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Journal articles on the topic 'NF-kB-mediated gene expression'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Fang, Deyu, та Heeyoung Yang. "Identification of a novel deubiquitinating enzyme DUBS6 that regulates Sirt6-mediated suppression of NF-κB in T cells (88.17)". Journal of Immunology 184, № 1_Supplement (1 квітня 2010): 88.17. http://dx.doi.org/10.4049/jimmunol.184.supp.88.17.

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Abstract The type III histone deacetylase Sirt6 is known as a regulator of aging in diverse species by regulating NF-kB-dependent gene expression. Here, using an LC-MS/MS approach combined with immunoprecipitation, we have identified a complex of Sirt6-interacting molecules (interactome) that contains about 40 proteins from mouse primary T cells. One of the interactome members is a novel deubiquitinating enzyme (DUB); we thus define this gene as a DUB of Sirt6 (DUBS6). Co-immunoprecipitation and western blotting analysis further validated that DUBS6 interacts with Sirt6 in transiently transfec

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Oliveira, Vasco A., Linda Mathews, Danielle Yarde, Xingyu Wang, David Boulware, Lori A. Hazlehurst, Dung-Tsa Chen, Amer Beg, and William S. Dalton. "NF-kB as a Regulator of FA/BRCA Gene Expression in Multiple Myeloma." Blood 110, no. 11 (November 16, 2007): 3508. http://dx.doi.org/10.1182/blood.v110.11.3508.3508.

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Abstract Results to date argue compellingly that disruption of FA/BRCA gene expression plays a pivotal role in human somatic carcinogenesis. Melphalan, a DNA cross-linker, is one of the most widely used and effective drugs in the treatment of multiple myeloma (MM). Although most patients respond to standard and high dose melphalan, eventually patients acquire resistance and develop progressive disease. In 1991, our laboratory reported that acquired resistance in a human myeloma cell line was associated with reduced DNA crosslinks, elevated glutathione levels, and increased radiation survival (

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3

Roh, Eunmiri, Heun-Sik Lee, Jeong-Ah Kwak, Sang Hun Jung, Sang-Bae Han, and Youngsoo Kim. "Novel chalcone JSH 4-4 inhibit NF-kB-regulated inflammatory gene expression via targeting LPS-binding site of MD-2 (98.4)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 98.4. http://dx.doi.org/10.4049/jimmunol.184.supp.98.4.

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Abstract Previous studies have shown that chalcone has beneficial effects with antioxidant and anti-inflammatory activities. However, molecular basis for these effects not yet fully understood. In this study, a chalcone derivative, 2’, 4’-dihydroxy-6’-isopentyloxy chalcone (JSH 4-4) was discovered as an inhibitor of NF-kB activation. To demonstrate molecular target affected by JSH 4-4, we examined a homotypic interaction of TLR4, using Ba/F3 cells stably expressing TLR4-Flag, TLR4-GFP CD14 and MD-2, seperately. As a result, JSH 4-4 inhibited the LPS-induced TLR4 oligomerization. Moreover, we d

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Kozloski, Goldi A., Xiaoyu Jiang, Shruti Bhatt, Rita Shaknovich, Ari M. Melnick, and Izidore S. Lossos. "Mirna-181a expression Lead to Longer Animal Survival and Slower Tumor-Growth Rate in Diffuse Large B-Cell Lymphoma Xenograft Models." Blood 124, no. 21 (December 6, 2014): 2963. http://dx.doi.org/10.1182/blood.v124.21.2963.2963.

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Abstract Introduction: Diffuse large B-cell lymphoma (DLBCL) is subdivided into the germinal center B-like (GCB) and activated B cell-like (ABC) subtypes by gene expression profiling, and these subtypes exhibit different clinical outcomes and signaling pathway deregulations. Compared to the GCB, the ABC-DLBCL subtype displays a more aggressive clinical course and shorter patient survival. Constitutive nuclear factor kappa-B (NF-kB) activity is often associated with the ABC-DLBCL subtype, however recent studies suggest that NF-kB signaling activation is also observed to a lower extent in the GC

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5

Zhu, Ningxi, Lubing Gu, Harry W. Findley, Kuang-Yueh Chiang та Muxiang Zhou. "Vitamin K3 Selectively Induces Apoptosis in Acute Lymphoblastic Leukemia Cells with Constitutive Activation of IKKα/NF-kB Activation." Blood 106, № 11 (16 листопада 2005): 859. http://dx.doi.org/10.1182/blood.v106.11.859.859.

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Abstract Although the cytotoxic effect of vitamin K3 (VK3) on human cancer cells has been repeatedly reported, no clear conclusions from either in vitro or in vivo tests have so far been made for VK3 as an anticancer agent due to marked inter-tumor variability of efficacy in response to VK3 treatment. Here, we report that sensitivity of neoplastic cells to VK3-induced killing depends on IKKα expression/NF-kB activation in the cells. We tested the sensitivity to VK3 of 14 leukemic cell lines established from children with acute lymphoblastic leukemia (ALL). The 14 lines were classified into thr

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6

Nakagawa, Masahiro, Munetake Shimabe, Nahoko Nishimoto, Naoko Watanabe-Okochi, Motoshi Ichikawa, Yasuhito Nannya, Yoichi Imai, and Mineo Kurokawa. "AML1/Runx1 Is a Cytoplasmic Attenuator of NF-Kb Signaling: Implication in Pathogenesis and Targeted Therapy of AML1-Related Leukemia." Blood 114, no. 22 (November 20, 2009): 1962. http://dx.doi.org/10.1182/blood.v114.22.1962.1962.

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Abstract Abstract 1962 Poster Board I-985 Introduction: AML1/Runx1 is one of the most frequent targets of chromosomal abnormalities in human leukemia. Functional impairment of AML1 caused by point mutation is also reported in patients with leukemia or myelodysplastic syndrome (MDS). However, molecular basis for leukemogenesis caused by functional impairment of AML1 is still elusive. In this study, we clarified the deregulated signaling pathway induced by loss of AML1. Results: To find the direct target of AML1, we compared gene expression profile between AML1-conditionally deleted and normal K

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Endale, Mehari, Tae-Hwan Kim, Yi-Seong Kwak, Na-Mi Kim, Seung-Hyung Kim, Jae Youl Cho, Bong-Sik Yun та Man-Hee Rhee. "Torilin Inhibits Inflammation by Limiting TAK1-Mediated MAP Kinase and NF-κB Activation". Mediators of Inflammation 2017 (2017): 1–13. http://dx.doi.org/10.1155/2017/7250968.

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Torilin, a sesquiterpene isolated from the fruits ofTorilis japonica,has shown antimicrobial, anticancer, and anti-inflammatory properties. However, data on the mechanism of torilin action against inflammation is limited. This study aimed at determining the anti-inflammatory property of torilin in LPS-induced inflammation using in vitro model of inflammation. We examined torilin’s effect on expression levels of inflammatory mediators and cytokines in LPS-stimulated RAW 264.7 macrophages. The involvement of NF-kB and AP-1, MAP kinases, and adaptor proteins were assessed. Torilin strongly inhibi

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8

Buhrmann, Constanze, Aranka Brockmueller, Anna-Lena Mueller, Parviz Shayan, and Mehdi Shakibaei. "Curcumin Attenuates Environment-Derived Osteoarthritis by Sox9/NF-kB Signaling Axis." International Journal of Molecular Sciences 22, no. 14 (July 16, 2021): 7645. http://dx.doi.org/10.3390/ijms22147645.

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Inflammation has a fundamental impact on the pathophysiology of osteoarthritis (OA), a common form of degenerative arthritis. It has previously been established that curcumin, a component of turmeric (Curcuma longa), has anti-inflammatory properties. This research evaluates the potentials of curcumin on the pathophysiology of OA in vitro. To explore the anti-inflammatory efficacy of curcumin in an inflamed joint, an osteoarthritic environment (OA-EN) model consisting of fibroblasts, T-lymphocytes, 3D-chondrocytes is constructed and co-incubated with TNF-α, antisense oligonucleotides targeting

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9

Lyu, Qingkang, Magdalena Wawrzyniuk, Victor P. M. G. Rutten, Willem van Eden, Alice J. A. M. Sijts, and Femke Broere. "Hsp70 and NF-kB Mediated Control of Innate Inflammatory Responses in a Canine Macrophage Cell Line." International Journal of Molecular Sciences 21, no. 18 (September 4, 2020): 6464. http://dx.doi.org/10.3390/ijms21186464.

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The pathogenesis of many inflammatory diseases is associated with the uncontrolled activation of nuclear factor kappa B (NF-κB) in macrophages. Previous studies have shown that in various cell types, heat shock protein 70 (Hsp70) plays a crucial role in controlling NF-κB activity. So far, little is known about the role of Hsp70 in canine inflammatory processes. In this study we investigated the potential anti-inflammatory effects of Hsp70 in canine macrophages as well as the mechanisms underlying these effects. To this end, a canine macrophage cell line was stressed with arsenite, a chemical s

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10

Dasgupta, Subhajit, Jackie Eudaly, Ivan Molano, DeAnna Baker, Meagan Mollenhauer, and Gary Gilkeson. "Involvement of estrogen receptor alpha on MCP1 production in C57BL/6 kidney mesangial cells (87.29)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 87.29. http://dx.doi.org/10.4049/jimmunol.184.supp.87.29.

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Abstract Abstract We demonstrate an estrogen independent involvement of ERα in TLR2 mediated expression of MCP1 in mesangial cells. In vitro treatment with the TLR2 ligands Pam3CysSK4, LTA and PGN-SA induced production of MCP1 in mesangial cells isolated from kidneys of female C57BL/6 mice in a dose dependent manner. Treatment with LTA to C57BL/6 mesangial cells was found to activate NF kB and induced its nuclear localization. Interestingly enough, we found LTA treatment induced phosphorylation of ERα in primary mesangial cells and also in SV40 virus transformed B6 mesangial cell line. Nuclear

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11

Yang, Bingyuan, Lisette A. Maddison, Karolina E. Zaborska, Chunhua Dai, Linlin Yin, Zihan Tang, Liqing Zang, David A. Jacobson, Alvin C. Powers та Wenbiao Chen. "RIPK3-mediated inflammation is a conserved β cell response to ER stress". Science Advances 6, № 51 (грудень 2020): eabd7272. http://dx.doi.org/10.1126/sciadv.abd7272.

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Islet inflammation is an important etiopathology of type 2 diabetes; however, the underlying mechanisms are not well defined. Using complementary experimental models, we discovered RIPK3-dependent IL1B induction in β cells as an instigator of islet inflammation. In cultured β cells, ER stress activated RIPK3, leading to NF-kB–mediated proinflammatory gene expression. In a zebrafish muscle insulin resistance model, overnutrition caused islet inflammation, β cell dysfunction, and loss in an ER stress–, ripk3-, and il1b-dependent manner. In mouse islets, high-fat diet triggered the IL1B expressio

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Friedrichsen, Sönke, Claire V. Harper, Sabrina Semprini, Michael Wilding, Antony D. Adamson, Dave G. Spiller, Glyn Nelson, John J. Mullins, Michael R. H. White та Julian R. E. Davis. "Tumor Necrosis Factor-α Activates the Human Prolactin Gene Promoter via Nuclear Factor-κB Signaling". Endocrinology 147, № 2 (1 лютого 2006): 773–81. http://dx.doi.org/10.1210/en.2005-0967.

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Pituitary function has been shown to be regulated by an increasing number of intrapituitary factors, including cytokines. Here we show that the important cytokine TNF-α activates prolactin gene transcription in pituitary GH3 cells stably expressing luciferase under control of 5 kb of the human prolactin promoter. Similar regulation of the endogenous rat prolactin gene by TNF-α in GH3 cells was confirmed using real-time PCR. Luminescence microscopy revealed heterogeneous dynamic response patterns of promoter activity in individual cells. In GH3 cells treated with TNF-α, Western blot analysis sh

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13

Le Clorennec, Christophe, Ibtissam Youlyouz-Marfak, Eric Adriaenssens, Jean Coll, Dominique Bordessoule, Georg W. Bornkamm, and Jean Feuillard. "Regulation of CD95 in EBV infected B-Cells." Blood 104, no. 11 (November 16, 2004): 81. http://dx.doi.org/10.1182/blood.v104.11.81.81.

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Abstract Expression of CD95 is regulated by various agents such as TNFa, IFNg, or Daunorubicine, able to induce the transcriptional factors NF-kB, STAT1 and p53 respectively. The CD95 promoter is known to harbour binding sites for these factors. These factors are modulated both in expression and activity during EBV infection of B-cells. EBV is known to induce CD95 expression. The objective of this work was to understand the contribution of p53, STAT1 and NF-kB in the regulation of CD95 expression by EBV. To control the activity of NF-kB, STAT1, p53 and LMP1, we have developed and used various

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14

De Curtis, Susan, та Stephen Aderaye. "Additive effect of TGF-ß with TNF-α on type VII collagen gene expression to activate the expression of an extracellular matrix-related gene". American Journal of BioMedicine 2, № 2 (2 червня 2014): 106–15. http://dx.doi.org/10.18081/2333-5106/014-01/56-66.

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Type VII collagen is the predominant, if not the exclusive, component of the anchoring fibrils, attachment structures stabilizing the association of the cutaneous basement membrane to the underlying dermis. In the skin, type VII collagen is synthesized by both dermal fibroblasts and epidermal keratinocytes. Alterations in the type VII collagen protein structure or lack of its expression due to mutations in the corresponding gene COL7A1 are the hallmark of dystrophic epidermolysis bullosa, a mechano-bullous skin disease characterized by extreme fragility of the skin and leading to development o

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15

Rahayu, Masruroh, M. Aris Widodo, Diana Lyrawati та Edi Widjadjanto. "ALPHA-PINENE ATTENUATES MICROGLIAL NF-ΚB ACTIVATION AND INOS EXPRESSION IN GP120-INDUCED NEUROINFLAMMATION". MNJ (Malang Neurology Journal) 7, № 1 (1 січня 2021): 80–84. http://dx.doi.org/10.21776/ub.mnj.2020.007.01.16.

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Background: Neuro-inflammation plays a role in the pathogenesis of HIV-associated dementia (HIV). Activation of microglia is essential for triggering inflammatory-mediated neurotoxicity. HIV-1 120 kDa envelope glycoprotein (gp120) induces microglial NF-κB signaling which in turn induce pro-inflammatory and iNOS gene transcription. Continuous or excessive activation of NF-κB signaling lead to persistent production of TNF-α and nitric oxide by microglia and induce neuronal apoptosis. Alpha-pinene is a natural substance found in pine tree and has efficacy on inhibiting NF-κB signaling. Objective:

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16

Ishihara, Yasuhiro, Sarah Y. Kado, Christiane Hoeper, Shelly Harel, and Christoph F. A. Vogel. "Role of NF-kB RelB in Aryl Hydrocarbon Receptor-Mediated Ligand Specific Effects." International Journal of Molecular Sciences 20, no. 11 (May 30, 2019): 2652. http://dx.doi.org/10.3390/ijms20112652.

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Here, we investigate the role of RelB in the regulation of genes which were identified to be induced in an aryl hydrocarbon receptor (AhR)-dependent manner and critically involved in regulation of immune responses. We analyzed the expression of genes of the AhR gene battery, cytokines, and immune regulatory enzymes in bone marrow-derived macrophages (BMM) and thymus of B6 wildtype (wt) mice and RelB knockout (RelB−/−) mice after treatment with various AhR ligands. The 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced expression of indoleamine 2,3-dioxygenase 1 (IDO1) and IDO2 was significantl

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17

Asare, Yaw, Erdenechimeg Shagdarsuren, Johannes Schmid, Pathricia Tilstam, Jochen Grommes, Omar El Bounkari, Anke Schütz та ін. "Endothelial CSN5 impairs NF-κB activation and monocyte adhesion to endothelial cells and is highly expressed in human atherosclerotic lesions". Thrombosis and Haemostasis 110, № 07 (2013): 141–52. http://dx.doi.org/10.1160/th13-02-0155.

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SummaryThe COP9 signalosome (CSN), a multifunctional protein complex involved in the regulation of cullin-RING-E3 ubiquitin ligases (CRLs), has emerged as a regulator of NF-κB signalling. As NF-κB drives the expression of pro-inflammatory and pro-atherosclerotic genes, we probed the yet unknown role of the CSN, in particular CSN5, on NF-KB-mediated atherogenic responses in endothelial cells. Co-immunoprecipitation in human umbilical vein endothelial cells (HUVECs) revealed the presence of a super-complex between IKK and CSN, which dissociates upon TNF-α stimulation. Furthermore, CSN5 silencing

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Kagoya, Yuki, Akihide Yoshimi, Shunya Arai, Keisuke Kataoka, Masahiro Nakagawa, Keiki Kumano та Mineo Kurokawa. "NF-κB/TNF-α Positive Feedback Loop with Active Proteasome Machinery Supports Myeloid Leukemia Initiating Cell Capacity". Blood 120, № 21 (16 листопада 2012): 654. http://dx.doi.org/10.1182/blood.v120.21.654.654.

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Abstract Abstract 654 Acute myeloid leukemia (AML) is an aggressive hematologic malignancy arising from leukemia initiating cells (LIC), and is comprised of highly heterogeneous groups with different cytogenetic and molecular abnormalities, which makes it difficult to establish a broadly effective therapeutic strategy. Since constitutive NF-kB pathway activation has been reported in different types of AML cells, it is one of the promising candidates which are universally involved in the LIC phenotype. However, the mechanism of activation and its significance in leukemia progression have not be

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19

Amin, Jakia, Ken-ichiro Otsuyama, Emi Uchida, Saeid Abroun, Karim Shamsasenjan, Khademul Islam та Michio M. Kawano. "The Potentials of Constitutive NF-κB Activation in U266 Cell Lines." Blood 108, № 11 (16 листопада 2006): 5008. http://dx.doi.org/10.1182/blood.v108.11.5008.5008.

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Abstract NF-κB has been described as a family of ubiquitously expressed transcription factors, composed of a dimer of distinct members of the Rel protein family (RelA/p65, cRel, RelB, p50, p52), and after stimulation, NF-κB dimer translocate into the nucleus to activate the transcription of various target genes. In the present study, we aimed to elucidate the mechanism of constitutive activation of NF-κB in human myeloma cells. For this purpose here, we used a human myeloma cell line, U266 cells, and performed gel shift assay and also examined the expression of different target genes of NF-κB

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Milone, Michael C., Roddy OConnor, Michael May, Steven Albelda, and Benjamin Philipson. "4-1BB-Costimulated CAR-Mediated Non-Canonical NF-Kb Signaling Enhances CAR T Cell Survival and Suppresses Bim Expression." Blood 132, Supplement 1 (November 29, 2018): 3713. http://dx.doi.org/10.1182/blood-2018-99-119522.

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Abstract Chimeric Antigen Receptor (CAR) T cell therapy induces deep and durable responses in a large percentage of patients with B-cell malignancies. These responses often correlate with CAR T cell persistence in patients. The first two FDA-approved CAR-T cell therapies employ 2nd generation CARs that use different costimulatory domains derived from either CD28 or 4-1BB. Data from pre-clinical studies as well as clinical trials suggest that 4-1BB CAR (BBz) T cells persist longer than CD28 CAR (28z) T cells. One signal associated with cellular survival and activated by endogenous 4-1BB, but no

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21

Gu, Lubing, Ningxi Zhu, Harry W. Findley, William G. Woods та Muxiang Zhou. "Identification and Characterization of the IKKα Promoter". Journal of Biological Chemistry 279, № 50 (5 жовтня 2004): 52141–49. http://dx.doi.org/10.1074/jbc.m407915200.

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IKKα, a subunit of IkBα kinase (IKK) complex, has an important role in the activation of nuclear factor-kB (NF-kB), a key regulator of normal and tumor cell proliferation, apoptosis, and response to chemotherapy. However, little is known about the transcriptional regulation of theIKKα gene itself. The present study revealed that the transcriptional induction of theIKKα gene is positively regulated by binding ETS-1, the protein product of theETS-1proto-oncogene. Furthermore, ETS-1 mediated activation of IKKα is negatively regulated by p53 binding to ETS-1. By analyzing the genomic DNA sequence,

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Otsuyama, Ken-ichiro, Zi Ma, Shangqin Liu, Saeid Abroun, Hideki Asaoku та Michio M. Kawano. "PPARβ-Mediated Suppression of the Growth and Survival in Human Myeloma Cells Conteracting NF-kB Activity." Blood 106, № 11 (16 листопада 2005): 5053. http://dx.doi.org/10.1182/blood.v106.11.5053.5053.

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Abstract PPAR(peroxisomal proliferators-activated receptor)β is considered to be involved in the lipid metabolism and regulating the inflammatory response and in human myeloma cells PPARβis predominantly expressed among these PPARs. However, it remains to be clarified what is the functional role of PPARβ in myeloma cells. In order to identify what are the ligands for PPARβ, we constructed the PPREβ-luciferase reporter gene and performed the reporter assay in Hela cells. Since we have already identified several reagents (DHEA (dehydroepiandrosterone), DHEA-S, baicalein, baicalin, dexamethasone)

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Li, Ailing, Ying Liang, Yi Liu, and Gary VanZant. "Latexin Regulates Stem Cell Numbers Via a NF-êB-Dependent Pathway." Blood 112, no. 11 (November 16, 2008): 1400. http://dx.doi.org/10.1182/blood.v112.11.1400.1400.

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Abstract Latexin was first discovered in the developing lateral cortex of the brain and is the only known endogenous carboxypeptidase A (CPA) inhibitor in mammals. Our recent studies have revealed that latexin exerted a novel function in regulating murine hematopoietic stem cell number by repressing stem cell self-renewal and enhancing apoptosis (Liang et al., Nat. Gen.39:178, 2007) . However, the underlying mechanism remains obscure. To test whether latexin acts through its canonical mechanism in hematopoietic cells we used fluorescence immunohistochemistry to reveal that latex and CPA did no

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Kammala, Ananth Kumar, Samantha Sheller-Miller, Enkhtuya Radnaa, Talar Kechichian, Hariharan Subramanian, and Ramkumar Menon. "Sodium Hydrogen Exchanger Regulatory Factor-1 (NHERF1) Regulates Fetal Membrane Inflammation." International Journal of Molecular Sciences 21, no. 20 (October 20, 2020): 7747. http://dx.doi.org/10.3390/ijms21207747.

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The fetal inflammatory response, a key contributor of infection-associated preterm birth (PTB), is mediated by nuclear factor kappa B (NF-kB) activation. Na+/H+ exchanger regulatory factor-1 (NHERF1) is an adapter protein that can regulate intracellular signal transduction and thus influence NF-kB activation. Accordingly, NHERF1 has been reported to enhance proinflammatory cytokine release and amplify inflammation in a NF-kB-dependent fashion in different cell types. The objective of this study was to examine the role of NHERF1 in regulating fetal membrane inflammation during PTB. We evaluated

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WILD, Angela C., Jerry J. GIPP та R. Timothy MULCAHY. "Overlapping antioxidant response element and PMA responseelement sequences mediate basal and β-naphthoflavone-induced expression of the human γ-glutamylcysteine synthetase catalytic subunit gene". Biochemical Journal 332, № 2 (1 червня 1998): 373–81. http://dx.doi.org/10.1042/bj3320373.

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γ-Glutamylcysteine synthetase (GCS), the rate-limiting enzyme in the de novo synthesis of GSH, is a heterodimer, consisting of a catalytic (GCSh) and a regulatory subunit (GCSl). We previously demonstrated that the constitutive and β-naphthoflavone (β-NF)-induced expression of the GCSh gene is mediated by a distal antioxidant response element (ARE), ARE4, located 3.1 kb upstream of the transcriptional start site [Mulcahy, Wartman, Bailey and Gipp (1997) J. Biol. Chem. 272, 7445–7454]. ARE4 consists of a consensus ARE sequence (5´-GTGACTCAGCG-3´) containing an embedded PMA-responsive element (T

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Imamura, Yasuhiro, Yoshimasa Makita, Kazuya Masuno, and Hourei Oh. "Inhibitory Mechanism of IL-6 Production by Orento in Oral Squamous Cell Carcinoma Cell Line CAL27 Stimulated by Pathogen-Associated Molecular Patterns from Periodontopathogenic Porphyromonas gingivalis." International Journal of Molecular Sciences 24, no. 1 (December 31, 2022): 697. http://dx.doi.org/10.3390/ijms24010697.

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Orento is a traditional Japanese medicinal kampo preparation that is also prescribed in oral care. In oral squamous cell carcinoma cell line CAL27, orento significantly inhibited periodontopathogenic bacterium Porphyromonas gingivalis lipopolysaccharide (LPS) and lipoproteins (PAMP)-stimulated production of interleukin (IL)-6. This suggests that orento negatively regulates PAMP-mediated toll-like receptor (TLR) signaling. Orento significantly suppressed PAMP-stimulated activation of the IL-6 promoter, indicating that orento may suppress the production of IL-6 by PAMP at the transcriptional lev

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Park, JH, and L. Levitt. "Overexpression of mitogen-activated protein kinase (ERK1) enhances T- cell cytokine gene expression: role of AP1, NF-AT, and NF-KB." Blood 82, no. 8 (October 15, 1993): 2470–77. http://dx.doi.org/10.1182/blood.v82.8.2470.2470.

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Abstract Transfected Jurkat cells overexpressing extracellular signal-regulated kinase (ERK1), also referred to as mitogen-activated protein (MAP) kinase, were selected by Western blotting assay using anti-ERK1 and antiphosphotyrosine antibodies in combination with a functional MAP kinase assay. We then asked whether enhanced ERK1 expression had any effect on induction of T-cell cytokine genes. The results show that overexpression of ERK1 enhances expression of T-cell interleukin-2 (IL- 2), IL-3, and granulocyte-macrophage colony-stimulating factor mRNA; no change was seen in expression of the

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Park, JH, and L. Levitt. "Overexpression of mitogen-activated protein kinase (ERK1) enhances T- cell cytokine gene expression: role of AP1, NF-AT, and NF-KB." Blood 82, no. 8 (October 15, 1993): 2470–77. http://dx.doi.org/10.1182/blood.v82.8.2470.bloodjournal8282470.

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Transfected Jurkat cells overexpressing extracellular signal-regulated kinase (ERK1), also referred to as mitogen-activated protein (MAP) kinase, were selected by Western blotting assay using anti-ERK1 and antiphosphotyrosine antibodies in combination with a functional MAP kinase assay. We then asked whether enhanced ERK1 expression had any effect on induction of T-cell cytokine genes. The results show that overexpression of ERK1 enhances expression of T-cell interleukin-2 (IL- 2), IL-3, and granulocyte-macrophage colony-stimulating factor mRNA; no change was seen in expression of the alpha-ac

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Arai, Ayako, Mayumi Takahashi, Ken-Ichi Imadome, Takatoshi Koyama, Yasunori Saitoh, Shoji Yamaoka, Shigeyoshi Fujiwara та Osamu Miura. "NF-κB Is Constitutively Activated in EBV-Infected T or NK Cells and Can Be a Molecular Target for EBV-Positive T/NK-Cell Lymphoproliferative Disease Treatment". Blood 116, № 21 (19 листопада 2010): 1998. http://dx.doi.org/10.1182/blood.v116.21.1998.1998.

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Abstract Abstract 1998 Epstein-Barr virus (EBV) can infect not only B cells but also rarely T or NK cells and causes EBV-positive T/NK-cell lymphoproliferative disease (EBV-T/NK-LPD), such as extranodal NK/T-cell lymphoma (ENKL), aggressive NK-cell leukemia, and chronic active EBV infection (CAEBV). However, why and how EBV infects T or NK cells and the mechanism of action responsible for the development of these EBV-induced malignancies have not been elucidated to date. Furthermore, optimal chemotherapy for these, especially for CAEBV, has not been established and the prognosis of EBV-T/NK-LP

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Suh, Han Na, Young Kyu Kim, Ju Young Lee, Goo-Hwa Kang, and Jeong Ho Hwang. "Dissect the immunity using cytokine profiling and NF-kB target gene analysis in systemic inflammatory minipig model." PLOS ONE 16, no. 6 (June 4, 2021): e0252947. http://dx.doi.org/10.1371/journal.pone.0252947.

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Minipigs have remarkably similar physiology to humans, therefore, they it can be a good animal model for inflammation study. Thus, the conventional (serum chemistry, histopathology) and novel analytic tools [immune cell identification in tissue, cytokine level in peripheral blood mononuclear cells (PBMC) and serum, NF-kB target gene analysis in tissue] were applied to determine inflammation in Chicago Miniature Swine (CMS) minipig. Lipopolysaccharide (LPS)-induced acute systemic inflammation caused liver and kidney damage in serum chemistry and histopathology. Immunohistochemistry (IHC) also s

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Molinero, Luciana, Michelle Miller, Mona Mashayekhi, Luqiu Chen, Ping Zhou, Nicole Tramontini, Monica Michelotti, Xindong Liu, Xiaoping Zhu та Maria-Luisa Alegre. "NF-κB controls IL-7 receptor expression in T cells (P6295)". Journal of Immunology 190, № 1_Supplement (1 травня 2013): 184.9. http://dx.doi.org/10.4049/jimmunol.190.supp.184.9.

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Abstract IL-7 and tonic TCR signaling control naïve T cell homeostasis. The transcription factor NF-κB plays a key role during T cell activation, proliferation and survival, but little is known on the role of basal NF-κB in quiescent T cells. Using mice bearing NF-κB impaired T cells (IκBαΔN), we show that basal levels of NF-κB signaling in naïve T cells are required for cell survival both in vivo and in vitro. In vitro, IκBαΔN T cells display reduced survival to IL-7, IL-7-mediated STAT5 phosphorylation and Bcl2 upregulation. Indeed, protein levels of IL-7Rα, but not common γc subunit (CD13

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Ganan-Gomez, Irene, Yue Wei, Hui Yang, Maria Carmen Boyano-Adánez, and Guillermo Garcia-Manero. "Overexpression Of Mir-125a In Bone Marrow CD34+ cells Of Patients With Myelodysplastic Syndrome Is Correlated To a Poor Prognosis and May Contribute To The Pathogenesis Of The Disease Through The Modulation Of NF-Kb Activation and Enhancement Of Differentiation Arrest." Blood 122, no. 21 (November 15, 2013): 5206. http://dx.doi.org/10.1182/blood.v122.21.5206.5206.

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Abstract Myelodysplastic syndromes (MDS) are a group of clonal malignancies characterized by impaired proliferation and differentiation of hematopoietic stem cells and precursors. The involvement of toll-like receptor (TLR)-mediated signalling in the modulation of myeloid differentiation and its participation in the pathogenesis of MDS are well documented (Wei et al 2013). Increased signaling through this pathway leads to the constitutive activation of NF-kB, which regulates the production of cytokines and mediates cell proliferation and apoptosis (Starczynowski 2010). In addition to the expre

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Wessel, Alex, Amy Hsu, Jevgenia Zilberman-Rudenko, Raphaela Goldbach-Mansky, Richard Siegel, and Eric Hanson. "Inflammatory disease and impaired antiviral immunity due to unbalanced NF-kB and IRF3 activation result from a de novo human NEMO mutation (P1415)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 57.19. http://dx.doi.org/10.4049/jimmunol.190.supp.57.19.

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Abstract The RIG-I-like receptors mediate antiviral signaling through NEMO-dependent activation of transcription factors NF-kB and IRF3, which are recognized for their roles in inflammation and the induction of Type I Interferon, respectively. We identified an individual with increased susceptibility to viral infection and persistent inflammatory disease. Sanger sequencing revealed a de novo synonymous mutation in the gene encoding NEMO that results in an in-frame splicing event and exclusive production of a shortened protein. To understand the role of NEMO in regulating the antiviral response

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Ruland, Jürgen, and Tak Mak. "MALT1 Is an Essential Regulator of Antigen Receptor Mediated NF-kappaB Activation." Blood 104, no. 11 (November 16, 2004): 347. http://dx.doi.org/10.1182/blood.v104.11.347.347.

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Abstract The translocation t(11;18)(q21;q21) is the most common chromosomal abnormality in lymphomas of mucosa associated lymphoid tissue (MALT lymphoma). Molecular cloning of the breakpoint demonstrated that t(11;18) leads to the fusion of the IAP2 gene to the novel gene MALT1. MALT1 encodes a paracaspase that can bind to BCL10 but its cellular function was unknown. We have previously demonstrated that BCL10, which is involved in independent MALT lymphoma translocations, functions as a positive regulator of lymphocyte proliferation. BCL10 connects antigen receptor signaling in B and T cells t

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Biswas, Polash Kumar, Sang Rok Park, Jongyub An, Kyung Min Lim, Ahmed Abdal Dayem, Kwonwoo Song, Hye Yeon Choi, et al. "The Orphan GPR50 Receptor Regulates the Aggressiveness of Breast Cancer Stem-like Cells via Targeting the NF-kB Signaling Pathway." International Journal of Molecular Sciences 24, no. 3 (February 1, 2023): 2804. http://dx.doi.org/10.3390/ijms24032804.

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The expression of GPR50 in CSLC and several breast cancer cell lines was assessed by RT-PCR and online platform (UALCAN, GEPIA, and R2 gene analysis). The role of GPR50 in driving CSLC, sphere formation, cell proliferation, and migration was performed using shGPR50 gene knockdown, and the role of GPR50-regulated signaling pathways was examined by Western blotting and Luciferase Assay. Herein, we confirmed that the expression of G protein-coupled receptor 50 (GPR50) in cancer stem-like cells (CSLC) is higher than that in other cancer cells. We examined that the knockdown of GPR50 in CSLC led to

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Murphy, Michael, Xiong Yanbao, and Andrei Medvedev. "Pellino-1 and Pellino-3b in endotoxin tolerance and TLR signaling (INM9P.458)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 189.11. http://dx.doi.org/10.4049/jimmunol.192.supp.189.11.

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Abstract Endotoxin tolerance (ET) reprograms Toll-like receptor (TLR) 4-inducible responses in monocytes and macrophages by attenuating expression of pro-inflammatory cytokines without suppressing anti-inflammatory cytokines and antimicrobial effectors. We previously demonstrated deficient LPS-mediated TLR4-driven activation of IL-1 receptor-associated kinase (IRAK) 4 and IRAK1 as critical hallmarks of endotoxin tolerance. E3 ubiquitin ligases Pellino regulate TLR signaling pathways via modifications of IRAK kinases. We examined the impact of ET on Pellino-1/3b expression and utilized overexpr

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Gautam, SC, KR Pindolia, CJ Noth, N. Janakiraman, YX Xu, and RA Chapman. "Chemokine gene expression in bone marrow stromal cells: downregulation with sodium salicylate." Blood 86, no. 7 (October 1, 1995): 2541–50. http://dx.doi.org/10.1182/blood.v86.7.2541.2541.

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Abstract Chemotactic cytokines, chemokines, have been shown to influence the proliferation of hematopoietic progenitor cells. Thus, regulation of chemokine production by bone marrow accessory cells is a critical aspect of stromal cell regulation of hematopoiesis. We have previously reported that monocyte chemotactic protein-1 (MCP-1 or MCP-1/JE) and interferon inducible protein 10 kD (IP-10) are both induced in murine bone marrow stromal cells +/(+)-1.LDA11 after stimulation with the inflammatory agents interleukin-1 alpha (IL-1 alpha), interferon-gamma (IFN-gamma), or lipopolysaccharide (LPS)

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Gautam, SC, KR Pindolia, CJ Noth, N. Janakiraman, YX Xu, and RA Chapman. "Chemokine gene expression in bone marrow stromal cells: downregulation with sodium salicylate." Blood 86, no. 7 (October 1, 1995): 2541–50. http://dx.doi.org/10.1182/blood.v86.7.2541.bloodjournal8672541.

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Chemotactic cytokines, chemokines, have been shown to influence the proliferation of hematopoietic progenitor cells. Thus, regulation of chemokine production by bone marrow accessory cells is a critical aspect of stromal cell regulation of hematopoiesis. We have previously reported that monocyte chemotactic protein-1 (MCP-1 or MCP-1/JE) and interferon inducible protein 10 kD (IP-10) are both induced in murine bone marrow stromal cells +/(+)-1.LDA11 after stimulation with the inflammatory agents interleukin-1 alpha (IL-1 alpha), interferon-gamma (IFN-gamma), or lipopolysaccharide (LPS). In the

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Fang, Jing, Brenden Barker, Lyndsey Bolanos, Xiaona Liu, Andres Jerez, Hideki Makishima, Dinesh S. Rao, et al. "SQSTM1/p62 Is a Necessary Cofactor In MDS/AML With Deletion Of Mir-146a." Blood 122, no. 21 (November 15, 2013): 747. http://dx.doi.org/10.1182/blood.v122.21.747.747.

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Abstract Deletions involving chromosome 5 (del(5q)) are the most common genetic abnormalities in Myelodysplastic Syndrome (MDS) and secondary Acute Myeloid Leukemia (AML). Chromosome 5q deletions extending beyond q34 portend a worse overall survival, are associated with high-risk (HR) disease, and exhibit significant downregulation of miR-146a, a gene residing on the extended deleted region on 5q34. Additional evidence linking miR-146a loss to HR del(5q) MDS/AML comes from mouse genetic studies; miR-146a-/- mice develop a myeloid proliferative disease and myeloid tumors, in part by derepressio

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Fang, Jing, Andres Jerez, Christopher Rasch, Lyndsey Bolanos, Jaroslaw P. Maciejewski та Daniel T. Starczynowski. "Haploinsufficiency of Mir-146a in High-Risk Del(5q) MDS/AML Requires an Intrachromosomal Gene Network Involving p62/TRAF6/NF-κB". Blood 120, № 21 (16 листопада 2012): 557. http://dx.doi.org/10.1182/blood.v120.21.557.557.

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Abstract Abstract 557 Deletion of chromosome 5q (del(5q)) is one of the most common cytogenetic abnormalities in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). Commonly deleted regions (CDR) have been mapped to 5q31.1 and 5q33.1 in del(5q) AML and MDS, respectively. Although there has been extensive efforts to identify candidate genes within the CDRs and decipher which genes contribute to the high-risk versus low-risk phenotypes, more recent findings indicate that deletions involving the telomeric bands of 5q are associated with more aggressive forms of del(5q) MDS/AML (Jerez

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Pessara, U., and N. Koch. "Tumor necrosis factor alpha regulates expression of the major histocompatibility complex class II-associated invariant chain by binding of an NF-kappa B-like factor to a promoter element." Molecular and Cellular Biology 10, no. 8 (August 1990): 4146–54. http://dx.doi.org/10.1128/mcb.10.8.4146-4154.1990.

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Expression of the major histocompatibility complex (MHC) class I and class II antigens and the class II-associated invariant chain (Ii) is strongly increased by treatment of cells with tumor necrosis factor alpha (TNF-alpha) and gamma interferon. We investigated elevation of expression of the invariant chain gene by TNF-alpha. Rat fibroblast cells transfected with the mouse Ii gene containing 802 base pairs of 5' sequences could be stimulated for Ii expression by treatment with TNF-alpha. Analysis of 5'-deleted Ii gene promoter-CAT constructs provided evidence for the presence of a TNF-alpha r

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Pessara, U., and N. Koch. "Tumor necrosis factor alpha regulates expression of the major histocompatibility complex class II-associated invariant chain by binding of an NF-kappa B-like factor to a promoter element." Molecular and Cellular Biology 10, no. 8 (August 1990): 4146–54. http://dx.doi.org/10.1128/mcb.10.8.4146.

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Expression of the major histocompatibility complex (MHC) class I and class II antigens and the class II-associated invariant chain (Ii) is strongly increased by treatment of cells with tumor necrosis factor alpha (TNF-alpha) and gamma interferon. We investigated elevation of expression of the invariant chain gene by TNF-alpha. Rat fibroblast cells transfected with the mouse Ii gene containing 802 base pairs of 5' sequences could be stimulated for Ii expression by treatment with TNF-alpha. Analysis of 5'-deleted Ii gene promoter-CAT constructs provided evidence for the presence of a TNF-alpha r

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Al-Rashed, Fatema, Reeby Thomas, Areej Al-Roub, Fahd Al-Mulla, and Rasheed Ahmad. "LPS Induces GM-CSF Production by Breast Cancer MDA-MB-231 Cells via Long-Chain Acyl-CoA Synthetase 1." Molecules 25, no. 20 (October 14, 2020): 4709. http://dx.doi.org/10.3390/molecules25204709.

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Granulocyte–macrophage colony-stimulating factor (GM-CSF) is a monomeric glycoprotein that has been implicated in the tumor growth and progression of different types of cancer. GM-CSF is produced by various non-immune cells including MDA-MB-231 in response to various stimuli. However, the role of lipopolysaccharide (LPS) in the regulation of GM-CSF in MDA-MB-231 breast cancer cells so far remains unclear. Herein, we asked whether LPS could induce GM-CSF production in MDA-MB-231 cells, and if so, which signaling pathway was involved. MDA-MB-231 cells were treated with LPS or tumor necrosis fact

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Alrashed, Fatema, Reeby Thomas, Areej Al-Roub, Fahd AL-Mulla, and Rasheed Ahmad. "LPS Induces GM-CSF Production by Breast Cancer MDA-MB-231 Cells via Long-Chain Acyl-CoA Synthetase 1." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 56.20. http://dx.doi.org/10.4049/jimmunol.206.supp.56.20.

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Abstract Granulocyte–macrophage colony-stimulating factor (GM-CSF) is a monomeric glycoprotein that has been implicated in the tumor growth and progression of different types of cancer. GM-CSF is produced by various non-immune cells including MDA-MB-231 in response to various stimuli. However, the role of lipopolysaccharide (LPS) in the regulation of GM-CSF in MDA-MB-231 breast cancer cells so far remains unclear. Herein, we asked whether LPS could induce GM-CSF production in MDA-MB-231 cells, and if so, which signaling pathway was involved. MDA-MB-231 cells were treated with LPS or tumor necr

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45

Otsuyama, Ken-ichiro, Jakia Amin, Emi Uchida, Saeid Abroun, Karim Shamsasenjan, Khademul Islam, Hideki Asaoku, and Michio M. Kawano. "Baicalein Combined with Dexamethasone Can Induce the Marked PPARß-Mediated Suppression of Growth and Survival in Human Myeloma Cells." Blood 108, no. 11 (November 16, 2006): 5085. http://dx.doi.org/10.1182/blood.v108.11.5085.5085.

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Abstract PPAR (Peroxisome proliferator-activated receptor) ß is ubiquitously expressed in all cells and considered to be involved in the lipid metabolism and regulating the inflammatory response and cell proliferation. However, it remain to be clarified the role of PPARß in human myeloma cells. In order to identify the possible ligands for PPARß, we constructed the PPARß response element (PPREß)-lusiferase reporter gene and performed the reporter assay in Hela cell. We found that adrenal cortex hormones (DHEA and DHEA-S etc), dexamethasone (Dex) and baicalein augmented the expression of report

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Cheng, Qilai, Meixiang Liao, Haibo Hu, Hongliang Li, and Longhuo Wu. "Asiatic Acid (AA) Sensitizes Multidrug-Resistant Human Lung Adenocarcinoma A549/DDP Cells to Cisplatin (DDP) via Downregulation of P-Glycoprotein (MDR1) and Its Targets." Cellular Physiology and Biochemistry 47, no. 1 (2018): 279–92. http://dx.doi.org/10.1159/000489806.

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Background/Aims: P-glycoprotein (P-gp, i.e., MDR1) is associated with the phenotype of multidrug resistance (MDR) and causes chemotherapy failure in the management of cancers. Searching for effective MDR modulators and combining them with anticancer drugs is a promising strategy against MDR. Asiatic acid (AA), a natural triterpene isolated from the plant Centella asiatica, may have an antitumor activity. The present study assessed the reversing effect of AA on MDR and possible molecular mechanisms of AA action in MDR1-overexpressing cisplatin (DDP)-resistant lung cancer cells, A549/DDP. Method

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Alrashed, Fatema, Zunair Ahmad, Reeby Thomas, Abdulwa Alghaith, Motasem Melhem та Rasheed Ahmad. "Neutral sphingomyelinase 2 regulates inflammatory responses in monocytes/macrophages induced by TNF-α". Journal of Immunology 204, № 1_Supplement (1 травня 2020): 59.26. http://dx.doi.org/10.4049/jimmunol.204.supp.59.26.

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Abstract Obesity is associated with elevated levels of TNF-α and proinflammatory CD11c monocytes/macrophages. TNF-α mediated dysregulation in the plasticity of monocytes/macrophages is concomitant with pathogenesis of several inflammatory diseases, including metabolic syndrome, but the underlying mechanisms are incompletely understood. Since neutral sphingomyelinase 2 (nSMase2; product of the sphingomyelin phosphodiesterase 3 gene, SMPD3) is a key enzyme for ceramide production involved in inflammation, we investigated whether the nSMase2 contributed to the inflammatory changes in the monocyte

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Varney, Melinda, Andres Jerez, Jing Fang, David Miller, Lyndsey Bolanos, Aly Karsan, Jaroslaw P. Maciejewski та Daniel T. Starczynowski. "Tifab, a Novel Candidate Gene in Deletion Chromosome 5q, Contributes to Deregulation of NF-κB Signaling in MDS/AML." Blood 120, № 21 (16 листопада 2012): 2812. http://dx.doi.org/10.1182/blood.v120.21.2812.2812.

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Abstract Abstract 2812 Myelodysplastic syndromes (MDS) are hematologic disorders defined by blood cytopenias due to ineffective hematopoiesis, altered cytogenetics, and predisposition to acute myeloid leukemia (AML). The most common cytogenetic alteration in de novo and treatment-related MDS is deletion of chromosome 5q (del(5q)). There are two commonly deleted regions (CDR) mapped to chr 5q, however the gene(s) in these regions responsible for the manifestation of del(5q) MDS are not clearly defined. A search of annotated genes revealed that TRAF-interacting protein with forkhead-associated d

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Ellegast, Jana M., Gabriela Alexe, Amanda Hamze, Shan Lin, Maxim Pimkin, Linda Ross, Neekesh V. Dharia, et al. "Unleashing Cell-Intrinsic Inflammation As a Strategy to Kill AML Blasts." Blood 138, Supplement 1 (November 5, 2021): 3305. http://dx.doi.org/10.1182/blood-2021-151511.

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Abstract Leukemic blasts are immune cells gone awry. We hypothesized that dysregulation of inflammatory pathways contributes to the maintenance of their leukemic state and can be exploited as cell-intrinsic, self-directed immunotherapy. To test the hypothesis, we analyzed three large, independent data collections from primary acute myeloid leukemia (AML) samples and identified an AML subgroup of approximately 40% of all samples enriched for immune and inflammatory pathways. Moreover, we observed a positive correlation between the enrichment of inflammatory response and a monocytic lineage sign

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Kuncio, Gerald S., Mariya Tsyganskaya, Jianling Zhu, Shu-Ling Liu, Laszlo Nagy, Vilmos Thomazy, Peter J. A. Davies та Mark A. Zern. "TNF-α modulates expression of the tissue transglutaminase gene in liver cells". American Journal of Physiology-Gastrointestinal and Liver Physiology 274, № 2 (1 лютого 1998): G240—G245. http://dx.doi.org/10.1152/ajpgi.1998.274.2.g240.

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One of several postulated roles for tissue transglutaminase (tTG) is the stabilization and assembly of extracellular matrix via peptide cross-linking. We previously determined that tTG activity increased in an animal model of hepatic fibrogenesis and in human liver disease. To further study the role of tTG in liver disease, we initiated investigations into the effect of a proinflammatory mediator, tumor necrosis factor (TNF)-α, on tTG activity in cultured liver cells. Treatment of human Hep G2 cells with 1 ng/ml TNF-α increased [14C]putrescine cross-linking to cellular proteins. An increase in

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