proteinase Inhibitor 6 (P BYL-719 Mechanisms: PI3K- IPI-145 (INK-1197) Mechan Apoptosis Phospho-Specifi EGF Phospho-Specific Arra Angiogenesis (Human) Anti Angiogenesis (Human) Anti
#27356780 2016/07/19 Save this To Up
Biological effects of eukaryotic recombinant plasmid pReceiver-M61-BAI-1 transfection on T24 cells and HUVECs.The aim of the current study was to investigate the biological effect on T24 cells and human umbilical vein endothelial cells (HUVECs) of transfection with brain-specific angiogenesis inhibitor-1 (BAI-1). The recombinant plasmid pReceiver-M61-BAI-1 was transfected into human superficial bladder tumor cells (T24) and HUVECs, in parallel with the vector control. mRNA and protein expression levels of BAI‑1 were then detected by quantitative polymerase chain reaction (qPCR) and western blotting, respectively. Cell apoptosis of T24 cells and HUVECs prior and subsequent to transfection with BAI‑1 was analyzed by flow cytometric analysis. Proliferation of T24 cells and HUVECs prior and subsequent to transfection of BAI-1 was assessed by the MTT method. T24 cells and HUVECs transfected with pReceiver‑M61‑BA1‑1 were classed as the experimental group; T24 cells and HUVECs transfected with p‑Receiver‑M61 were the control group. qPCR and western blotting methods confirmed that there was positive expression of BAI‑1 in T24 cells and HUVECs transfected with pReceiver‑M61‑BAI‑1, however BAI‑1 was not expressed in T24 cells and HUVECs transfected with pReceiver‑M61. The results of the MTT assay demonstrated that absorbance was markedly reduced in HUVECs at 12, 48 and 72 h subsequent to transfection with pReceiver-M61-BAI-1 when compared with that of the control group and in T24 cells transfected with p‑Receiver-M61-BAI-1. Furthermore, flow cytometry results also indicated that the apoptotic rate of HUVECs transfected with p‑Receiver‑M61‑BAI‑1 was significantly increased compared with that of the control group and T24 cells transfected with p‑Receiver‑M61‑BAI‑1. BAI‑1 was observed to markedly inhibit the proliferation of vascular endothelial cells in vitro, however, no direct inhibition by BAI‑1 was observed in T24 cells. In conclusion, BAI-1 is suggested to be a potential novel therapautic target for the inhibition of tumor neovascularization.
2029 related Products with: Biological effects of eukaryotic recombinant plasmid pReceiver-M61-BAI-1 transfection on T24 cells and HUVECs.Macrophage Colony Stimula RANK Ligand Soluble, Huma Recombinant HBsAg adr [fr Recombinant HBsAg adr [fr Recombinant Human HGF [fr Recombinant Human HGF [fr Recombinant Human IL-4 [f Recombinant Human IL-6 (I Recombinant Canine ApoJ C Recombinant Canine ApoJ C Recombinant Human OPG TNF Recombinant Human OPG TNF
#26222696 2015/07/30 Save this To Up
BAI1-Associated Protein 2-Like 1 (BAIAP2L1) Is a Potential Biomarker in Ovarian Cancer.Brain-specific angiogenesis inhibitor 1 (BAI1)-associated protein 2-like 1 (BAIAP2L1), also known as insulin receptor tyrosine kinase substrate (IRTKS), is involved in plasma membrane protrusion and actin formation during cell morphogenesis and migration. BAIAP2L1 is recently reported to promote cell proliferation through activation of the EGFR-ERK pathway in hepatocellular carcinoma. In this study, we report the first comprehensive study of BAIAP2L1 upregulation in human ovarian cancer. Upregulation of BAIAP2L1 in ovarian tumors was first found during RNA screening and confirmed by immunohistochemical studies on ovarian cancers and other cancer types. Significant upregulation of BAIAP2L1 in ovarian cancer was validated by analyzing multiple independent cohorts in publicly available data sets. Furthermore, BAIAP2L1 protein expression in metastatic lesions was higher than the corresponding primary tumors. Functional assays in ovarian cancer cells revealed that BAIAP2L1 is involved in promoting cell proliferation and avoiding apoptosis. In conclusion, results of this study not only indicate that BAIAP2L1 can be used as a biomarker for human ovarian cancer but also reveal its role in cancer biology. Further elucidation of the role of BAIAP2L1 in context of the insulin receptor signaling pathways of cancer cells is warranted for developing cancer therapeutics by targeting cancer-specific metabolism.
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#26075824 2015/07/03 Save this To Up
Apoptotic cells trigger a membrane-initiated pathway to increase ABCA1.Macrophages clear millions of apoptotic cells daily and, during this process, take up large quantities of cholesterol. The membrane transporter ABCA1 is a key player in cholesterol efflux from macrophages and has been shown via human genetic studies to provide protection against cardiovascular disease. How the apoptotic cell clearance process is linked to macrophage ABCA1 expression is not known. Here, we identified a plasma membrane-initiated signaling pathway that drives a rapid upregulation of ABCA1 mRNA and protein. This pathway involves the phagocytic receptor brain-specific angiogenesis inhibitor 1 (BAI1), which recognizes phosphatidylserine on apoptotic cells, and the intracellular signaling intermediates engulfment cell motility 1 (ELMO1) and Rac1, as ABCA1 induction was attenuated in primary macrophages from mice lacking these molecules. Moreover, this apoptotic cell-initiated pathway functioned independently of the liver X receptor (LXR) sterol-sensing machinery that is known to regulate ABCA1 expression and cholesterol efflux. When placed on a high-fat diet, mice lacking BAI1 had increased numbers of apoptotic cells in their aortic roots, which correlated with altered lipid profiles. In contrast, macrophages from engineered mice with transgenic BAI1 overexpression showed greater ABCA1 induction in response to apoptotic cells compared with those from control animals. Collectively, these data identify a membrane-initiated pathway that is triggered by apoptotic cells to enhance ABCA1 within engulfing phagocytes and with functional consequences in vivo.
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#25751059 2015/04/02 Save this To Up
BAI1 regulates spatial learning and synaptic plasticity in the hippocampus.Synaptic plasticity is the ability of synapses to modulate the strength of neuronal connections; however, the molecular factors that regulate this feature are incompletely understood. Here, we demonstrated that mice lacking brain-specific angiogenesis inhibitor 1 (BAI1) have severe deficits in hippocampus-dependent spatial learning and memory that are accompanied by enhanced long-term potentiation (LTP), impaired long-term depression (LTD), and a thinning of the postsynaptic density (PSD) at hippocampal synapses. We showed that compared with WT animals, mice lacking Bai1 exhibit reduced protein levels of the canonical PSD component PSD-95 in the brain, which stems from protein destabilization. We determined that BAI1 prevents PSD-95 polyubiquitination and degradation through an interaction with murine double minute 2 (MDM2), the E3 ubiquitin ligase that regulates PSD-95 stability. Restoration of PSD-95 expression in hippocampal neurons in BAI1-deficient mice by viral gene therapy was sufficient to compensate for Bai1 loss and rescued deficits in synaptic plasticity. Together, our results reveal that interaction of BAI1 with MDM2 in the brain modulates PSD-95 levels and thereby regulates synaptic plasticity. Moreover, these results suggest that targeting this pathway has therapeutic potential for a variety of neurological disorders.
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#24642458 2014/04/24 Save this To Up
The BAI subfamily of adhesion GPCRs: synaptic regulation and beyond.The brain-specific angiogenesis inhibitors 1-3 (BAI1-3) comprise a subfamily of adhesion G-protein-coupled receptors (GPCRs). These receptors are highly expressed in the brain and were first studied for their ability to inhibit angiogenesis and tumor formation. Subsequently, BAI1 was found to play roles in apoptotic cell phagocytosis and myoblast fusion. Until recently, however, little was known about the physiological importance of the BAI subfamily in the context of normal brain function. Recent work has provided evidence for key roles of BAI1-3 in the regulation of synaptogenesis and dendritic spine formation. In this review, we summarize the current understanding of the BAI subfamily with regard to downstream signaling pathways, physiological actions, and potential importance as novel drug targets in the treatment of psychiatric and neurological diseases.
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#23932496 2013/09/20 Save this To Up
Macrophages engulfing apoptotic thymocytes produce retinoids to promote selection, differentiation, removal and replacement of double positive thymocytes.The thymus provides the microenvironment in which thymocytes develop into mature T-cells, and interactions with thymic stromal cells are thought to provide the necessary signals for thymocyte maturation. Recognition of self-MHC by T-cells is a basic requirement for mature T-cell functions, and those thymocytes that do not recognize or respond too strongly to the peptide-loaded self-MHC molecules found in the thymus undergo apoptosis. As a result, 95% of the thymocytes produced will die and be subsequently cleared by macrophages. This review describes a complex crosstalk between developing thymocytes and engulfing macrophages which is mediated by retinoids produced by engulfing macrophages. The interaction results in the harmonization of the rate of cell death of dying double positive cells with their clearance and replacement, and in promotion of the differentiation of the selected cells in the thymus.
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#23827879 2013/08/19 Save this To Up
The integrin inhibitor cilengitide enhances the anti-glioma efficacy of vasculostatin-expressing oncolytic virus.Oncolytic viral (OV) therapy has been considered as a promising treatment modality for brain tumors. Vasculostatin, the fragment of brain-specific angiogenesis inhibitor-1, shows anti-angiogenic activity against malignant gliomas. Previously, a vasculostatin-expressing oncolytic herpes simplex virus-1, Rapid Antiangiogenesis Mediated By Oncolytic virus (RAMBO), was reported to have a potent antitumor effect. Here, we investigated the therapeutic efficacy of RAMBO and cilengitide, an integrin inhibitor, combination therapy for malignant glioma. In vitro, tube formation was significantly decreased in RAMBO and cilengitide combination treatment compared with RAMBO or cilengitide monotherapy. Moreover, combination treatment induced a synergistic suppressive effect on endothelial cell migration compared with the control virus. RAMBO, combined with cilengitide, induced synergistic cytotoxicity on glioma cells. In the caspase-8 and -9 assays, the relative absorption of U87ΔEGFR cell clusters treated with cilengitide and with RAMBO was significantly higher than that of those treated with control. In addition, the activity of caspase 3/7 was significantly increased with combination therapy. In vivo, there was a significant increase in the survival of mice treated with combination therapy compared with RAMBO or cilengitide monotherapy. These results indicate that cilengitide enhanced vasculostatin-expressing OV therapy for malignant glioma and provide a rationale for designing future clinical trials combining these two agents.
1025 related Products with: The integrin inhibitor cilengitide enhances the anti-glioma efficacy of vasculostatin-expressing oncolytic virus.Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rabbit anti PKC theta (Ab Rat Anti-CCT theta Antibo Rabbit Anti-Theophylline Sheep Anti-Theophylline 3 FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Normal mouse multiple org Normal rat multiple organ Normal rat multiple organ
#23782696 2013/08/05 Save this To Up
Brain-specific angiogenesis inhibitor-1 signaling, regulation, and enrichment in the postsynaptic density.Brain-specific angiogenesis inhibitor-1 (BAI1) is an adhesion G protein-coupled receptor that has been studied primarily for its anti-angiogenic and anti-tumorigenic properties. We found that overexpression of BAI1 results in activation of the Rho pathway via a Gα(12/13)-dependent mechanism, with truncation of the BAI1 N terminus resulting in a dramatic enhancement in receptor signaling. This constitutive activity of the truncated BAI1 mutant also resulted in enhanced downstream phosphorylation of ERK as well as increased receptor association with β-arrestin2 and increased ubiquitination of the receptor. To gain insights into the regulation of BAI1 signaling, we screened the C terminus of BAI1 against a proteomic array of PDZ domains to identify novel interacting partners. These screens revealed that the BAI1 C terminus interacts with a variety of PDZ domains from synaptic proteins, including MAGI-3. Removal of the BAI1 PDZ-binding motif resulted in attenuation of receptor signaling to Rho but had no effect on ERK activation. Conversely, co-expression with MAGI-3 was found to potentiate signaling to ERK by constitutively active BAI1 in a manner that was dependent on the PDZ-binding motif of the receptor. Biochemical fractionation studies revealed that BAI1 is highly enriched in post-synaptic density fractions, a finding consistent with our observations that BAI1 can interact with PDZ proteins known to be concentrated in the post-synaptic density. These findings demonstrate that BAI1 is a synaptic receptor that can activate both the Rho and ERK pathways, with the N-terminal and C-terminal regions of the receptor playing key roles in the regulation of BAI1 signaling activity.
2853 related Products with: Brain-specific angiogenesis inhibitor-1 signaling, regulation, and enrichment in the postsynaptic density.Brain-Specific Angiogenes Brain Specific Angiogenes CAL-101 Mechanisms: PI3K- IPI-145 (INK-1197) Mechan AMPK Signaling Phospho-Sp GPCR Signaling to MAPK ER IGF-1R Signaling Phospho- p53 Signaling Phospho-Spe T-Cell Receptor Signaling TGF-Beta Signaling Phosph PathwayReady™ PI3 K Akt PathwayReady™ EGFR Sign
#23761815 2013/06/13 Save this To Up
Expression of brain-specific angiogenesis inhibitor 1 is inversely correlated with pathological grade, angiogenesis and peritumoral brain edema in human astrocytomas.As the most common intracranial malignant neoplasms, astrocytomas are characterized by high neovascularization and severe peritumoral brain edema (PTBE). Angiogenesis is a prerequisite for the growth of solid tumors, including astrocytoma, and brain-specific angiogenesis inhibitor 1 (BAI1) is a novel angiogenesis inhibitor. In the present study, the expression levels of BAI1, vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were investigated using immunohistochemical methods in 90 human brain astrocytoma specimens of various pathological grades and in 11 normal human brain tissues. Vascular endothelial cells were stained for CD105 and the microvessel density (MVD) was assessed. The volume of astrocytoma and PTBE in each case was evaluated by magnetic resonance imaging (MRI). The results showed that BAI1 was highly expressed in the normal brain tissues, but that the expression decreased with the rising pathological grades of astrocytoma, MVD number and PTBE, indicating that BAI1 expression was inversely correlated with these factors. Furthermore, it was observed that the expression of VEGF and bFGF were inversely correlated with BAI1 expression in the human brain astrocytomas. These results indicate that the BAI1 gene may be used as a marker of decreased tumor progression and tumoral neovascularization, as well as PTBE.
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