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Creative Bioarray provides cell proliferation assay service for our customer. We are capable of performing different cell proliferation assays based on several concepts, which are measuring rate of DNA replication, analysis of metabolic activity, cell surface antigen recognitions, detecting proliferation markers, ATP measurement, measures of membrane integrity and so on.
... Abstract ...The cell proliferation assay is an important tool in the assessment of... Introduction ...Cell proliferation assays are employed frequently in immunological ca...,Cell,Proliferation,Assays,biological,advanced biology technology,biology laboratory technology,biology device technology,latest biology technology
BioAssay record AID 1077586 submitted by ChEMBL: Antiproliferative activity against human PLC/PRF/5 cells assessed as inhibition of cell proliferation at 10 to 100 uM by MTT dye uptake assay.
Little knockdown but big effect on proliferation - posted in siRNA, microRNA and RNAi: Hi folks,Hope you are well all !! I did knockdown lately on cell line expressed in GOI and it was tested by qPCR. The results showed that i got moderate suppression in mRNA level in my GOI, following the knockdown i did cell proliferation ( cell viability ) and the results showed that there is an effect on proliferation rate.]My question is how was an effect on proliferation when there was little...
We have shown that 4-1BB in myeloid cells, particularly in APCs, negatively regulates peripheral T cell responses in vivo. Thus, adoptively transferred CD4+ and CD8+ T cells showed the enhanced T cell proliferation in tumor-bearing RAG2−/−4-1BB−/− mice, and DCs and IL-15 were primarily responsible for this enhanced T cell proliferation. However, isolated 4-1BB+/+ and 4-1BB−/− DCs made comparable levels of IL-15, and individual 4-1BB−/− DCs induced T cell responses in vivo less efficiently than 4-1BB+/+ DCs. Therefore, we concluded that 4-1BB deficiency in myeloid cells in vivo induces the enhanced proliferation of peripheral T cells by promoting the accumulation of DCs in secondary lymphoid organs.. Although enhanced T cell responses were first reported when 4-1BB−/− mice were generated more than a decade ago (29), the underlying mechanism was not understood. Other studies have also pointed to a negative regulatory function of 4-1BB in modulating T cell responses. Thus, ...
Creative Proteomics offers sensitive, reliable, and accurate Cell Proliferation Assay via DNA Synthesis to study cell proliferation.
A serum-free or serum-depleted medium for the short- and long-term proliferation and development of cells, particularly hematopoietic cells and bone marrow stromal cells, the medium comprising cell proliferation and development effective amounts of: a standard culture medium such as Iscoves modified Dulbeccos medium; serum albumin; transferrin; a source of lipids and fatty acids; cholesterol; a reducing agent; pyruvate; a glucocorticoid (when the cells to be cultured are hematopoietic cells); nucleosides for synthesis of DNA and RNA; growth factors that stimulate the proliferation and development of stromal cells and cells from a variety of tissues or organs, such as epidermal growth factor, fibroblast growth factor, platelet derived growth factor, and insulin; and extracellular matrix materials, such as collagen, fibronectin, and laminin.
NSCLC is the most prevalent cancer types and has highest mortality rate in China [1]; however, the progression mechanisms of NSCLC have largely remained elusive. Ample evidence indicates a crucial role for miRNAs in human cancer [21], especially the miRNAs participate in the initiation, promotion, and progression of NSCLC. For instance, miR-21 promotes growth and invasion of NSCLC [22]. In addition, miR-494, miR-101, miR-1254, miR-574-5p, miR-143 and miR-181a were demonstrated to be involved in NSCLC [23-25]. In the present study, we certified that miR-361-3p was frequently down-regulated in NSCLC, and first found that the reduced miR-361-3p expression was closely related to advanced stage and lymph node metastasis of NSCLC. Furthermore, we demonstrated that overexpression of miR-361-3p could suppress NSCLC cell proliferation, migration and invasion in vitro and in vivo. The versatile functions of miR-361-3p in tumor cell proliferation, migration and invasion suggest its potential application as ...
Breast cancer is one of the most lethal types of cancer in women worldwide due to the late stage detection and resistance to traditional chemotherapy. The human epidermal growth factor receptor 2 (HER2) is considered as a validated target in breast cancer therapy. Even though a substantial effort has been made to develop HER2 inhibitors, only lapatinib has been approved by the U.S. Food and Drug Administration (FDA). Side effects were observed in a majority of the patients within one year of treatment initiation. Here, we took advantage of bioinformatics tools to identify novel effective HER2 inhibitors. The structure-based virtual screening combined with ADMET (absorption, distribution, metabolism, excretion and toxicity) prediction was explored. In total, 11,247 natural compounds were screened. The top hits were evaluated by an in vitro HER2 kinase inhibition assay. The cell proliferation inhibition effect of identified inhibitors was evaluated in HER2-overexpressing SKBR3 and BT474 cell lines. We
CD44 is a causal factor for tumor invasion, metastasis and acquisition of resistance to apoptosis. CD44 knockdown using inducible short hairpin RNA (shRNA) significantly reduces cell growth and invasion. Short hairpin RNA against CD44 and pGFP-V-RS-vector was used for knockdown of CD44 expression in SW620 colon cancer cells. Cell growth, invasion and migration assay, immunofluorescence for β-catenin expression and western blotting for Wnt signaling molecules were analyzed. Cell cycle analysis and western blot analysis for apoptotic molecules were evaluated. Short hairpin RNA against CD44 reduced the expression of CD44. Cell proliferation, migration and invasion were markedly inhibited and apoptosis was increased in shRNA CD44-transfected cells. Knockdown of CD44 decreased the phosphorylation of PDK1, Akt and GSK3β, and β-catenin levels. Decreased phosphorylated Akt led to an increase in phosphorylated FoxO1 and induced cell cycle arrest in the G0-G1 phase and a decrease in the S phase. The ...
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Perifosine and CCI 779 co-operate to induce cell death and decrease proliferation in PTEN-intact and PTEN-deficient PDGF-driven murine glioblastoma.
Plants and animals evolved significantly different strategies of regulation of the cell proliferation and differentiation. Identification and comparison of molecular mechanisms driving those different strategies in plants, animals and microorganisms might contribute to the identification of their common principles. The project is based on collaboration of laboratories involved in the study of the processes of the cell proliferation and differentiation in those different model organisms including human beings. Collaboration of the laboratories with expertise in (i) molecular plant physiology, (ii) molecular mechanisms maintaining the genome stability, (iii) proliferation, differentiation and programmed cell death of cancer cells and (iv) bioinformatics will result into a multidisciplinary, while still functional team that will guarantee successful solution of scheduled tasks. Participation of multiple, recently collaborating laboratories including Core lab will allow effective employment of ...
: Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed. We determined the expression, biological functions, and regulatory mechanisms of MIEN1 in the prostate. The results of immunohistochemical analysis indicated that MIEN1 was expressed specifically in epithelial cells and significantly higher in adenocarcinoma as compared to in normal tissues. MIEN1 enhanced in vitro cell proliferation, invasion, and in vivo tumorigenesis. Meanwhile, MIEN1 attenuated cisplatin-induced apoptosis in PC-3 cells. Overexpression of NF-ĸB-inducing kinase (NIK) enhanced MIEN1 expression, while overexpression of NF-ĸB inhibitor α (IĸBα) blocked MIEN1 expression in PC-3 cells. In prostate carcinoma cells, MIEN1 provoked Akt phosphorylation; moreover, MIEN1 downregulated N-myc downstream regulated 1 (NDRG1) but upregulated interleukin-6 (IL-6) gene expression. MK2206, an
ATCC Cell Proliferation Assay kits are convenient and valuable tools for the quantitative evaluation of a cell populations response to external factors that affect cell viability and growth.
Probable proto-oncogene that regulates cell proliferation, growth, migration and epithelial to mesenchymal transition. Through the degradation of FBXW7, may act indirectly on the expression and downstream signaling of MTOR, JUN and MYC (PubMed:24344117). May play also a role in cell proliferation through activation of the ERK1/ERK2 signaling cascade (PubMed:25646692). May also be important for proper chromosome congression and alignment during mitosis through its interaction with KIF22 ...
Gentaur molecular products has all kinds of products like :search , Trevigen \ MTT Cell Proliferation Assay Kit \ 4890-25-K for more molecular products just contact us
Effect of GPC3 on cell proliferation and clonogenic capacity of liver CD90+GPC3+CSCs.(A) Cell proliferation was assessed after GPC3 knockdown in PLC CD90+GPC3+
A colorimetric cell proliferation assay using soluble tetrazolium sodium [(CellTiter 96? Aqueous One Remedy) cell proliferation reagent, comprising the (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium, inner salt) and an electron coupling reagent phenazine ethosulfate], was optimized and certified for quantitative dedication of IL-15 dependent CTLL-2 cell proliferation activity. of scripts written in the R Statistical Language and Environment utilizing a […]. ...
Fig. 2. Effect of low-dose PTX (A), BMS-275183 (B), EpoB (C), and 4-HC (D) on in vitro cell proliferation. The antiproliferative effects of the drugs were studied using both short-term (24 h, left) and prolonged continuous exposures (144 h, right) on the HUVEC, HMVEC-d, MDA-MB-435, T0.1, and NHDF cell lines. Columns and bars, mean values ± SE, respectively. aP , 0.05 versus HUVEC controls; bP , 0.05 versus HMVEC-d controls; cP , 0.05 versus MDA-MB-435 controls; dP , 0.05 versus T0.1 controls; eP , 0.05 versus NHDF controls; ∗P , 0.05 versus 144 h HUVEC controls; °P , 0.05 versus 144 h MDA-MB-435 controls; +P , 0.05 versus 24 h HUVEC controls; °P , 0.05 versus 24 h MDA-MB-435 controls.. ...
We report a novel mechanism of cellular growth control. Increasing the density of endothelial or smooth muscle cells in culture increased cell-cell contact and decreased cell spreading, leading to growth arrest. Using a new method to independently control cell-cell contact and cell spreading, we fou …
Introduction The difficulty in re-growing and mineralizing new bone after severe fracture can result in loss of ambulation or limb. Here we describe the sequential roles of FGF-2 in inducing gene expression, cell growth and BMP-2 in gene expression and mineralization of bone. Materials and methods The regulation of gene expression was determined using real-time RTPCR (qRTPCR) and cell proliferation was measured by thymidine incorporation or fluorescent analysis of DNA content in MC3T3E1 osteoblast-like cells. Photomicroscopy was used to identify newly mineralized tissue and fluorescence was used to quantify mineralization. Results Fibroblast growth factor-2 (FGF-2) had the greatest ability to induce proliferation after 24 hours of treatment when compared to transforming growth factor beta (TGFβ, insulin-like growth factor-1 (IGF-1), bone morphogenic protein (BMP-2), platelet derived growth factor (PDGF) or prostaglandin E2 (PGE2). We found that FGF-2 caused the most significant induction of ...
Cell proliferation assays are performed by four decades in cancer research to test the anti-proliferative activity of natural products and synthetic compounds in in vitro tumor models such as cell lines. However, current parameters used to quantify growth inhibition lead to a misinterpretation of results based on the exponential, and not linear, proliferation of cells in culture. We recently published in Journal of Cellular Physiology the development and experimental validation of a new parameter for the analysis of growth inhibition in proliferation assays, termed relative doubling capacity, that can be used to properly quantify the anti-proliferative activity of tested compounds in cell cultures and compare drug efficacy between distinct cell models. ...
[109 Pages Report] Check for Discount on Global Cell Proliferation Kit Sales Market Report 2017 report by QYResearch Group. In this report, the global Cell Proliferation Kit market is...
Definition of Cell proliferation with photos and pictures, translations, sample usage, and additional links for more information.
Figure 1: Effects of PKR on the proliferation and translation. (a) Effects of PKR on the proliferation of HeLa cells. After being transfected with plasmids PKR, PKR siRNA, or GFP, HeLa cells were plated in multiple wells of a 96-well plate and grown for 24 hr for cell proliferation assays. Cells from the sample preparations were collected for immunoblotting. Proliferation rate of the control sample was normalized to 100%. PKR, WT PKR; si-PKR, PKR siRNA; Ctrl, GFP. Upper panel, averaged data (N=4 ...
The master regulator p53 is a prominent tumor suppressor gene, functioning in the cell as a tetrameric (dimer of dimers) sequence-specific transcription factor, able to bind to two copies of a decameric sequence with the RRRCWWGYYY consensus (where R stands for a purine, W for A/T and Y for a pyrimidine) representing the so called p53-response element (p53-RE) [1]. p53 is known to be inducible in response to a large number of cellular stress signals that, besides genotoxic stress, include carbon and oxygen deficiencies, perturbations of the translation apparatus, excessive proliferation signals, alteration in microtubule dynamics [2, 3]. There are ,100 established p53 targets genes that link p53 to cell cycle arrest, apoptosis, DNA repair and inhibition of angiogenesis [3-6]. More recently, p53 was demonstrated to modulate the expression of genes able to modify glucose as well as lipid metabolism, induction of autophagy, immune responses and cell motility [7-11].. A direct role of p53 on the ...
Cell proliferation analyses are crucial for cell growth and differentiation studies, and are often used to evaluate both compound toxicity and inhibition of tumor cell growth during drug development. Proliferation measurements are typically based on average DNA content or cellular metabolism, or they quantify DNA synthesis.
Molecular mechanism of microRNA-93 in suppressing the cell proliferation of cervical cancer by adjusting the EGFR/AKT signal pathway, Xue Dong, Yan Wang
MicroRNA-331-3p promotes cell proliferation and invasion in breast cancer by targeting SRCIN1, Yonghua Hu, Wenjun Liu, Che Chen, Aihua Hou
Find and order buffers and products like this Ready-to-use Cell Proliferation Colorimetric Reagent, WST-1 on www.antibodies-onli... | Order product ABIN1304384.
Abstract: miRNA-221 was a carcinogenic factor in many cancers, however, it is limited that the correlation between miRNA-221 and progression of cervical cancer. So we here aimed to determine the function of miRNA-221 in cervical cancer proliferation and a
Concurrent in vivo proliferation and CTL activity by gB-specific CD8+ T cells in the PLNs after cutaneous infection with HSV-1. (A) CFSE-labeled lymph node cell
To determine the effect of protein treatments in cell proliferation, MDA-MB-231 breast cancer cells were first injected into the mammary fat pad of nude mice, and when tumors grew to 10 mm in diameter, mice were treated once only with purified Endo (20 mg/kg), CD (40 mg/kg), or EndoCD (60 mg/kg) proteins plus 500 mg/kg 5-FC, a clinically sufficient dose of 5-FU (15 mg/kg; 1× 5-FU), or 10 times the clinically sufficient dose (150 mg/kg; 10× 5-FU). The choice of 20 mg/kg Endo was based on a previous preclinical study (15) and is also within the dose tested in the phase I clinical trial (ref. 18; 15-600 mg/m2 in human is equivalent to 4.8-194.4 mg/kg in mouse; ref. 30). Tumors were harvested from mice 48 hours after treatment and labeled with bromodeoxyuridine (BrdU) antibody for in vivo BrdU incorporation analysis. The results show that EndoCD/5-FC most significantly reduced cancer cell proliferation (Fig. 2B) compared with all other treatment groups.. The potent inhibitory activity of ...
Trouvez tous les livres de Lam, Eric W-F - Phosphoinositide 3-Kinase Signalling Pathway: The Key to Cell Proliferation and Death. Sur eurolivre.fr,vous pouvez commander des livres anciens et neufs.COMPARER ET acheter IMMÉDIATEMENT au meilleur prix. 9781860946264
This inhibition concerns cell proliferation and the expression of IL-8, u-PA, and MMP - 9, which can AZD0530 proposes inhibit invasion of cancer cells in the
Gen5 allows measuring cell proliferation as both an end point and kinetic imaging assay and can be run with temperature and gas control.
A method for treating a disorder characterized by excessive cell proliferation in a patient by administering to the patient a therapeutically effective amount of sclareolide.
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Cells are structural and functional unit of our body that control and maintain the function of all unicellular and multicellular organisms
Liu, X., Go, M.-L. (2006-01-01). Antiproliferative properties of piperidinylchalcones. Bioorganic and Medicinal Chemistry 14 (1) : 153-163. [email protected] Repository. https://doi.org/10.1016/j.bmc.2005.08. ...
I do a proliferation assay after pulsing PBMCS with CFSE (5micromol for 2-10million cells) and then staining with CD3. I sort the cells and then stimulate them for proliferation with PHA(2microlitre). I also stain the cells with CD4 and CD8 on the day of analysis. I add PI jus before running the cells on the flow cytometer to discriminate for live vs dead cells.I am worried because I only get a single peak for each day (1-5 days expt). am i using too much CFSE? is that making it difficult to discern the peaks? Can somebody help with the trouble shooting. I also apply single compensation controls for the first day and find no spill for the rest of the days by using the same settings ...
I do a proliferation assay after pulsing PBMCS with CFSE (5micromol for 2-10million cells) and then staining with CD3. I sort the cells and then stimulate them for proliferation with PHA(2microlitre). I also stain the cells with CD4 and CD8 on the day of analysis. I add PI jus before running the cells on the flow cytometer to discriminate for live vs dead cells.I am worried because I only get a single peak for each day (1-5 days expt). am i using too much CFSE? is that making it difficult to discern the peaks? Can somebody help with the trouble shooting. I also apply single compensation controls for the first day and find no spill for the rest of the days by using the same settings ...
Cell labeling probes (both antibodies and non- antibodies) can be used in a number of applications, including cell cycle, apoptosis, viability, cell proliferation, cell movement. Check out our upgraded Cell Health and Proliferation webpage to learn more about how these reagents work and how they can aid you.
Full Text - Inducing cardiomyocyte proliferation is a hopeful approach for cardiac regeneration following myocardial infarction. Previous studies have shown that p21 inhibits the cardiomyocyte proliferation and cardiac regeneration. Deacetylation of p21 by Sirt1 deacetylase may reduce p21 abundance and remove p21-induced cell cycle arrest. However, whether p21 deacetylation and Sirt1 deacetylate control cardiomyocyte proliferation is unclear. Here, we show that acetylation of p21 induces cardiomyocyte proliferation arrest, whereas blocking the acetylation of p21 increases cardiomyocyte proliferation. P21 can be acetylated by Sirt1, and Sirt1 activate p21 ubiquitination through deacetylation. Additionally, overexpression of Sirt1 induces EdU-, pH3-, and Aurora B-positive cardiomyocytes in neonatal and adult mice. In contrast, depletion of Sirt1 reduces cardiomyocyte proliferation in vitro and in vivo. Moreover, Sirt1 protects cardiac function, reduces cardiac remodeling, inhibits
The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation ...
We have previously demonstrated, that 15 days after female rats pace the sexual interaction, there is an increase in the number of new cells that reach the granular cell layer (GrL) of the accessory olfactory bulb (AOB). The aim of the present study was to evaluate, if the first sexual experience in the female rat increases cell proliferation in the subventricular zone (SVZ) and the rostral migratory stream (RMS). We also tested if this behavior promotes the survival of the new cells that integrate into the main olfactory bulb (MOB) and AOB 45 days after the behavioral test. Sexually, naive female rats were injected with the DNA synthesis marker 5′-bromo-2′-deoxyuridine (BrdU) on the day of the behavioral test. They were randomly divided into the following groups: Female rats placed alone in the mating cage (1); Females exposed to amyl acetate odor [banana scent, (2)]; Females that could see, hear, and smell the male but physical contact was not possible [exposed to male, (3)]; Female rats that
Markers of crypt cell proliferation are frequently employed in studies of the impact of genetic and exogenous factors on human colonic physiology. Human studies often rely on the assessment of tissue acquired at endoscopy. Modulation of cell proliferation by bowel preparation with oral laxatives may confound the findings of such studies, but there is little data on the impact of commonly used bowel preparations on markers of cell proliferation. Crypt length, crypt cellularity and crypt cell proliferation were assessed in biopsies acquired after preparation with either Klean-Prep or Picolax. Crypt cell proliferation was assessed by whole-mount mitotic figure count, and by two different immunohistochemical (IHC) labelling methods (Ki-67 and pHH3). Subsequent biopsies were obtained from the same patients without bowel preparation and similarly assessed. Parameters were compared between groups using analysis of variance and paired t-tests. There were significant differences in labelling indices (LI) between
Tumor cell metastasis and proliferation are crucial for tumor development and result in loss of life of tumor individuals. TLR4 signaling pathway. It offers fresh insights for the systems of tumor advancement and metastasis, and suggests targeting TLR4 and OPN as an intervention in the ovarian cancer treatment. proliferation activity of tumor cells. Without LPS stimulation, the proliferation activity of tumor cells increased during 12 h. The cell proliferation significantly changed by LPS stimulation, and the maximum absorbance value at 429 nm was present after 6 h, with a proliferation rate of approximately 137.1% compared to cells without stimulation (Figure 2AC2B). To investigate the effect of TLR4 signal block on cell proliferation, the TLR4 inhibitor TAK-242 was used. The LPS-stimulated increase in the proliferation of tumor cells was significantly reduced with TAK-242 pretreatment, whereas no significant change was observed in cells treated with TAK-242 alone (Figure ?(Figure2C).2C). These ...
PC cell-derived growth factor (PCDGF), also called epithelin/granulin precursor (GEP), is an 88-kDa secreted glycoprotein with the ability to stimulate cell proliferation in an autocrine fashion. In addition, some studies indicated that PCDGF participated in invasion, metastasis and survival of cancer cells by regulating cell migration, adhesion and proliferation. Yet the effects of PCDGF on proliferation and invasion of ovarian cancer cells in vitro and the mechanisms by which PCDGF mediates biological behaviors of ovarian cancer have rarely been reported. In the present study we investigated whether and how PCDGF/GEP mediated cell proliferation and invasion in ovarian cancer. PCDGF/GEP expression level in three human ovarian cancer cell lines of different invasion potential were detected by RT-PCR and western blot. Effects of inhibition of PCDGF expression on cell proliferation and invasion capability were determined by MTT assay and Boyden chamber assay. Expression levels of cyclin D1 and CDK4 and
Regulation of mRNAs is one way to control protein levels and thereby important cellular processes such as growth, invasion and apoptosis. G3BPs constitute a family of mRNA-binding proteins, shown to be overexpressed in several cancer types, including breast, colon and pancreas cancer. G3BP has been reported to both stabilize and induce degradation of specific mRNAs. Here, we show that G3BP1, but not G3BP2, supports proliferation of several breast cancer cell lines. Global gene expression analyses of G3BP1- and G3BP2-depleted cells indicate that primarily G3BP1, and much less G3BP2, influences mRNA expression levels. Peripheral myelin protein 22 (PMP22) was one gene that was significantly influenced by G3BP1 depletion which led to a 2-3 fold increased expression. Depletion of PMP22 resulted in increased proliferation and the G3BP1-mediated effect on proliferation was not seen upon PMP22-depletion. This indicates a novel role for G3BP1 in the regulation of cell proliferation in breast cancer cells,
KDM5c is a histone demethylase that specifically demethylates trimethylated and dimethylated H3 Lys-4 to play a central role in transcriptional repression. C-Jun is a proto-oncogene and promotes cell proliferation when ectopically accumulated, but can be ubiquitinated by SCF (FBXW7), leading to its degradation. FBXW7 is an E3 ubiquitin ligase of c-Jun, and exhibits carcinostasis in colon cancer. Here, we report that overexpression of KDM5c in human colon cancer cells results in attenuated FBXW7 transcription and accumulated c-Jun protein, leading to increased proliferation of colon cancer cells. We show that overexpression of KDM5c can result in increased c-Jun protein levels and decreased ubiquitin levels, with no significant change in mRNA levels of c-Jun. KDM5c overexpression blocks the ubiquitin-proteasome proteolytic pathway of c-Jun by down-regulating the expression of FBXW7. KDM5c down-regulation of FBXW7 occurs by demethylation of H3K4me3 at TSS and downstream of the FBXW7 gene. And interaction
Various assays, using different strategies, are available for assessing cultured cell proliferation. These include measurement of metabolic activity (tetrazolium salts and alamarBlue), DNA quantification using fluorophores (Hoechst 33258 and PicoGreen), uptake of radioactively-labeled DNA precursors such as [3H]thymidine, and physical counting (hemocytometer). These assays are well established in characterizing cell proliferation in two-dimensional (2D), monolayer cultures of low cell densities. However, increasing interest in 3D cultures has prompted the need to evaluate the effectiveness of using these assays in high cell density or 3D cultures. We show here that typical cell proliferation assays do not necessarily correlate linearly with increasing cell densities or between 2D and 3D cultures, and are either not suitable or only rough approximations in quantifying actual cell numbers in a culture. Prudent choice of techniques and careful interpretation of data are therefore recommended when ...
p,Here, we ask how neural stem cells (NSCs) transition in the developing neocortex from a rapidly to a slowly proliferating state, a process required to maintain lifelong stem cell pools. We identify LRIG1, known to regulate receptor tyrosine kinase signaling in other cell types, as a negative regulator of cortical NSC proliferation. LRIG1 is expressed in murine cortical NSCs as they start to proliferate more slowly during embryogenesis and then peaks postnatally when they transition to give rise to a portion of adult NSCs. Constitutive or acute loss of Lrig1 in NSCs over this developmental time frame causes stem cell expansion due to increased proliferation. LRIG1 controls NSC proliferation by associating with and negatively regulating the epidermal growth factor receptor (EGFR). These data support a model in which LRIG1 dampens the stem cell response to EGFR ligands within the cortical environment to slow their proliferation as they transition to postnatal adult NSCs.,/p,. ...
TY - JOUR. T1 - α-1 Adrenergic receptors stimulation induces the proliferation of neural progenitor cells in vitro. AU - Hiramoto, Takeshi. AU - Ihara, Yoshiaki. AU - Watanabe, Yasuhiro. PY - 2006/11/6. Y1 - 2006/11/6. N2 - The proliferation of neural progenitor cells (NPCs) is regulated by classical neurotransmitters such as dopamine, serotonin and acetylcholine, via its own receptors. Previous studies have reported that the depletion of l-norepinephrine decreases the proliferation of NPCs in the adult rat hippocampus and it has been suggested that l-norepinephrine regulates the proliferation of NPCs. However, it remains unknown whether or not adrenergic receptors are involved in the increased proliferation of NPCs. In the present study, an MTT cell proliferation assay was carried out in order to investigate the roles played by adrenergic receptors in the proliferation of NPCs. We demonstrated that l-epinephrine enhanced the proliferation of embryonic NPCs in vitro. In addition, the α-1 ...
TY - JOUR. T1 - Conflicting evidence for the role of JNK as a target in breast cancer cell proliferation. T2 - comparisons between pharmacological inhibition and selective shRNA knockdown approaches. AU - Wood, Rachel A.. AU - Barbour, Mark J.. AU - Gould, Gwyn W.. AU - Cunningham, Margaret R.. AU - Plevin, Robin J.. N1 - © 2017 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.. PY - 2018/2/28. Y1 - 2018/2/28. N2 - As a target, the JNK pathway has been implicated in roles including cell death, proliferation, and inflammation in variety of contexts which span cardiovascular disease, neurodegenerative pathologies, and cancer. JNK1 and JNK2 have recently been demonstrated to function independently, highlighting a new parameter in the study of the JNK pathway. In order for JNK1 and JNK2-specific roles to be defined, better tools need to be employed. Previous ...
OBJECTIVE: This study explored the effect of miR-26a-5p on cell proliferation, migration, and invasion in gastric cancer by targeting COL10A1. MATERIALS
ADSCs are a promising candidate for clinical applications. They are easily derived from adipose tissue, with strong proliferation potential. Compared with other sources of MSCs such as bone marrow, umbilical cord and umbilical cord blood, ADSCs have a shorter doubling time. Therefore, numerous studies on ADSCs, especially on ADSC in vitro proliferation, have been performed to date. To date, hypoxia has been applied on stem cell cultures including ADSC culture. This study aimed to evaluate the effects of hypoxia on ADSC proliferation.. First, ADSCs were successfully isolated and confirmed by usual methods and assays. Similarly to previous studies, the obtained ADSCs fully exhibited several MSCs characteristics, including adherence to the surface of plastic flasks with a fibroblast-like shape; they also successfully differentiated into three kinds of mesoderm cells including adipocytes, osteoblasts and chondroblasts. Flow cytometry analysis with surface markers revealed that they expressed ...
F the soft agar colony formation in comparison with vector control cells exposed to arsenite for eight weeks. A single explanation of these information is the
Measurement of cell proliferation is necessary for testing the effects of pharmacological agents or growth factors, assessing cytotoxicity or investigating circumstances of cell activation. In a cell proliferation assay, the increase in number of cells or change in the proportion of cells that is dividing is assessed. Trevigen® offers a Calcein-AM based kit to determine cell viability as well as the tetrazolium salts MTT and XTT metabolic cell proliferation assay kits.. ...
Cell proliferation is a process of increasing cell number, including cell development and cell division [46]. This intern responsible to increase in cell mass and ultimately the organism development. In certain cells, proliferation is restricted while it remains continue in some of the cells throughout lifetime. In certain situation cell proliferation becomes abnormal which further augment the tumor cell formation [40]. In the body, cell proliferation process is highly regulated by cell division and apoptosis [2]. Apoptosis is programmed cell death mechanism that destroys unwanted cells and also involved in defense mechanism of the body. It also plays a role in morphological and cellular mechanisms of cell, caspases functioning, translocation of phosphatidyl serine and DNA fragmentation [43, 47]. This complex process comprises intrinsic pathway and extrinsic pathway which are also called as mitochondrial pathway and cytoplasmic pathway or death receptor pathway, respectively (Fig. 4) [5]. In ...
This paper represents a study on the effect of electrical pulses on adult stem cells, especially on proliferation control and also as a method of deliverin
TY - JOUR. T1 - Tumor growth dynamics with nutrient limitation and cell proliferation time delay. AU - Alsheri, Ahuod. AU - Alzahrani, Ebraheem O.. AU - Asiri, Asim. AU - El-Dessoky, Mohamed M.. AU - Kuang, Yang. PY - 2017/12/1. Y1 - 2017/12/1. N2 - It is known that avascular spherical solid tumors grow monotonically, often tends to a limiting final size. This is repeatedly confirmed by various mathematical models consisting of mostly ordinary differential equations. However, cell growth is limited by nutrient and its proliferation incurs a time delay. In this paper, we formulate a nutrient limited compartmental model of avascular spherical solid tumor growth with cell proliferation time delay and study its limiting dynamics. The nutrient is assumed to enter the tumor proportional to its surface area. This model is a modification of a recent model which is built on a two-compartment model of cancer cell growth with transitions between proliferating and quiescent cells. Due to the limitation of ...
The Wnt signal pathway is composed of β-catenin and transcriptional factor TCF-4 (2 , 3 , 19, 20, 21) . These factors activate the target genes that preserve the consensus motif (A/TA/TCAAAG) for TCF-4 binding in the promoter region (6) . Recent studies have shown that cyclin D1, c-myc, MMP7, and c-jun could be target genes for the Wnt signal pathway (7, 8, 9, 10) . Therefore, Wnt signal may induce cell proliferation through activation of these target genes (22, 23, 24, 25) . To our knowledge, there is no report on RCCs regarding the significance of the Wnt signal factors in cell proliferation and/or apoptosis through regulation of downstream target genes. In this study, we evaluated the significance of the Wnt signal pathway in RCC through the analysis of cyclin D1, c-myc, MMP7, and c-jun in relation to β-catenin and TCF-4 alterations.. TCF-4 expression has been intensively investigated in the epithelium of the gastrointestinal tract (26 , 27) , and the presence of splicing isoforms in TCF-4 ...
Transforming growth factor-β (TGF-β) plays an important role in regulating hematopoiesis, inhibiting proliferation while stimulating differentiation when appropriate. We previously demonstrated that the type III TGF-β receptor (TβRIII, or betaglycan) serves as a novel suppressor of cancer progression in epithelial tumors; however, its role in hematologic malignancies is unknown. Here we demonstrate that TβRIII protein expression is decreased or lost in the majority of human multiple myeloma specimens. Functionally, restoring TβRIII expression in myeloma cells significantly inhibited cell growth, proliferation, and motility, largely independent of its ligand presentation role. In a reciprocal fashion, shRNA-mediated silencing of endogenous TβRIII expression enhanced cell growth, proliferation, and motility. Although apoptosis was not affected, TβRIII inhibited proliferation through induction of the cyclin-dependent kinase inhibitors p21 and p27. TβRIII further regulated myeloma cell ...
Genome-wide mutant strain collections have increased demand for high throughput cellular phenotyping (HTCP). For example, investigators use HTCP to investigate interactions between gene deletion mutations and additional chemical or genetic perturbations by assessing differences in cell proliferation among the collection of 5000 S. cerevisiae gene deletion strains. Such studies have thus far been predominantly qualitative, using agar cell arrays to subjectively score growth differences. Quantitative systems level analysis of gene interactions would be enabled by more precise HTCP methods, such as kinetic analysis of cell proliferation in liquid culture by optical density. However, requirements for processing liquid cultures make them relatively cumbersome and low throughput compared to agar. To improve HTCP performance and advance capabilities for quantifying interactions, YeastXtract software was developed for automated analysis of cell array images. YeastXtract software was developed for kinetic growth
Genome-wide mutant strain collections have increased demand for high throughput cellular phenotyping (HTCP). For example, investigators use HTCP to investigate interactions between gene deletion mutations and additional chemical or genetic perturbations by assessing differences in cell proliferation among the collection of 5000 S. cerevisiae gene deletion strains. Such studies have thus far been predominantly qualitative, using agar cell arrays to subjectively score growth differences. Quantitative systems level analysis of gene interactions would be enabled by more precise HTCP methods, such as kinetic analysis of cell proliferation in liquid culture by optical density. However, requirements for processing liquid cultures make them relatively cumbersome and low throughput compared to agar. To improve HTCP performance and advance capabilities for quantifying interactions, YeastXtract software was developed for automated analysis of cell array images. YeastXtract software was developed for kinetic growth
Lack of IGF2 in mice results in diminished embryonic growth due to diminished cell proliferation. Here we show that mouse embryonic fibroblasts lacking the RNA-binding protein IMP1 (IGF2 mRNA-binding protein 1) have defective splicing and translation of IGF2 mRNAs, markedly reduced IGF2 polypeptide production, and diminished proliferation. The proliferation of the IMP1-null fibroblasts can be restored to wild-type levels by IGF2 in vitro or by re-expression of IMP1, which corrects the defects in IGF2 RNA splicing and translation. The ability of IMP1 to correct these defects is dependent on IMP1 phosphorylation at Ser181, which is catalyzed cotranslationally by mTOR complex 2 (mTORC2). Phosphorylation strongly enhances IMP1 binding to the IGF2-leader 3 5 untranslated region, which is absolutely required to enable IGF2-leader 3 mRNA translational initiation by internal ribosomal entry. These findings uncover a new mechanism by which mTOR regulates organismal growth by promoting IGF2 production in ...
Visit CellSignal.com to view our Cellular Assay Kits materials including Cell Proliferation Assays & more. CST - Customer satisfaction is our highest priority.
Visit CellSignal.com to view our Cellular Assay Kits materials including Cell Proliferation Assays & more. CST - Customer satisfaction is our highest priority.
Visit CellSignal.com to view our Cellular Assay Kits materials including Cell Proliferation Assays & more. CST - Customer satisfaction is our highest priority.
Fibulins not only function as molecular bridges within the cellular microenvironment but also influence cell behavior. Thus, fibulins may contribute to create a permissive microenvironment for tumor growth but can also stimulate different mechanisms that may impede tumor progression. This is the case with Fibulin-5, which has been shown to display both tumor-promoting and tumor-protective functions by mechanisms that are not totally defined. We show new evidence on the tumor-protective functions displayed by Fibulin-5 in MCF-7, T47D and MDA-MB-231 breast cancer cells including the inhibition of invasion and proliferation capacity and hampering the ability to form mammospheres. Reduction in the level of phosphorylation of Ser residues involved in the nuclear translocation of β-catenin may underlie these antitumor effects. We also found that Fibulin-5 reduces the level of expression of Ki-67, a nuclear protein associated with cell proliferation. Moreover, reduction in Fibulin-5 expression ...
The present study, to the best of the authors knowledge, demonstrated for the first time, that miR-614 was upregulated in OC clinical tissues and cells. Increased expression of miR-614 led to the promotion of cell proliferation and colony-forming abilities, and conversely, decreased the apoptotic rate of OC cells. Additionally, PPP2R2A may act as a novel target of miR-614. The present study indicated that miR-614 may act as a novel tumor promoter in OC by targeting PPP2R2A.. Accumulating evidence suggests that miRNAs exhibit an essential role in human cancer pathological proceedings via controlling different target genes, including those involved in cell proliferation, migration, invasion, cycle and apoptosis (15-18). Dysregulation of miRNA frequently occurs in novel types of cancers, including ovarian cancer. miR-21-3p inhibits cell proliferation and invasion of ovarian cancer by targeting RNA binding protein with multiple splicing, RCC1 and BTB domain containing protein 1 and Zinc finger ...
miRNAs are emerging as critical regulators in carcinogenesis and tumor progression. Recently, microRNA-122 (miR-122) has been proved to play an important role in hepatocellular carcinoma, but its functions in the context of breast cancer (BC) remain unknown. In this study, we report that miR-122 is commonly downregulated in BC specimens and BC cell lines with important functional consequences. Overexpression of miR-122 not only dramatically suppressed cell proliferation, colony formation by inducing G1-phase cell-cycle arrest in vitro, but also reduced tumorigenicity in vivo. We then screened and identified a novel miR-122 target, insulin-like growth factor 1 receptor (IGF1R), and it was further confirmed by luciferase assay. Overexpression of miR-122 would specifically and markedly reduce its expression. Similar to the restoring miR-122 expression, IGF1R downregulation suppressed cell growth and cell-cycle progression, whereas IGF1R overexpression rescued the suppressive effect of miR-122. To identify
Both cell proliferation and cell size control are fundamental biological processes that must be carefully orchestrated, and dysregulation of either can lead to diseases such as cancer. In contrast to our understanding of the mechanisms that control cell proliferation, less is known about the mechanisms that control cell size and, particularly, the mechanisms by which cell proliferation and cell size are coordinately regulated. Recently, we identified a novel protein named FIP200, which plays an important role in the regulation of cell cycle progression (Abbi et al., 2002). In this study, we showed that FIP200 can also regulate cell size through interaction with the TSC1-TSC2 complex and activation of S6K. These results identify FIP200 as a regulator that plays roles in both cell proliferation and cell size control.. Most other proteins known to play roles in both cell proliferation and cell size usually regulate these two cellular processes in a similar manner. For example, PTEN can inhibit cell ...
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Ng F, Ye J, et al. PERK promotes cancer cell proliferation and tumor development by limiting oxidative DNA harm. Oncogene 29: 38813895. 42. Min L, Ji Y, Bakiri
Antibodies for proteins involved in positive regulation of B cell proliferation pathways, according to their Panther/Gene Ontology Classification
Supervisor: Golnar Kolahgar. The intestinal epithelium constantly regenerates from stem cells, which adjust their behaviour to the changing physiological conditions the gut is exposed to. For example, stem cell proliferation rates can transiently increase to speed up regeneration after tissue loss or in response to the diet, before reverting to steady-state levels once correct tissue size is reached. This plasticity is essential for intestinal function, as lack of regeneration causes tissue atrophy whereas unrestricted stem cell proliferation promotes cancer. We use the genetically tractable Drosophila gut to identify the secreted and physical factors regulating gut plasticity. In particular, we use targeted genetic screens and functional analyses, to identify novel extracellular signalling molecules regulating cell proliferation in contexts that trigger reversible changes in gut size. As the regulation of intestinal proliferation is largely conserved between Drosophila and mammals this work has ...
Reduction of Prep1 Levels Affects Differentiation of Normal and Malignant B Cells and Accelerates Myc Driven Lymphomagenesis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Background: Cisplatin, a DNA damaging agent, induces apoptosis through increasing DNA fragmentation.However, identification of intrinsic resistance molecules against Cisplatin is vital to estimate the success of therapy.Bag-1 (Bcl-2-associated anthanogene) is one anti-apoptotic protein involved in drug resistance impacting ontherapeutic efficiency. Elevated levels of this protein are related with increase cell proliferation rates, motilityand also cancer development. For this reason, we aimed to understand the role of Bag-1 expression in Cisplatininducedapoptosis in HeLa cervix cancer cells. Cisplatin decreased cell viability in time- and dose-dependentmanner in wt and Bag-1L+HeLa cells. Although, 10μM Cisplatin treatment induced cell death within 24h byactivating caspases in wt cells, Bag-1L stable transfection protected cells against Cisplatin treatment. To assess thepotential protective role of Bag-1, we first checked the expression profile of interacting anti-apoptotic partners ofBag-1. We found
RESULTS: 775 genes were differentially expressed and clustered in terms of their growth factor responsiveness. As well as identifying uncharacterized genes as novel targets of ErbB2-dependent signalling, ErbB2 overexpression augmented the induction of multiple genes involved in proliferation (e.g. MYC, MAP2K1, MAP2K3), autocrine growth factor signalling (VEGF, PDGF) and adhesion/cytoskeletal regulation (ZYX, THBS1, VCL, CNN3, ITGA2, ITGA3, NEDD9, TAGLN), linking them to the hyper-poliferative and altered adhesive phenotype of the ErbB2-overexpressing cells. We also report ErbB2-dependent down-regulation of multiple interferon-stimulated genes that may permit ErbB2-overexpressing cells to resist the anti-proliferative action of interferons. Finally, IGFBP3 was unique in its pattern of regulation and we further investigated a possible role for IGFBP3 down-regulation in ErbB2-dependent transformation through suppressed IGF1 signalling. We show that IGF1-dependent signalling and proliferation were ...
The application discloses novel 2-alkoxyestradiol analogs which exhibit anti-proliferative properties, and methods of making and using such compounds to inhibit undesired cell proliferation and tumor growth. Additionally, methods are disclosed of treating diseases associated with undesired angiogenesis and undesired proliferation, and methods of treating infectious disease wherein the infectious agent is particularly susceptible to inhibition by agents that disrupt microtubule organization and function.
目的:探讨反义脱氧寡核苷酸封闭HSP70基因对体外宫颈癌 HeLa 细胞增殖、凋亡及化疗敏感性的影响。方法:1)将体外培养的宫颈癌 HeLa 细胞分为正常对照组(Ctrl组)、反义寡核苷酸处理组(AS组)、正义寡核苷酸处理组(S组)、随机寡核苷酸处理组(R组),每组各5例,分别转染体外培养的宫颈癌 HeLa 细胞,采用Western免疫印迹检测各组细胞HSP70蛋白表达。2)将顺铂处理体外培养的宫颈癌 HeLa 细胞分为正常对照组(Ctrl组)、单纯顺铂处理组(Cis组)、反义寡核苷酸+顺铂处理组(AS +Cis组)、正义寡核苷酸+顺铂处理组(S +Cis组)、随机寡核苷酸+顺铂处理组 (R +Cis组),每组各8例。采用四甲基偶氮唑蓝光吸收法(methyl thiazolyl tetrazolium,MTT) 法检测 HeLa 细胞的生长抑制率; 流式细胞术检测 HeLa 细胞的凋亡率。结果:1)Ctrl组、AS组、S组、R组HSP70灰度比值分别为1.365±0.187,0.379±0.134,1.403±0.163和1.410±0
One potential model of type 2 diabetes etiology is that those with the disease were born with less β-cell mass making them susceptible to stressors such as obesity. Thus, it would be of therapeutic potential to find mechanisms that increase functional β-cell mass. One candidate that has been studied in our lab is Connective tissue growth factor (Ctgf). Ctgf is a secreted protein known to be involved in cell adhesion, migration and, in some cell types, proliferation. Previous studies in our lab have shown that Ctgf is crucial for β-cell development, with loss of Ctgf resulting in fewer β-cells and decreased β-cell proliferation, thus decreased β-cell mass at birth. Ctgf is also important in situations of metabolic stress, such as pregnancy or β-cell loss. Haploinsufficiency during pregnancy results in decreased maternal β-cell proliferation while in contrast, over-expression of Ctgf results in increased β-cell proliferation and regeneration in a model of partial β-cell ablation. ...
MTT Cell Proliferation and Cytotoxicity Assay Kit, For quantitation of viable cell number in proliferation and cytotoxicity assays
Oncotarget | https://doi.org/10.18632/oncotarget.26824 Francisca Guardiola-Serrano, Roberto Beteta-Göbel, Raquel Rodríguez-Lorca, Maitane Ibarguren, David J. López, Silvia Terés, María Alonso-Sande, Mónica...