Search results for: Human Galectin-1 Galectin-1
#27430422 2016/08/08 Save this To Up
Sulforaphane-cysteine suppresses invasion via downregulation of galectin-1 in human prostate cancer DU145 and PC3 cells.Our previous study showed that sulforaphane (SFN) inhibits invasion in human prostate cancer DU145 cells; however, the underlying mechanisms were not profoundly investigated. In the present study, we found that sulforaphane-cysteine (SFN-Cys), as a metabolite of SFN, inhibits invasion and possesses a novel mechanism in prostate cancer DU145 and PC3 cells. The scratch and Transwell assays showed that SFN-Cys (15 µM) inhibited both migration and invasion, with cell morphological changes, such as cell shrinkage and pseudopodia shortening. The cell proliferation (MTS) assay indicated that cell viability was markedly suppressed with increasing concentrations of SFN‑Cys. Furthermore, the Transwell assay showed that inhibition of SFN‑Cys‑triggered invasion was tightly linked to the sustained extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. Western blot analysis revealed that SFN-Cys downregulated galectin-1 protein, an invasion‑related protein, and that the galectin‑1 reduction could be blocked by ERK1/2 inhibitor PD98059 (25 µM). Moreover, immunofluorescence staining showed that the expression level of galectin-1 protein was significantly reduced in the cells treated with SFN‑Cys. Hence, SFN‑Cys‑inhibited invasion resulted from the sustained ERK1/2 phosphorylation and ERK1/2‑triggered galectin-1 downregulation, suggesting that galectin-1 is a new SFN-Cys target inhibiting invasion apart from ERK1/2, in the treatment of prostate cancer.
1299 related Products with: Sulforaphane-cysteine suppresses invasion via downregulation of galectin-1 in human prostate cancer DU145 and PC3 cells.Macrophage Colony Stimula anti H inh human blood an anti CD7 All T cells Reco anti Transferrin receptor Prostate cancer tissue ar Prostate cancer tissue ar Prostate cancer and norma Prostate cancer tissue ar Prostate cancer test tiss Prostate cancer test tiss Prostate cancer test tiss Top 4 types of cancer (co
#26397183 2015/12/22 Save this To Up
Pharmacological activation of estrogen receptors-α and -β differentially modulates keratinocyte differentiation with functional impact on wound healing.Estrogen deprivation is considered responsible for many age-related processes, including poor wound healing. Guided by previous observations that estradiol accelerates re‑epithelialization through estrogen receptor (ER)‑β, in the present study, we examined whether selective ER agonists [4,4',4''-(4-propyl [1H] pyrazole-1,3,5-triyl)‑trisphenol (PPT), ER‑α agonist; 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN), ER‑β agonist] affect the expression of basic proliferation and differentiation markers (Ki‑67, keratin‑10, ‑14 and ‑19, galectin‑1 and Sox‑2) of keratinocytes using HaCaT cells. In parallel, ovariectomized rats were treated daily with an ER modulator, and wound tissue was removed 21 days after wounding and routinely processed for basic histological analysis. Our results revealed that the HaCaT keratinocytes expressed both ER‑α and ‑β, and thus are well-suited for studying the effects of ER agonists on epidermal regeneration. The activation of ER‑α produced a protein expression pattern similar to that observed in the control culture, with a moderate expression of Ki‑67 being observed. However, the activation of ER‑β led to an increase in cell proliferation and keratin‑19 expression, as well as a decrease in galectin‑1 expression. Fittingly, in rat wounds treated with the ER‑β agonist (DPN), epidermal regeneration was accelerated. In the present study, we provide information on the mechanisms through which estrogens affect the expression patterns of selected markers, thus modulating keratinocyte proliferation and differentiation; in addition, we demonstrate that the pharmacological activation of ER-α and -β has a direct impact on wound healing.
2904 related Products with: Pharmacological activation of estrogen receptors-α and -β differentially modulates keratinocyte differentiation with functional impact on wound healing.Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone Estrogen Receptor; Clone Estrogen Receptor; Clone c-erbB-2 Oncoprotein c-erbB-2 Oncoprotein c-erbB-3 Oncoprotein; Cl c-erbB-3 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl c-erbB-2 Oncoprotein; Cl
#25662337 2015/08/17 Save this To Up
Panel of Urinary Diagnostic Markers for Non-Invasive Detection of Primary and Recurrent Urothelial Urinary Bladder Carcinoma.To determine the combination of urinary protein markers for noninvasive detection of primary and recurrent urothelial bladder carcinomas.
2537 related Products with: Panel of Urinary Diagnostic Markers for Non-Invasive Detection of Primary and Recurrent Urothelial Urinary Bladder Carcinoma.Bladder carcinoma (multi Breast invasive ductal ca Human Urinary Trypsin Inh Human Urinary Trypsin Inh Human Urinary Trypsin Inh Primary antibody Caspase Primary antibody FLIP An Carcinoma with adjacent t Stomach carcinoma (multi Stomach carcinoma tissue Esophageal carcinoma (mul Esophageal carcinoma (mul
#25491384 2015/04/13 Save this To Up
The placental immune milieu is characterized by a Th2- and anti-inflammatory transcription profile, regardless of maternal allergy, and associates with neonatal immunity.How maternal allergy affects the systemic and local immunological environment during pregnancy and the immune development of the offspring is unclear.
2668 related Products with: The placental immune milieu is characterized by a Th2- and anti-inflammatory transcription profile, regardless of maternal allergy, and associates with neonatal immunity.Rabbit Anti-Human Androge Rabbit Anti-Human Androge Rabbit Anti-Human Androge Goat Anti-Human Androgen Rabbit Anti-Rat Androgen Rabbit anti Androgen Rece Anti-Androgen Receptor pr Anti Androgen Receptor pr MOUSE ANTI BOVINE ROTAVIR Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon
#25231117 2014/09/19 Save this To Up
Involvement of IL‑10 and granulocyte colony‑stimulating factor in the fate of monocytes controlled by galectin‑1.The process of differentiation from monocytes to dendritic cells is critical in immune modulation. Monocyte apoptosis is a key regulator in balancing the immune response. Galectin‑1 has been reported to induce tolerogenic dendritic cells by the autocrine interleukin (IL)‑10 in monocytes. However, IL‑10 has been found to induce apoptosis in IL‑4/granulocyte macrophage colony‑stimulating factor (CSF) stimulating and non‑stimulating monocytes, whereas galectin‑1 has not. After analyzing the factors secreted by galectin-1-activated CD14 monocytes isolated from the peripheral blood, the present study revealed that galectin‑1 upregulates IL‑10 and granulocyte (G)-CSF expression. Furthermore, G‑CSF inhibited IL‑10‑induced apoptosis, implying that galectin‑1 may enhance the immune‑modulating functions of G‑CSF by inducing tolerogenic dendritic cells and maintaining their survival. Therefore, G‑CSF may be further applied in immune therapy, particularly in the IL‑10‑presenting microenvironment.
1475 related Products with: Involvement of IL‑10 and granulocyte colony‑stimulating factor in the fate of monocytes controlled by galectin‑1.Macrophage Colony Stimula CELLKINES MACROPHAGE COLO MACROPHAGE COLONY STIMULA CELLKINES MACROPHAGE COLO MACROPHAGE COLONY STIMULA Human Granulocyte Macroph Human Granulocyte Colony Macrophage Colony Stimula Macrophage Colony Stimula Mouse Granulocyte Colony Rat Granulocyte Macrophag G CSF | granulocyte colon
#21511956 2011/06/17 Save this To Up
Galectin-1-expressing stromal cells constitute a specific niche for pre-BII cell development in mouse bone marrow.In the bone marrow (BM), stromal cells constitute a supportive tissue indispensable for the generation of pro-B/pre-BI, pre-BII, and immature B lymphocytes. IL-7-producing stromal cells constitute a cellular niche for pro-B/pre-BI cells, but no specific stromal cell microenvironment was identified for pre-BII cells expressing a functional pre-B cell receptor (pre-BCR). However expression of the pre-BCR represents a crucial checkpoint during B-cell development. We recently demonstrated that the stromal cell derived-galectin1 (GAL1) is a ligand for the pre-BCR, involved in the proliferation and differentiation of normal mouse pre-BII cells. Here we show that nonhematopoietic osteoblasts and reticular cells in the BM express GAL1. We observed that pre-BII cells, unlike the other B-cell subsets, were specifically localized in close contact with GAL1(+) reticular cells. We also determined that IL-7(+) and GAL1(+) cells represent 2 distinct mesenchymal populations with different BM localization. These results demonstrate the existence of a pre-BII specific stromal cell niche and indicate that early B cells move from IL-7(+) to GAL1(+) supportive BM niches during their development.
2733 related Products with: Galectin-1-expressing stromal cells constitute a specific niche for pre-BII cell development in mouse bone marrow.GFP Expressing Human Inte Rat Anti-Mouse Dendritic MOUSE ANTI BOVINE ROTAVIR anti HSV (II) gB IgG1 (mo anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl MOUSE ANTI BORRELIA BURGD Mouse Stromal Cell-Derive GLP 1 ELISA Kit, Rat Gluc Glucagon ELISA KIT, Rat G Cell cycle antibody array Cell Cycle Control Phosph
#19068473 2009/09/28 Save this To Up
Proteomic analysis of human osteoprogenitor response to disordered nanotopography.Previous studies have shown that microgroove-initiated contact guidance can induce bone formation in osteoprogenitor cells (OPGs) and produce changes in the cell proteome. For proteomic analysis, differential in-gel electrophoresis (DIGE) can be used as a powerful diagnostic method to provide comparable data between the proteomic profiles of cells cultured in different conditions. This study focuses on the response of OPGs to a novel nanoscale pit topography with osteoinductive properties compared with planar controls. Disordered near-square nanopits with 120 nm diameter and 100 nm depth with an average 300 nm centre-to-centre spacing (300 nm spaced pits in square pattern, but with +/-50 nm disorder) were fabricated on 1x1 cm2 polycaprolactone sheets. Human OPGs were seeded onto the test materials. DIGE analysis revealed changes in the expression of a number of distinct proteins, including upregulation of actin isoforms, beta-galectin1, vimentin and procollagen-proline, 2-oxoglutarate 4-dioxygenase and prolyl 4-hydroxylase. Downregulation of enolase, caldesmon, zyxin, GRASP55, Hsp70 (BiP/GRP78), RNH1, cathepsin D and Hsp27 was also observed. The differences in cell morphology and mineralization are also reported using histochemical techniques.
2929 related Products with: Proteomic analysis of human osteoprogenitor response to disordered nanotopography.Analysis Tool for Custom Human IgG (total) ELISA K TOM1-like protein 2 antib TOK-1 alpha antibody Sour Recombinant Human IFN-alp Recombinant Human Interfe Recombinant Human IFN-alp Recombinant Human TOP1 Pr Recombinant Human TOP1 Pr Recombinant Human TOP1 Pr TOM1L1 antibody Source Ra Anti beta3 AR Human, Poly
#18284189 2008/04/04 Save this To Up
New protein clustering of breast cancer tissue proteomics using actin content as a cellularity indicator.In the present study, we report the comparative proteome profiles of proteins solubilized from 37 breast cancer surgical tissues, normalized for the actin content. Blood-derived proteins were excluded from the analysis. Among the tumor-derived protein spots, a large proportion (39%) was found present in all patients. These included several glycolytic enzymes, detox and heat shock proteins, members of annexin and S100 protein families, cathepsin D, and two "rare" proteins, DDAH2 involved in the angiogenesis control, and the oncogene PARK7. Other proteins, such as psoriasin, galectin1, cofilin, peroredoxins, SH3L1, and others, showed sporadic presence and high expression level, which suggests their possible role for patient stratification.
2467 related Products with: New protein clustering of breast cancer tissue proteomics using actin content as a cellularity indicator.Breast cancer and matched Breast cancer and matched Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer tissue arra Breast cancer frozen tiss Breast adjacent normal ti
#11983026 2002/05/01 Save this To Up
Effect of 5-azacytidine and galectin-1 on growth and differentiation of the human b lymphoma cell line bl36.BACKGROUND: 5-AzaCytidine (AzaC) is a DNA demethylating drugs that has been shown to inhibit cell growth and to induce apoptosis in certain cancer cells. Induced expression of the galectin1 (Gal1) protein, a galactoside-binding protein distributed widely in immune cells, has been described in cultured hepatoma-derived cells treated with AzaC and this event may have a role in the effect of the drug. According to this hypothesis, we investigated the effect of AzaC and Gal1 on human lymphoid B cells phenotype. METHODS: The effect of AzaC and Gal1 on cell growth and phenotype was determined on the Burkitt lymphoma cell line BL36. An immunocytochemical analysis for detection of Gal1 protein expression was performed in AzaC-treated cells. To investigate the direct effects of Gal1, recombinant Gal1 was added to cells. RESULTS: Treatment of lymphoid B cells with AzaC results in: i) a decrease in cell growth with an arrest of the cell cycle at G0/G1 phase, ii) phenotypic changes consistent with a differentiated phenotype, and iii) the expression of p16, a tumor-suppressor gene whose expression was dependent of its promoter demethylation, and of Gal1. A targeting of Gal 1 to the plasma membrane follows its cytosolic expression. To determine which of the effects of AzaC might be secondary to the induction of Gal1, recombinant Gal1 was added to BL36 cells. Treated cells displayed growth inhibition and phenotypic changes consistent with a commitment toward differentiation. CONCLUSIONS: Altered cell growth and expression of the cell surface plasma cell antigen, CD138 are detectable in BL36 cells treated by AzaC as well as by Gal1. It seems that AzaC-induced Gal1 expression and consequent binding of Gal1 on its cell membrane receptor may be, in part, involved in AzaC-induced plasmacytic differentiation.
1437 related Products with: Effect of 5-azacytidine and galectin-1 on growth and differentiation of the human b lymphoma cell line bl36.Growth Differentiation Fa Growth Differentiation Fa Anti C Reactive Protein A Epidermal Growth Factor ( Epidermal Growth Factor ( Human Fibroblast Growth F Human Growth and Differen Human Growth and Differen Human Fibroblast Growth F Human Transforming Growth Human Growth and Differen Rabbit Anti-Human Androge
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