Effect of miR-503 Down-Regulation on Growth and Invasion of Esophagus Carcinoma and Related Immune Function - Order reprints #895518
Xie, W., Xie, H., Liu, F., Li, W., Dan, J., Mei, Y., Dan, L., Xiao, X., Li, J. and Chen, X. (2013), Propranolol induces apoptosis of human umbilical vein endothelial cells through downregulation of CD147. British Journal of Dermatology, 168: 739-748. doi: 10.1111/bjd.12193 ...
Dr. Katzmanns Protein Sorting and Receptor Downregulation Lab at Mayo Clinic looks at ESCRTs and associated factors facilitate the MVB sorting process.
(KudoZ) English to Portuguese translation of marked down-regulation: regulação descendente marcante, regulação descendente acentuada [Medical (general) (Medical)].
TY - JOUR. T1 - Tiazofurin down-regulates expression of c-Ki-ras oncogene in a leukemic patient. AU - Weber, G.. AU - Nagai, M.. AU - Natsumeda, Y.. AU - Eble, J. N.. AU - Jayaram, H. N.. AU - Paulik, E.. AU - Zhen, W.. AU - Hoffman, R.. AU - Tricot, G.. PY - 1991/1/1. Y1 - 1991/1/1. UR - http://www.scopus.com/inward/record.url?scp=0025806199&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0025806199&partnerID=8YFLogxK. M3 - Article. C2 - 1705812. AN - SCOPUS:0025806199. VL - 3. SP - 61. EP - 66. JO - Oncology Research. JF - Oncology Research. SN - 0965-0407. IS - 3. ER - ...
The antileukemic effect of inhibiting bromodomain and extra-terminal domain-containing (BET-containing) proteins (BETPs) such as BRD4 has largely been largely attributed to transcriptional downregulation of cellular anabolic and antiapoptotic processes, but its effect on the bone marrow microenvironment, a sanctuary favoring the persistence of leukemic stem/progenitor cells, is unexplored. Sustained degradation of BETP with the small-molecule BET proteolysis-targeting chimera (PROTAC) ARV-825 resulted in a marked downregulation of surface CXCR4 and CD44, key proteins in leukemia-microenvironment interactions, in acute myeloid leukemia (AML) cells. Abrogation of surface CXCR4 expression impaired SDF-1α-directed migration and was mediated through transcriptional downregulation of PIM1 kinase, which in turn phosphorylates CXCR4 and facilitates its surface localization. Downregulation of CD44, including isoforms CD44v8-10 impaired cystine uptake, lowered intracellular reduced glutathione, and ...
The antileukemic effect of inhibiting bromodomain and extra-terminal domain-containing (BET-containing) proteins (BETPs) such as BRD4 has largely been largely attributed to transcriptional downregulation of cellular anabolic and antiapoptotic processes, but its effect on the bone marrow microenvironment, a sanctuary favoring the persistence of leukemic stem/progenitor cells, is unexplored. Sustained degradation of BETP with the small-molecule BET proteolysis-targeting chimera (PROTAC) ARV-825 resulted in a marked downregulation of surface CXCR4 and CD44, key proteins in leukemia-microenvironment interactions, in acute myeloid leukemia (AML) cells. Abrogation of surface CXCR4 expression impaired SDF-1α-directed migration and was mediated through transcriptional downregulation of PIM1 kinase, which in turn phosphorylates CXCR4 and facilitates its surface localization. Downregulation of CD44, including isoforms CD44v8-10 impaired cystine uptake, lowered intracellular reduced glutathione, and ...
In addition to initiating signaling events, the activation of cell surface receptors also triggers regulatory processes that restrict the duration of signaling. Acute attenuation of signaling can be accomplished either via ligand-induced internalization of receptors (endocytic downregulation) or via ligand-induced receptor desensitization. These phenomena have traditionally been viewed in the context of adaptation wherein the receptor system enters a refractory state in the presence of sustained ligand stimuli and thereby prevents the cell from over-responding to the ligand. Here we use the epidermal growth factor receptor (EGFR) and G-protein coupled receptors (GPCR) as model systems to respectively examine the effects of downregulation and desensitization on the ability of signaling receptors to decode time-varying ligand stimuli. Using a mathematical model, we show that downregulation and desensitization mechanisms can lead to tight and efficient input-output coupling thereby ensuring synchronous
By default, all articles on GreenMedInfo.com are sorted based on the content type which best reflects the data which most users are searching for. For instance, people viewing substances are generally most interested in viewing diseases that these substances have shown to have positive influences. This section is for allowing more advanced sorting methods. Currently, these advanced sorting methods are available for members only. If you are already a member, you can sign in by clicking here. If you do not currently have a user account, and would like to create one/become a member, click here to begin the singup process ...
5-HT1a and 5-ht7 receptors The functional need for 5-HT1A and 5-HT7 receptors dimerization is continues to be revised (Matthys et al., 2011; Gellynck et al., 2013; Herrick-Davis, 2013); indicating that it differentially regulates receptor signaling and trafficking (Renner et al., 2012). But nonetheless we have no idea the implications of the in storage formation and amnesic circumstances; hence, the analysis of signaling linked to 5-HT7 receptor in memory space development, amnesia and forgetting may provide significant insights (Meneses, 2014a,b). For example, as the association of 5-HT7 receptor activation, improved memory space and improved cAMP appears to be dependable findings; certainly elements such as for example differential rules of hippocampal manifestation aswell as individual variations might be essential (observe Meneses, 2013). Furthermore, a biphasic and brain-region selective down-regulation of cAMP concentrations is definitely observed assisting object acknowledgement in the ...
Oncogenic Ras downregulates CD24 expression in NIH/3T3 cells. CD24 mRNA expression in vector control (Control) and RasV12 cells was determined by (A) RT-PCR and
title: Role of targeting integrin-linked kinase in suppression of invasion and metastasis through downregulation of epithelial to mesenchymal transition in renal cell carcinoma, doi: none, category: Thesis
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 ...
when a ligan binds, the signal produced by the liogand must be stopped. one way is receptor downregulation, in which the receptor is internalized and degraded in the lysosome ...
I have more to say on some of the ensuing discussion on the direction of causality when I procure some other references, but for now lets fast forward a bit. Taubes goes on to describe metabolic adaptation, regulation and homeostasis. The implication he makes in this discussion is that human metabolism is extremely varied and adaptable. Yes, there are differences due to hormonal levels (e.g. hypothyroidism is a basic example), and different macronutrients elicit different thermogenic effects, but there are limits. Hormonal signals can downregulate metabolism, lower body temp, etc. But theres only so far this can go ... or we die! By the same token, overfeeding studies have demonstrated time and again that whatever signalling and adaptations (futile cycling) may occur in response cannot prevent considerable weight gain. Taubes basically implies that no matter what we may do consciously to (a) maintain caloric balance, (b) induce positive caloric balance, or (c) induce a caloric deficit, our ...
Down-regulation of Akt1 in IGF-IR cells induces migration and EMT. (A, top) The motility of IGF-IR cells with isoform-specific down-regulation of Akt was assess
Oncotarget | https://doi.org/10.18632/oncotarget.1174 Xu Di, Guofeng Zhang, Yaqin Zhang, Kazuyo Takeda, Leslie A. Rivera Rosado, Baolin Zhang
Book now at Article One - American Grill in Washington, explore menu, see photos and read 217 reviews: A very nice atmosphere. We did, however, have to contend with a screaming baby at the front desk. Otherwise, the staff was very polite and attentive.
TY - JOUR. T1 - PPARα is down-regulated following liver transplantation in mice. AU - Nakagawa, Kan. AU - Tanaka, Naoki. AU - Morita, Miwa. AU - Sugioka, Atsushi. AU - Miyagawa, Shin Ichi. AU - Gonzalez, Frank J.. AU - Aoyama, Toshifumi. PY - 2012/3. Y1 - 2012/3. N2 - Background & Aims: Graft dysfunction is one of the major complications after liver transplantation, but its precise mechanism remains unclear. Since steatotic liver grafts are susceptible to post-transplant dysfunction, and peroxisome proliferator-activated receptor (PPAR) α plays an important role in the maintenance of hepatic lipid homeostasis, we examined the role of PPARα in liver transplantation. Methods: Livers were harvested from Sv/129 wild-type (Ppara +/+) mice and PPARα-null (Ppara -/-) mice and transplanted orthotopically into syngeneic Ppara +/+ mice. Results: Hepatocellular damage was unexpectedly milder in transplanted Ppara -/- livers compared with Ppara +/+ ones. This was likely due to decreased lipid peroxides ...
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Our recent work established the essential role of β-arrestin in the internalization of the M2 mAChR [9]. The present study extends the observations of previous work and demonstrates that the agonist-promoted down-regulation of M1 and M2 mAChRs is β-arrestin dependent, and that the ubiquitination pattern of β-arrestin has a critical role in the differential down-regulation for M1 vs M2 mAChRs.. It has been previously established in a variety of cell lines that a prolonged activation of M1 or M2 mAChRs induces receptor down-regulation. In agreement with these findings, long-term stimulation of M1 or M2 mAChRs induced receptor down-regulation with the M1 mAChR showing significantly more down-regulation than M2 subtype. This observation suggests that the two subtypes are differentially regulated by endogenous β-arrestins. No down-regulation of either mAChR subtype occurred in the absence of β-arrestin and either β-arrestin subtype was able to rescue receptor down-regulation.. The observations ...
Sustained endotoxemia leads to marked down-regulation of early steps in the insulin-signaling cascade. Crit Care Med. 2001 Apr; 29(4):839-46 ...
The disialoganglioside GD3 plays a major role in proliferation, differentiation, and apoptosis. It has been reported that ganglioside GD3 can induce apoptosis through bcl-2 mediated mitochondrial pathway. However, the relationship between ganglioside GD3 and B-cell/CLL lymphoma 2 (Bcl-2) is not full …
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PARACTIN®: is a patented extract of Andrographis Paniculata (containing Andrographolide, 14-Deoxyandrographolides, and Neoandrographolides). Multiple double-blind randomized controed trials (RTC) published in PubMed demonstrated that PARACTIN® reduces the activity of COX-2 enzyme and nproduction of TNF-α, IL-6, IL-1βand IL-10 through selective down-regulation of the genes involved in immune and inflammation processes ((TNFSF14, TNF, TNFRSF6, and IL1A, CCL8 and CXCL11, JAK3 and STAT5A, TLR4 and TLR8 and NF-κB). By inhibiting Nuclear Factor kappa B (NFkB) and other genes that participate in the inflammatory cascade, PARACTIN® inhibits the production of a range of pro-inflammatory cytokines and interleukins (signaling proteins used by our immune system) and other markers of inflammation (ESR, CRP, IgA, Rheumatoid factor) and modulates the dysregulated immune response. Studies showed that it is safe and as effective as NSAIDs or DMARDs for treating acute as we as ...
In chronic heart failure (HF), sympathetic nervous system overdrive induces the upregulation of G-protein-coupled receptor kinase 2 (GRK2) with a consequent β-adrenergic receptor downregulation/desensitization. Importantly, in failing myocardium, β-adrenergic receptor dysregulation is clinically seen by loss of inotropic reserve. Currently, β-blockers represent a solid pillar of HF therapy that at the molecular level efficiently counteracts both β-adrenergic receptor downregulation and GRK2 upregulation. GRK2 inhibition represents a promising new strategy to rescue the failing heart, and we have recently demonstrated that in some animal models, it could be used as a substitute for or in conjunction with β-blockers. GRK2 inhibition may be effective by interfering with other intracellular processes. The present study provides the first evidence of a direct and GRK2-dependent interaction between the β1-adrenergic receptor and the sphingosine-1-phosphate receptor 1 (S1PR1). We show that the ...
Activating transcription factor-3 (ATF3) is involved in the complex process of cellular stress response. However, its exact role in cancer is discussed controversially because both tumor suppressive and oncogenic effects have been described. Here we followed-up on our previous observation that inhibition of Hsp90 may increase ATF3 expression and sought to determine the role of ATF3 in colon cancer. Regulation of ATF3 was determined in cancer cells using signaling inhibitors and a heat-shock protein-90 (Hsp90) antagonist. Human HCT116 cancer cells were stably transfected with an ATF3-shRNA or a luciferase-shRNA expression plasmid and alterations in cell motility were assessed in migration assays. The impact of ATF3 down-regulation on cancer growth and metastasis were investigated in a subcutaneous tumor model, a model of hepatic tumor growth and in a model of peritoneal carcinomatosis. Human colon cancer tissues were analyzed for ATF3 expression. The results show that therapeutic Hsp90 inhibition
This study further elucidates the role of CYP33 in gene transcription by studying the effects of CYP33 overexpression and siRNA-mediated down-regulation on the expression of MLL target genes such as c-MYC, p21, p27, and HOXA9. CYP33 is a cis-trans prolyl isomerase (PPIase) which mediates repression of HOX gene expression after binding to the 3rd PHD finger of MLL through its own RRM domain. Upon binding to MLL, CYP33 increases recruitment of HDAC to the MLL repression domain which in turn leads to deacetylation of histone H3. This ultimately causes repression of MLL target genes (Xia et al. 2003). Chromosomal translocations involving the MLL gene (Mixed Lineage Leukemia) can lead to the production of fusion proteins with any of more than 60 different partner proteins and is implicated in the initiation of leukemia. Expression of MLL fusion proteins leads to increased expression of MLL target genes such as HOXA7, HOXA9 and MEIS1 (Hess et al., 2010). MLL-fusion proteins lack the 3rd PHD finger and ...
Head and thorax development in the Drosophila embryo requires the maternal determinant of the anterior patterning system bicoid (bcd) (Frohnhofer and Nusslein-Volhard, 1986). The Bcd protein is expressed as a maternal anteroposterior concentration gradient in the early developing embryo (Driever and Nusslein-Volhard, 1988b; Struhl et al., 1989) and it is necessary for the expression of numerous zygotic genes in distinct anterior domains. Among them, the gap gene hunchback (hb), which is required for the formation of the segmented part of the head and of the thorax, is activated by low levels of Bcd and expands from 54% to 100% of egg length (EL). In contrast to hb, the expression of another Bcd target gene, the head gap gene orthodenticle (otd), which is involved in the development of antennal and pre-antennal segments, is restricted to 100-70% of EL in the domain where high levels of Bcd concentration are found. Bcd is a homeodomain (HD)-containing transcription factor that probably activates ...
By studying activated DC, it was found that CD82 appeared to have an opposing function to CD37. Whereas CD37 expression was down-regulated following activation of DC, CD82 was up-regulated and restrained DC migration to lymph nodes. DC that were deficient in either CD37 or CD82 were unable to become fully functional and DC that were deficient in CD82 were able to spread much further than CD37 deficient DC. Thus, unactivated DC were observed to have high CD37 expression and low CD82 expression leading to a highly mobile cell that is able to travel easily around the body. Activated DC (DC that have sensed an infection) have low CD37 expression and high CD82 expression which limits mobility of the DC but is able to efficiently signal to immune cells that an infection is present ...
Interferon regulatory aspect (IRF)-3 may have a crucial function in viral and bacterial innate immune system replies by regulating the creation of type We interferon (IFN). cells. This inhibition was because of its suppression from the transcriptional activation TC-E 5001 of IRF-3, as proven by inhibition of IRF-3 PRD (III-I) luciferase activity along with the phosphorylation design of IRF-3 within the immunoblotting test. Furthermore, TQ targeted the autophosphorylation of TANK-binding kinase 1 (TBK1), an upstream essential enzyme in charge of IRF-3 activation. Used together, these results claim that TQ can downregulate IRF-3 activation via inhibition of TBK1, which would eventually decrease the creation of type I IFN. TQ also governed IRF-3, among the inflammatory transcription elements, offering a novel understanding into its anti-inflammatory actions. (TRIF). Upon arousal by LPS, TLR-4 recruits the adaptor proteins TRIF, which in turn recruits tumor necrosis TC-E 5001 aspect ...
Balikova, A., Jääger, K., Viil, J., Maimets, T. and Kadaja-Saarepuu, L. (2012). Leukocyte marker CD43 promotes cell growth in co-operation with β-catenin in non-hematopoietic cancer cells. Int J Oncol 41:299-309. Kadaja-Saarepuu, L., Lõoke, M., Balikova, A. and Maimets, T. (2011) Tumor suppressor p53 down-regulates expression of human leukocyte marker. CD43 in non-hematopoietic tumor cells. Int J Oncol 40(2):567-76. Kadaja-Saarepuu, L., Laos, S., Jääger, K., Viil, J., Balikova, A., Lõoke, M.,Hansson, G.C. and Maimets, T. (2008) CD43 promotes cell growth and. helps to evade FAS-mediated apoptosis in non-hematopoietic cancer cells lacking the tumor suppressors p53 or ARF. Oncogene 27(12):1705-15. ...
Androgen suppression mediates transcriptional downregulation of DNA repair genes. Stimulation with supraphysiologic levels of dihydrotestosterone induces formation of lethal DNA breaks through recruitment of topoisomerase II enzymes to fragile DNA sites. Bipolar castration and stimulation that contributes to increasing DNA damage represents a novel strategy of sensitizing prostate cancer to cytotoxic therapies, including radiotherapy. Clin Cancer Res; 22(13); 1-3. ©2016 AACR.. See related article by Hedayati et al., p. 3310 ...
TY - JOUR. T1 - Inhibition of NFκB and pancreatic cancer cell and tumor growth by curcumin is dependent on specificity protein down-regulation. AU - Jutooru, Indira. AU - Chadalapaka, Gayathri. AU - Lei, Ping. AU - Safe, Stephen. PY - 2010/8/13. Y1 - 2010/8/13. N2 - Curcumin activates diverse anticancer activities that lead to inhibition of cancer cell and tumor growth, induction of apoptosis, and antiangiogenic responses. In this study, we observed that curcumin inhibits Panc28 and L3.6pL pancreatic cancer cell and tumor growth in nude mice bearing L3.6pL cells as xenografts. In addition, curcumin decreased expression of p50 and p65 proteins and NFκB-dependent transactivation and also decreased Sp1, Sp3, and Sp4 transcription factors that are overexpressed in pancreatic cancer cells. Because both Sp transcription factors and NFκB regulate several common genes such as cyclin D1, survivin, and vascular endothelial growth factor that contribute to the cancer phenotype, we also investigated ...
Sigma-Aldrich offers abstracts and full-text articles by [Fei Gao, Jiyu Guan, Limei Liu, Sheng Zhang, Peipei An, Anran Fan, Guangqi Song, Peng Zhang, Tianchuang Zhao, Bo Tang, Xueming Zhang, Ziyi Li].
Evidence-Based Complementary and Alternative Medicine (eCAM) is an international peer-reviewed, Open Access journal that seeks to understand the sources and to encourage rigorous research in this new, yet ancient world of complementary and alternative medicine.
In the original manuscript, the text in figure 1 is illegible. Furthermore, there is an unnecessary carriage return (page 1716, ~line 18) crystallographic ... methods. [...]
Curcumin blocks CCL2 induced adhesion, motility and invasion, in part, through down-regulation of CCL2 expression and proteolytic activity is an eagle-i resource of type Journal article at Oregon Health & Science University.
Mutations in the parkin gene, which encodes a ubiquitin ligase, has been implicated as one of causative factor for genetic parkinsonism. Interestingly, parkin role has also been implicated in cancer as a putative tumor suppressor with the gene been frequently targeted by deletion and inactivation in several human malignant tumors. Here, we demonstrated a potential tumor suppressor role for parkin in gliomas. We found that parkin expression was dramatically reduced in glioma cells and that the restoration of parkin expression promoted G1 phase cell-cycle arrest and mitigated the proliferation rate of glioma cells in vitro and in vivo. Furthermore, parkin-expressing glioma cells showed a reduction in levels of cyclin D1, but not cyclin E, and a selective downregulation of Akt serine-473 phosphorylation and VEGF receptor levels. In accordance, cells derived from a parkin-null mouse model exhibited increased levels of cyclin D1, VEGF receptor, and Akt phosphorylation, and divided significantly ...
These findings reflect the selective downregulation of HLA-Bw4 by HIV infection and implicate educated KIR3DL1+ NK cells as the major NK population responding to HIV infection. To directly measure NK-mediated killing of DHIV3-infected cells, we assessed the viability of infected cells after co-culture with autologous NK cells. 77 unique alleles of are classified into four subtypes based on their surface expression density and sequence homology: alleles can be segregated further into or subtypes. In experiments using transfectant systems and tetramer binding, specific combinations of KIR3DL1 and HLA-Bw4 subtypes exhibit different receptor-ligand binding affinities and inhibitory strengths (13, 14, 21). KIR3DS1 and KIR3DL1-n subtypes are not known to engage Bw4 molecules on neighboring cells; however, specific peptides including those from HIV may facilitate engagement of KIR3DS1 by Bw4-80I (22). KIR3DL1-l and Ch subtypes, in contrast, bind both Bw4 subtypes, with ATN-161 trifluoroacetate salt ...
Conversely, if one supposes that internalized receptor is immune to down-regulation and that down-regulation occurs proportionately to occupancy of receptor by agonist in the membrane, then again, down-regulation is greater at low fenoterol concentrations than the model predicts. As before this proposal cannot be saved by supposing a saturable process because the down-regulation is a first order process.. Kinetic models that are consistent with the data can be constructed if a pool of receptor in addition to the endocytosed pool can be invoked. Here we propose a scheme (Fig. 7A, model II), the key features of which are that down-regulation can occur by either of two pathways; one pathway involving a high agonist affinity component with a low capacity that is independent of internalization and a second pathway using a low-affinity, high-capacity event that is closely correlated with internalization. This scheme provides an explanation for the dissociation of internalization from down-regulation ...
UCL Discovery is UCLs open access repository, showcasing and providing access to UCL research outputs from all UCL disciplines.
Cardiomyocyte death is currently recognized as a critical factor in the development of heart disease. heart. (Jin et al. 2002; Jonassen et al. 2001; Means et al. 2007). Its been recommended that Akt can be involved with cardioprotection mediated by preconditioning also, some short cycles of I/R in front of you sustained amount of ischemia (Mocanu et al. 2002; Steenbergen and Murphy 2008; Tong et al. 2000; Uchiyama et al. 2004). Diverse mobile Akt focuses on localized in a variety of BMS 378806 mobile compartments confer safety through transcriptional-(Brunet et al. 1999; Make et al. 2002; BMS 378806 Craig et al. 2001; Muraski et al. 2007) and post-transcriptional rules of pro-survival/pro-apoptotic protein (Datta et al. 1997; del Peso et al. 1997; Kuwahara et al. 2000; Rosenzweig and Matsui 2005; Cooper and Pap 1998; Shiojima and Walsh 2006). Excitement of receptors that activate PI3K outcomes in an upsurge in PIP3; this drives Akt translocation towards the plasma membrane where it turns into ...
IL-1 is a potent pro-inflammatory cytokine that activates intracellular signaling cascades a few of which might involve IL-1 receptor associated kinase-1 (IRAK1). become detected in moderate from cells treated with IFN- only or in conjunction with IL-1. Over-expression of IRAK1 resulted in improved constitutive and cytokine induced creation of CCL5 and CCL20. Inhibition of IRAK1 activity through RNAi or manifestation of a dominating negative mutant clogged creation of CCL5 and CCL20 but experienced SGX-145 no impact upon the IL-1 improvement of IFN- induced CXCL9, CXCL10 and CXCL11 creation. To conclude IL-1 regulates T cell focusing on chemokine creation in keratinocytes through IRAK1 reliant and self-employed pathways. These pathways may donate to severe and chronic pores and skin swelling. transcription in the current presence of biotin-16-UTP (Roche, Indianapolis, IN). The cRNA was purified using ArrayGrade cRNA Cleanup Package (SuperArray Bioscience Corp.) based on the producers guidelines ...
Wei, W.,Ming, X.,Yi, Z. Y.,et al. Autoimmunity Mediated Down-regulation Of B 2-adrenergic Receptor In COPD[J]. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE,2010,181 ...
By default, all articles on GreenMedInfo.com are sorted based on the content type which best reflects the data which most users are searching for. For instance, people viewing substances are generally most interested in viewing diseases that these substances have shown to have positive influences. This section is for allowing more advanced sorting methods. Currently, these advanced sorting methods are available for members only. If you are already a member, you can sign in by clicking here. If you do not currently have a user account, and would like to create one/become a member, click here to begin the singup process ...
This morning I had my Down Regulation appointment. This consisted of yet another internal scan. And being taught how to use the pen that holds my next lot of drugs. Somehow I get the feeling that sticking a needle in me is a whole lot different to sticking a needle into the little pad thing…
Mouse monoclonal antibody MX35 was developed against ovarian cancer. The antibody showed homogeneous reactivity with approximately 90% of human ovarian epithelial cancers and with a limited number of normal tissues by immunohistochemistry. Although mAb MX35 has been used in a number of clinical trials in ovarian cancer, it has been difficult to define the molecular identity of MX35. We report here that mAb MX35 recognizes the sodium-dependent phosphate transport protein 2b (NaPi2b) in human cancer cells. This conclusion is based on several lines of experimental evidence, including 1) the identification of SLC34A2, the gene coding for NaPi2b, by immunoscreening an ovarian cancer cell line cDNA expression library with mAb MX35; 2) mass spectrometry sequencing of peptides obtained by fragmentation from mAb MX35 affinity-purified antigen, which show complete sequence homology to amino acid sequences in NaPi2b; 3) selective down-regulation of SLC34A2 gene expression by RNA interference and the ...
miRNAs (microRNAs) have been shown to play a role in myocardial fibrosis. The present study was designed to analyse whether alterations in miRNA expression contribute to the progression of myocardial fibrosis in AS (aortic valve stenosis) patients through up-regulation of the pro-fibrotic factor TGF-β1 (transforming growth factor-β type 1). Endomyocardial biopsies were obtained from 28 patients with severe AS, and from the necropsies of 10 control subjects. AS patients presented increased myocardial CVF (collagen volume fraction) and TGF-β1 compared with the controls, these parameters being correlated in all patients. Patients were divided into two groups by cluster analysis according to their CVF: SF (severe fibrosis; CVF ,15%; n=15) and non-SF (CVF ≤15%; n=13). TGF-β1 was increased in patients with SF compared with those with non-SF. To analyse the involvement of miRNAs in SF, the miRNA expression profile of 10 patients (four with non-SF and six with SF) was analysed showing that 99 ...
No effective chemotherapy for the treatment of malignant brain tumors, especially glioblastoma, exists so far. Despite the progress in surgical techniques and advances in the irradiation treatment, the concomitant chemotherapy is essential for the prevention of relapse and of major importance for patient outcome. The introduction of temozolomide combined with radiation in clinical practice led to slightly improved long-term survival, but malignant gliomas remain resistant to cancer chemotherapy. Thus, new strategies for the treatment of brain tumors are still needed. Objectives of this work were the evaluation of the TmHU protein as siRNA transfection reagent (Chapter 2), investigations on new kinesin Eg5 inhibitors, which specifically inhibit cell division during mitosis (Chapter 3), and the exploration of new tariquidar analogs as ABCB1 and ABCG2 inhibitors (Chapter 4). Due to the selective down-regulation of oncogene expression by small interfering RNA, siRNAs are considered as promising ...
Aging is characterized by loss of function of the adaptive immune system, but the underlying causes are poorly understood. To assess the molecular effects of aging on B cell development, we profiled gene expression and chromatin features genome-wide, including histone modifications and chromosome conformation, in bone marrow pro-B and pre-B cells from young and aged mice. Our analysis reveals that the expression levels of most genes are generally preserved in B cell precursors isolated from aged compared with young mice. Nonetheless, age-specific expression changes are observed at numerous genes, including microRNA encoding genes. Importantly, these changes are underpinned by multi-layered alterations in chromatin structure, including chromatin accessibility, histone modifications, long-range promoter interactions, and nuclear compartmentalization. Previous work has shown that differentiation is linked to changes in promoter-regulatory element interactions. We find that aging in B cell precursors is
TY - JOUR. T1 - CDK4 down-regulation induced by paclitaxel is associated with G1 arrest in gastric cancer cells. AU - Yoo, Young Do. AU - Park, Jong Kuk. AU - Choi, Ju Youn. AU - Lee, Kee Ho. AU - Kang, Yoon Koo. AU - Kim, Chong Suk. AU - Shin, Sang Won. AU - Kim, Yeul Hong. AU - Kim, Jun Suk. PY - 1998. Y1 - 1998. N2 - Paclitaxel induces a cell cycle block at G2-M phase by preventing the depolymerization of microtubules and induces p53-independent apoptosis in many cancer cells. We observed that gastric cancer cells treated with paclitaxel have shown a cyclin-dependent kinase (CDK)4 down-regulation. This paclitaxel-induced CDK4 down-regulation resulted in a cell cycle arrest at G1-S phase. To confirm this observation, we prepared stable transfectants that overexpressed CDK4 and analyzed the cell cycle progression. Ectopic expression of CDK4 in SNU cells resulted in a release of paclitaxel-induced G1 arrest. The release of G1 arrest by enforced expression of CDK4 seems to make the cells more ...
Recent studies have shown that selenium-binding protein 1 (SELENBP1) is significantly down-regulated in a variety of solid tumors. Nevertheless, the clinical relevance of SELENBP1 in human bladder cancer has not been described in any detail, and the molecular mechanism underlying its inhibitory role in cancer cell growth is largely unknown. SELENBP1 expression levels in tumor tissues and adjacent normal tissues were evaluated using immunoblotting assay. The association of SELENBP1 expression, clinicopathological features, and clinical outcome was determined using publicly available dataset from The Cancer Genome Atlas bladder cancer (TCGA-BLCA) cohort. DNA methylation in SELENBP1 gene was assessed using online MEXPRESS tool. We generated stable SELENBP1-overexpression and their corresponding control cell lines to determine its potential effect on cell cycle and transcriptional activity of p21 by using flow cytometry and luciferase reporter assay, respectively. The dominant-negative mutant constructs,
Dopamine is one of the key neurotransmitters actively involved in the brain. Research shows that by increasing the levels of dopamine within the reward circuits in the brain, nicotine acts as a chemical with intense addictive qualities. In many studies it has been shown to be more addictive than cocaine and heroin.[citation needed] Like other physically addictive drugs, nicotine withdrawal causes down-regulation of the production of dopamine and other stimulatory neurotransmitters as the brain attempts to compensate for artificial stimulation. As dopamine regulates the sensitivity of nicotinic acetylcholine receptors decreases. To compensate for this compensatory mechanism, the brain in turn upregulates the number of receptors, convoluting its regulatory effects with compensatory mechanisms meant to counteract other compensatory mechanisms. An example is the increase in norepinephrine, one of the successors to dopamine, which inhibit reuptake of the glutamate receptors,[45] in charge of memory ...
Over the past few years, the discovery of miRNAs has changed the landscape of human genetics and they have been widely studied in the field of oncology, where altered miRNA expression has been observed in a variety of human cancers [28]. Indeed, miRNA-expression profiling of human epithelial malignancies has led to the identification of signatures associated with diagnosis, staging, progression, prognosis and even response to treatment [29, 30]. However, few mechanistic studies have been carried out to dissect the functional role of miRNA in RCC, particularly in the context of immune dysfunction which may underlie disease progression. In fact, attaining effective tumor immunity is a major goal of the modern biologic therapy, limited by the tumor microenvironment and regulatory mechanisms affecting T cell and NK cell effectors [31].. The major finding in this report is that CD8+ T cells isolated from RCC patients exhibit defects in proliferation and a propensity to undergo apoptotic cell death ...
Research on the regulation of fish muscle physiology and growth was addressed originally by classical in vivo approaches; however, systemic interactions resulted in many questions that could be better considered through in vitro myocyte studies. The first paper published by our group in this field was with Tom Moon on brown trout cardiomyocytes, where the insulin and IGF-I receptors were characterized and the down-regulatory effects of an excess of peptides demonstrated. We followed the research on cultured skeletal muscle cells through the collaboration with INRA focused on the characterization of IGF-I receptors and its signaling pathways through in vitro development. Later on, we showed the important metabolic role of IGFs, although these studies were only the first stage of a prolific area of work that has offered a useful tool to advance in our knowledge of the endocrine and nutritional regulation of fish growth and metabolism. Obviously, the findings obtained in vitro serve the purpose to ...
The central dogma postulates that genes are first copied into messenger RNAs, which are then decoded into proteins with the help of transfer RNAs and ribosomal RNAs. It has long been known that there is more to the world of RNA than just these three classes, but the development of high-throughput RNA sequencing has revealed just how active RNAs can be. Much of the genome is transcribed, without these transcripts being translated into proteins. As these non-coding RNAs have been characterized, it is clear that many of them have regulatory roles. It has also been revealed how chemical modifications to all classes of RNAs affect their behavior, such as what they interact with and when, and how long they hang around for before being degraded.. Genome Biology has recently published a special issue on RNA & gene regulation, exploring this new world.. Perhaps some of the best understood regulatory RNAs are the microRNAs, short RNAs that bind to mRNA which mostly causes downregulation by either ...
TY - JOUR. T1 - Down-Regulation of Serum/Glucocorticoid Regulated Kinase 1 in Colorectal Tumours Is Largely Independent of Promoter Hypermethylation. AU - Lessi, Francesca. AU - Beggs, Andrew. AU - De Palo, Mariagrazia. AU - Anti, Marcello. AU - Macarone Palmieri, Raffaele. AU - Francesconi, Simona. AU - Gomes, Vito. AU - Bevilacqua, Generoso. AU - Tomlinson, Ian. AU - Segditsas, Stefania. AU - Landsberger, Nicoletta. PY - 2010. Y1 - 2010. U2 - 10.1371/journal.pone.0013840. DO - 10.1371/journal.pone.0013840. M3 - Article. VL - 5. SP - e13840. JO - PLoS ONE. JF - PLoS ONE. SN - 1932-6203. IS - 11. ER - ...
Tryndyak, V. P., Ross, S. A., Beland, F. A. and Pogribny, I. P. (2009), Down-regulation of the microRNAs miR-34a, miR-127, and miR-200b in rat liver during hepatocarcinogenesis induced by a methyl-deficient diet. Mol. Carcinog., 48: 479-487. doi: 10.1002/mc.20484 ...
PIK-93 is a potent PI3K inhibitor. PIK93 selectively inhibits the type III PI 4-kinase beta enzyme, and small interfering RNA-mediated down-regulation of the individual PI 4-kinase enzymes, revealed that PI 4-kinase beta has a dominant role in ceramide transport between the ER and Golgi.
Our results show that genetic elimination of BAMBI as a modulator of the signaling of the family of TGF cytokines renders the almost-resistant C57BL/6 mouse strain more susceptible to the development of diabetic glomerular abnormalities, as determined by proteinuria with a widening of the FPs. This is associated with increased activation of ERK1/2 and Smad1/5 alternative TGF-β signaling pathways. The Vegfr2 and Angpt1 genes, which control glomerular endothelial survival and microvascular stability, were downmodulated in glomeruli from diabetic BAMBI−/− mice compared with BAMBI+/+ mice. Incubation of glomeruli from nondiabetic BAMBI+/+ or BAMBI−/− mice with TGF-β resulted in further downregulation of Angpt1 and Vegfr2 in glomeruli from BAMBI−/− compared with BAMBI+/+ mice. The enhanced downregulation of Vegfr2 in glomeruli of diabetic mice by eliminating BAMBI could be localized to glomerular endothelial cells using an H2B-EYFP reporter under the control of Vegfr2/Flk1 regulatory ...