Transcription Factor RelB
Transcription Factors
Transcription, Genetic
Promoter Regions, Genetic
DNA-Binding Proteins
Sp1 Transcription Factor
Gene Expression Regulation
Molecular Sequence Data
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Base Sequence
Transcriptional Activation
Binding Sites
Evidence for distinct intracellular signaling pathways in CD34+ progenitor to dendritic cell differentiation from a human cell line model. (1/327)
Intracellular signals that mediate differentiation of pluripotent hemopoietic progenitors to dendritic cells (DC) are largely undefined. We have previously shown that protein kinase C (PKC) activation (with phorbol ester (PMA) alone) specifically induces differentiation of primary human CD34+ hemopoietic progenitor cells (HPC) to mature DC. We now find that cytokine-driven (granulocyte-macrophage CSF and TNF-alpha) CD34+ HPC-->DC differentiation is preferentially blocked by inhibitors of PKC activation. To further identify intracellular signals and downstream events important in CD34+ HPC-->DC differentiation we have characterized a human leukemic cell line model of this process. The CD34+ myelomonocytic cell line KG1 differentiates into dendritic-like cells in response to granulocyte-macrophage CSF plus TNF-alpha, or PMA (with or without the calcium ionophore ionomycin, or TNF-alpha), with different stimuli mediating different aspects of the process. Phenotypic DC characteristics of KG1 dendritic-like cells include morphology (loosely adherent cells with long neurite processes), MHC I+/MHC IIbright/CD83+/CD86+/CD14- surface Ag expression, and RelB and DC-CK1 gene expression. Functional DC characteristics include fluid phase macromolecule uptake (FITC-dextran) and activation of resting T cells. Comparison of KG1 to the PMA-unresponsive subline KG1a reveals differences in expression of TNF receptors 1 and 2; PKC isoforms alpha, beta I, beta II, and mu; and RelB, suggesting that these components/pathways are important for DC differentiation. Together, these findings demonstrate that cytokine or phorbol ester stimulation of KG1 is a model of human CD34+ HPC to DC differentiation and suggest that specific intracellular signaling pathways mediate specific events in DC lineage commitment. (+info)Constitutive nuclear translocation of NF-kappa B in B cells in the absence of I kappa B degradation. (2/327)
Members of the NF-kappa B/Rel family of transcription factors are involved in many aspects of B lymphocyte development and function. NF-kappa B is constitutively active in these cells, in contrast with most other cell types. In the inactive form, NF-kappa B/Rel proteins are sequestered in the cytoplasm by members of the I kappa B family of NF-kappa B inhibitors. When activated, NF-kappa B is translocated to the nucleus, a process that involves the phosphorylation and proteasomal degradation of I kappa B proteins. Thus, NF-kappa B activation is accompanied by the rapid turnover of I kappa B proteins. We show that while this "classical" mode of NF-kappa B activation is a uniform feature of IgM+ B cell lines, all IgG+ B cells analyzed contain nuclear NF-kappa B yet have stable I kappa B alpha, I kappa B beta, and I kappa B epsilon. Furthermore, I kappa beta epsilon levels are at least 10 times lower in IgG+ B cells than in IgM+ B cells, an additional indication that the regulation of constitutive NF-kappa B activity in these two types of B cells is fundamentally different. These data imply the existence of a novel mechanism of NF-kappa B activation in IgG+ B cells that operates independently of I kappa B degradation. They further suggest that different isoforms of the B cell receptor may have distinct roles in regulating NF-kappa B activity. (+info)Dendritic cells and the pathogenesis of rheumatoid arthritis. (3/327)
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease in which unknown arthrogenic autoantigen is presented to CD4+ T cells. The strong association of the disease with an epitope within the HLA-DR chain shared between various alleles of HLA-DR4 and DR1 emphasizes the importance of antigen presentation. This immune response predominantly occurs in the synovial tissue and fluid of the joints and autoreactive T cells are readily demonstrable in both the synovial compartment and blood. Circulating dendritic cells (DC) are phenotypically and functionally identical with normal peripheral blood (PB) DC. In the synovial tissue, fully differentiated perivascular DC are found in close association with T cells and with B cell follicles, sometimes containing follicular DC. These perivascular DC migrate across the activated endothelium from blood and receive differentiative signals within the joint from monocyte-derived cytokines and CD40-ligand+ T cells. In the SF, DC manifest an intermediate phenotype, similar to that of monocyte-derived DC in vitro. Like a delayed-type hypersensitivity response, the rheumatoid synovium represents an effector site. DC at many effector sites have a characteristic pattern of infiltration and differentiation. It is important to note that the effector response is not self-limiting in RA autoimmune inflammation. In this article, we argue that the presentation of self-antigen by DC and by autoantibody-producing B cells is critical for the perpetuation of the autoimmune response. Permanently arresting this ongoing immune response with either pharmaceutical agents or immunotherapy is a major challenge for immunology. (+info)c-Rel and p65 trans-activate the monocyte chemoattractant protein-1 gene in interleukin-1 stimulated mesangial cells. (4/327)
BACKGROUND: The chemokine monocyte chemoattractant protein-1 (MCP-1) is secreted by human glomerular mesangial cells in response to interleukin-1 (IL-1) and has a central role in amplifying the inflammatory response during glomerulonephritis. However, the mechanism by which IL-1 regulates its transcription is not understood. Specific members of the nuclear factor kappaB/rel (NF-kappaB) proteins may regulate MCP-1 expression in a stimulus- and tissue-specific manner. METHODS: Electrophoretic mobility shift assays and Western blot analysis characterized the members of the NF-kappaB family that bound the two NF-kappaB sites of the MCP-1 enhancer (A1 and A2) in vitro. Trans-activation of the MCP-1 gene was investigated by transfer of the MCP-1 enhancer DNA to mesangial cells. RESULTS: Primary human mesangial cells contained in addition to p50 (NF-kappaB1) and p65 (Rel A) NF-kappaB proteins, the oncoprotein c-rel, and Rel B, but not p52 (NF-kappaB2). IL-1 induced c-rel to form a complex with p65, which bound the MCP-1 A2 site but not the A1 or IL-6 NF-kappaB sites in vitro. IL-1 up-regulated transfected MCP-1 enhancer activity. Cotransfer of the MCP-1 enhancer together with individual members of the NF-kappaB family showed that the heterodimer c-relp65 or (p65)2 can selectively trans-activate the MCP-1 gene via its A1 and A2 sites in mesangial cells. CONCLUSIONS: This study demonstrates for the first time that the c-rel oncoprotein can enhance MCP-1 transcription in mesangial cells and suggests that it may have an important role in amplifying gene expression in the inflamed glomerulus. (+info)Caerulein-induced NF-kappaB/Rel activation requires both Ca2+ and protein kinase C as messengers. (5/327)
The eukaryotic transcription factor NF-kappaB/Rel is activated by a large variety of stimuli. We have recently shown that NF-kappaB/Rel is induced during the course of caerulein pancreatitis. Here, we show that activation of NF-kappaB/Rel by caerulein, a CCK analog, requires increasing intracellular Ca2+ levels and protein kinase C activation. Caerulein induces a dose-dependent increase of nuclear NF-kappaB/Rel binding activity in pancreatic lobules, which is paralleled by degradation of IkappaBalpha. IkappaBbeta was only slightly affected by caerulein treatment. Consistent with an involvement of Ca2+, the endoplasmic reticulum-resident Ca2+-ATPase inhibitor thapsigargin activated NF-kappaB/Rel in pancreatic lobules. The intracellular Ca2+ chelator TMB-8 prevented IkappaBalpha degradation and subsequent nuclear translocation of NF-kappaB/Rel induced by caerulein. BAPTA-AM was less effective. Cyclosporin A, a Ca2+/calmodulin-dependent protein phosphatase (PP2B) inhibitor, decreased caerulein-induced NF-kappaB/Rel activation and IkappaBalpha degradation. The inhibitory effect of bisindolylmaleimide suggests that protein kinase C activity is also required for caerulein-induced NF-kappaB/Rel activation. These data suggest that Ca2+- as well as protein kinase C-dependent mechanisms are required for caerulein-induced NF-kappaB/Rel activation. (+info)The NF-kappa B family member RelB is required for innate and adaptive immunity to Toxoplasma gondii. (6/327)
The NF-kappa B family of transcription factors are associated with the regulation of innate and adaptive immunity to infection. Infection of C57BL/6 mice with Toxoplasma gondii resulted in up-regulation of NF-kappa B activity that included the NF-kappa B family member RelB. To assess the role of RelB in the regulation of the immune response to this infection, we challenged RelB-deficient mice (RelB-/-) and wild-type (WT) littermate controls with T. gondii. Although WT controls were resistant to T. gondii, RelB-/- mice succumbed 10-15 days after infection. Examination of accessory cell functions associated with resistance to T. gondii revealed that RelB-/- macrophages stimulated with IFN-gamma plus LPS or TNF-alpha produced IL-12 as well as reactive nitrogen intermediates and inhibited parasite replication similar to WT macrophages. Analysis of the systemic responses of RelB-/- and WT mice revealed that infected mice had similar serum levels of IL-12. However, RelB-/- mice challenged with T. gondii produced negligible levels of IFN-gamma and had reduced NK cell activity compared with WT mice. Similarly, splenocytes from uninfected RelB-/- mice stimulated with polyclonal stimuli were deficient in their ability to produce IFN-gamma. Together, our results demonstrate that RelB is essential for the development of innate NK and adaptive T cell responses that lead to the production of IFN-gamma and resistance to T. gondii. (+info)RelB modulation of IkappaBalpha stability as a mechanism of transcription suppression of interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necrosis factor alpha in fibroblasts. (7/327)
Members of the NF-kappaB/RelB family of transcription factors play important roles in the regulation of inflammatory and immune responses. RelB, a member of this family, has been characterized as a transcription activator and is involved in the constitutive NF-kappaB activity in lymphoid tissues. However, in a previous study we observed an overexpression of chemokines in RelB-deficient fibroblasts. Here we show that RelB is an important transcription suppressor in fibroblasts which limits the expression of proinflammatory mediators and may exert its function by modulating the stability of IkappaBalpha protein. Fibroblasts from relb(-/-) mice overexpress interleukin-1alpha (IL-1alpha), IL-1beta, and tumor necrosis factor alpha in response to lipopolysaccharide (LPS) stimulation. These cells have an augmented and prolonged LPS-inducible IKK activity and an accelerated degradation which results in a diminished level of IkappaBalpha protein, despite an upregulated IkappaBalpha mRNA expression. Consequently, NF-kappaB activity was augmented and postinduction repression of NF-kappaB activity was impaired in these cells. The increased kappaB-binding activity and cytokine overexpression was suppressed by introducing RelB cDNA or a dominant negative IkappaBalpha into relb(-/-) fibroblasts. Our findings suggest a novel transcription suppression function of RelB in fibroblasts. (+info)Expression of the RelB transcription factor correlates with the activation of human dendritic cells. (8/327)
The RelB gene product is a member of the nuclear factor (NF)-kappaB family of transcription factors. It has been identified recently within mouse antigen-presenting cells and human monocyte-derived dendritic cells (DC). Disruption of the mouse RelB gene is accompanied, amongst other phenotypes, by abnormalities in the antigen-presenting cell lineages. In order to define RelB expression during human DC differentiation, we have analysed RelB mRNA by reverse transcriptase-polymerase chain reaction and RelB protein by intracellular staining in CD34+ precursors and different types of DC preparations. RelB mRNA was not detected in CD34+ precursor populations. Fresh blood DC (lineage-human leucocyte antigen-DR+ (lin-HLA-DR+)) lacked RelB mRNA and cytoplasmic RelB protein but a period of in vitro culture induced RelB expression in blood DC. Purified Langerhans' cells (LC) (CD1a+ HLA-DR+) failed to express RelB mRNA. Immunocytochemical staining identified RelB protein in human skin epithelium. RelB protein was expressed in a very few CD1a+, CD83+ or CMRF-44+ dermal DC but was not present in CD1a+ LC. Tonsil DC (lin-HLA-DR+ CMRF-44+) were positive for RelB mRNA and RelB protein. Intestinal DC (HLA-DR+) also lacked immunoreactive RelB protein. The majority of interdigitating CD83+, CMRF-44+, CMRF-56+ or p55+ DC located in paracortical T-lymphocyte areas of lymph node and tonsil contained RelB protein. The expression of RelB mRNA and RelB protein correlates with the activated phase of blood DC and the postmigration cell (activated) stage of tissue DC development. (+info)Transcription Factor RelB is a member of the NF-κB family, functioning as a homodimer or heterodimer to regulate gene expression, primarily involved in immune and inflammatory responses, cell survival, and proliferation.
Transcription factor RelB is a member of the NF-κB (nuclear factor kappa B) family, which plays a crucial role in regulating immune responses, cell survival, and inflammation. RelB forms a heterodimer with other NF-κB family members, such as p50 or p52, and binds to specific DNA sequences called κB sites in the promoter regions of target genes. This binding leads to the activation or repression of gene transcription, ultimately influencing various cellular processes, including immune response regulation, development, and oncogenesis. RelB is unique among NF-κB family members because it can shuttle between the cytoplasm and nucleus even in unstimulated cells, although its activity is enhanced upon stimulation by various signals.
Transcription factors are specialized proteins that regulate the transcription of genetic information from DNA to RNA by binding to specific DNA sequences, thereby acting as molecular switches that turn genes on or off.
Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.
Transcription, Genetic is the process of creating an RNA copy of a sequence of DNA through the action of RNA polymerase and various transcription factors, which serves as a template for protein synthesis or other cellular functions.
Genetic transcription is the process by which the information in a strand of DNA is used to create a complementary RNA molecule. This process is the first step in gene expression, where the genetic code in DNA is converted into a form that can be used to produce proteins or functional RNAs.
During transcription, an enzyme called RNA polymerase binds to the DNA template strand and reads the sequence of nucleotide bases. As it moves along the template, it adds complementary RNA nucleotides to the growing RNA chain, creating a single-stranded RNA molecule that is complementary to the DNA template strand. Once transcription is complete, the RNA molecule may undergo further processing before it can be translated into protein or perform its functional role in the cell.
Transcription can be either "constitutive" or "regulated." Constitutive transcription occurs at a relatively constant rate and produces essential proteins that are required for basic cellular functions. Regulated transcription, on the other hand, is subject to control by various intracellular and extracellular signals, allowing cells to respond to changing environmental conditions or developmental cues.
'Promoter regions, genetic' are specific DNA sequences located primarily upstream of a gene that serve as binding sites for RNA polymerase and transcription factors, thereby regulating the initiation and rate of transcription of that gene.
Promoter regions in genetics refer to specific DNA sequences located near the transcription start site of a gene. They serve as binding sites for RNA polymerase and various transcription factors that regulate the initiation of gene transcription. These regulatory elements help control the rate of transcription and, therefore, the level of gene expression. Promoter regions can be composed of different types of sequences, such as the TATA box and CAAT box, and their organization and composition can vary between different genes and species.
'DNA-binding proteins' are defined as a category of proteins that interact with DNA, recognizing and binding to specific sequences or structures, thereby playing crucial roles in various cellular processes such as transcription regulation, DNA replication, repair, and recombination.
DNA-binding proteins are a type of protein that have the ability to bind to DNA (deoxyribonucleic acid), the genetic material of organisms. These proteins play crucial roles in various biological processes, such as regulation of gene expression, DNA replication, repair and recombination.
The binding of DNA-binding proteins to specific DNA sequences is mediated by non-covalent interactions, including electrostatic, hydrogen bonding, and van der Waals forces. The specificity of binding is determined by the recognition of particular nucleotide sequences or structural features of the DNA molecule.
DNA-binding proteins can be classified into several categories based on their structure and function, such as transcription factors, histones, and restriction enzymes. Transcription factors are a major class of DNA-binding proteins that regulate gene expression by binding to specific DNA sequences in the promoter region of genes and recruiting other proteins to modulate transcription. Histones are DNA-binding proteins that package DNA into nucleosomes, the basic unit of chromatin structure. Restriction enzymes are DNA-binding proteins that recognize and cleave specific DNA sequences, and are widely used in molecular biology research and biotechnology applications.
Sp1 Transcription Factor is a widely expressed zinc finger protein that binds to GC-rich motifs in the promoter regions of many housekeeping genes and some tissue-specific genes, acting as a transcriptional activator or repressor to regulate their expression.
Sp1 (Specificity Protein 1) transcription factor is a protein that binds to specific DNA sequences, known as GC boxes, in the promoter regions of many genes. It plays a crucial role in the regulation of gene expression by controlling the initiation of transcription. Sp1 recognizes and binds to the consensus sequence of GGGCGG upstream of the transcription start site, thereby recruiting other co-activators or co-repressors to modulate the rate of transcription. Sp1 is involved in various cellular processes, including cell growth, differentiation, and apoptosis, and its dysregulation has been implicated in several human diseases, such as cancer.
'Gene expression regulation' is the process by which the transcription or translation of a gene into functional products (proteins or RNA) is controlled, thus determining the amount and timing of protein synthesis that occurs in response to various intracellular and extracellular signals.
'Gene expression regulation' refers to the processes that control whether, when, and where a particular gene is expressed, meaning the production of a specific protein or functional RNA encoded by that gene. This complex mechanism can be influenced by various factors such as transcription factors, chromatin remodeling, DNA methylation, non-coding RNAs, and post-transcriptional modifications, among others. Proper regulation of gene expression is crucial for normal cellular function, development, and maintaining homeostasis in living organisms. Dysregulation of gene expression can lead to various diseases, including cancer and genetic disorders.
'Molecular sequence data' refers to the specific arrangement of molecules, such as nucleotides in DNA or amino acids in proteins, that are represented in a linear fashion and used to identify, compare, and analyze biological characteristics or relationships among organisms at the molecular level.
Molecular sequence data refers to the specific arrangement of molecules, most commonly nucleotides in DNA or RNA, or amino acids in proteins, that make up a biological macromolecule. This data is generated through laboratory techniques such as sequencing, and provides information about the exact order of the constituent molecules. This data is crucial in various fields of biology, including genetics, evolution, and molecular biology, allowing for comparisons between different organisms, identification of genetic variations, and studies of gene function and regulation.
In molecular biology, the "base sequence" refers to the specific order of nucleotides (adenine, thymine, guanine, and cytosine) that make up a DNA or RNA molecule, which is critical for encoding genetic information and determining the function of genes.
A base sequence in the context of molecular biology refers to the specific order of nucleotides in a DNA or RNA molecule. In DNA, these nucleotides are adenine (A), guanine (G), cytosine (C), and thymine (T). In RNA, uracil (U) takes the place of thymine. The base sequence contains genetic information that is transcribed into RNA and ultimately translated into proteins. It is the exact order of these bases that determines the genetic code and thus the function of the DNA or RNA molecule.
Transcriptional activation is the process by which transcription factors, usually bound to specific cis-acting elements in the DNA, recruit coactivators and other proteins to promote the initiation or increase the rate of transcription of a particular gene or set of genes.
Transcriptional activation is the process by which a cell increases the rate of transcription of specific genes from DNA to RNA. This process is tightly regulated and plays a crucial role in various biological processes, including development, differentiation, and response to environmental stimuli.
Transcriptional activation occurs when transcription factors (proteins that bind to specific DNA sequences) interact with the promoter region of a gene and recruit co-activator proteins. These co-activators help to remodel the chromatin structure around the gene, making it more accessible for the transcription machinery to bind and initiate transcription.
Transcriptional activation can be regulated at multiple levels, including the availability and activity of transcription factors, the modification of histone proteins, and the recruitment of co-activators or co-repressors. Dysregulation of transcriptional activation has been implicated in various diseases, including cancer and genetic disorders.
In Biochemistry and Pharmacology, 'binding sites' refer to specific regions on a macromolecule (such as a protein or nucleic acid) where another molecule (like a drug, ligand, or cofactor) can attach or bind, often influencing the function, activity, or conformation of the macromolecule.
In the context of medical and biological sciences, a "binding site" refers to a specific location on a protein, molecule, or cell where another molecule can attach or bind. This binding interaction can lead to various functional changes in the original protein or molecule. The other molecule that binds to the binding site is often referred to as a ligand, which can be a small molecule, ion, or even another protein.
The binding between a ligand and its target binding site can be specific and selective, meaning that only certain ligands can bind to particular binding sites with high affinity. This specificity plays a crucial role in various biological processes, such as signal transduction, enzyme catalysis, or drug action.
In the case of drug development, understanding the location and properties of binding sites on target proteins is essential for designing drugs that can selectively bind to these sites and modulate protein function. This knowledge can help create more effective and safer therapeutic options for various diseases.
Trans-activators are proteins that bind to specific DNA sequences in the promoter or enhancer regions of genes and increase the transcription rate of those genes by interacting with other components of the transcription machinery.
Trans-activators are proteins that increase the transcriptional activity of a gene or a set of genes. They do this by binding to specific DNA sequences and interacting with the transcription machinery, thereby enhancing the recruitment and assembly of the complexes needed for transcription. In some cases, trans-activators can also modulate the chromatin structure to make the template more accessible to the transcription machinery.
In the context of HIV (Human Immunodeficiency Virus) infection, the term "trans-activator" is often used specifically to refer to the Tat protein. The Tat protein is a viral regulatory protein that plays a critical role in the replication of HIV by activating the transcription of the viral genome. It does this by binding to a specific RNA structure called the Trans-Activation Response Element (TAR) located at the 5' end of all nascent HIV transcripts, and recruiting cellular cofactors that enhance the processivity and efficiency of RNA polymerase II, leading to increased viral gene expression.
RELB
Transcription factor RelB is a protein that in humans is encoded by the RELB gene. RELB has been shown to interact with NFKB2, ... which in association with RelB appears in the nucleus as RelB:p52 NF-κB heterodimers. RelB:p52 activates the expression ... Demarchi F, d'Adda di Fagagna F, Falaschi A, Giacca M (July 1996). "Activation of transcription factor NF-kappaB by the Tat ... Basak S, Shih VF, Hoffmann A (May 2008). "Generation and activation of multiple dimeric transcription factors within the NF- ...
Pyroptosis
HPV infection causes the upregulation of sirtuin 1 protein, which disrupts the transcription factor for AIM2, RelB. Knockdown ... These receptors upregulate expression of inflammatory cytokines such as IFN α/β, tumour necrosis factor (TNF), IL-6 and IL-12 ...
NFKBIE
NFKB1 or NFKB2 is bound to REL, RELA, or RELB to form the NF-κB transcription factor complex. The NF-κB complex is inhibited by ... activation requires NF-κB interaction with other transcription factors, such as STAT (see STAT6), AP-1 (JUN), and NFAT (see ... Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon, also known as NFKBIE, is a protein which ... "Entrez Gene: NFKBIE nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon". Whiteside ST, ...
RELA
Transcription factor p65 also known as nuclear factor NF-kappa-B p65 subunit is a protein that in humans is encoded by the RELA ... Seven proteins encoded by five genes are involved in the NF-κB complex, namely p105, p100, p50, p52, RELA, c-REL and RELB. Like ... "BRCA1 augments transcription by the NF-kappaB transcription factor by binding to the Rel domain of the p65/RelA subunit". The ... Xia C, Cheshire JK, Patel H, Woo P (Dec 1997). "Cross-talk between transcription factors NF-kappa B and C/EBP in the ...
Interleukin-1 receptor associated kinase
... and subsequent phosphorylation of the transcription factors p100/RelB in an IKKα-dependent mechanism. It was observed that IRAK ... IRF7 is a transcription factor that translocates into the nucleus when activated and initiates transcription of IFN-α. IRAK-1 ... TAK1 can then activate two transcription pathways, the nuclear factor-κB (NF-κB) pathway and the mitogen-activated protein ... Phosphorylated JNK/p38 can then translocate into the nucleus and phosphorylate and activate transcription factors such as c-Fos ...
TANK-binding kinase 1
... and activates two distinct transcription factors, NF-kappa B and IFN-regulatory factor-3, in the Toll-like receptor signaling ... This subunit dimerizes with RelB and mediates gene expression. In the canonical NFkB pathway, the NF-kappa-B (NFKB) complex of ... TANK-binding kinase 1 has been shown to interact with: NCK1, TANK, TRAF2 and TBKBP1 aka SINTBAD Transcription factors activated ... Subsequently, it phosphorylates the transcription factor IRF3, which is translocated to the nucleus, and promotes production of ...
NF-κB
... primary transcription factors, i.e., transcription factors that are present in cells in an inactive state and do not require ... Then p52 dimerizes with RelB to appear as a nuclear RelB:p52 DNA binding activity. RelB:p52 regulates the expression of ... Escárcega RO, Fuentes-Alexandro S, García-Carrasco M, Gatica A, Zamora A (March 2007). "The transcription factor nuclear factor ... Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is a protein complex that controls transcription of DNA ...
TRIM14
... was shown to interact with transcription factor PU.1 (SPI1) and inhibit its activity. PU.1 is a transcription factor critical ... They are ifna, il6 (ifnb2), isg15, raf-1, NF-kB (nf-kb1, rela, nf-kb2, relb), grb2, grb3-3, traf3ip2, junB, c-myb, pu.1, akt1, ... interaction with the transcription factors common to TRIM proteins. The mouse homologue of TRIM14, the "Pub protein", ... TRIM14 transfected HEK293 cell show increased transcription of eighteen genes involved in the innate immune system. ...
NFKBID
IκBNS is a member of the atypical inhibitors of NF-κB (also called the nuclear IκBs). NF-κB is a transcription factor, which ... It was reported that NFKBID interacts with p50, which is a subunit of NF-κB, p52, p65, RelB, and c-Rel. NFKBID binds these ... After NF-κB activation atypical IκBs are induced by the transcription factor Atypical IκBs, in turn, can regulate the NF-κB ... protein mediates regulatory T cell development via induction of the Foxp3 transcription factor". Immunity. 37 (6): 998-1008. ...
TANGO2
This region was used to determine transcription factor interactions. Some of the main transcription factors that bind to the ... C22orf25 has been shown to interact with NFKB1, RELA, RELB, BTRC, RPS27A, BCL3, MAP3K8, NFKBIA, SIN3A, SUMO1, Tat. Mutations in ...
Thymic epithelial cell
The most important transcription factor for all stages of TEC development in embryonic and postnatal thymus is a Foxn1. Foxn1 ... In contrast, mTEC development is dependent on the presence of Relb, NFκB signals and the TNFR superfamily but it could be ... The first steps of TEC development are regulated by the transcription factors (Hoxa3, Pax1/9, Eya1, Six1/4, Tbx1), most of ... and transcription factors, which have an effect on thymocyte development. TECs, situated in the corticomedullary junction, ...
Aryl hydrocarbon receptor
The first is the basic-region (b), which is involved in the binding of the transcription factor to DNA. The second is the helix ... Vogel CF, Sciullo E, Li W, Wong P, Lazennec G, Matsumura F (December 2007). "RelB, a new partner of aryl hydrocarbon receptor- ... The bHLH motif is located in the N-terminal of the protein and is a common entity in a variety of transcription factors. ... Sequential recruitment of transcription factors and differential phosphorylation of C-terminal domain of RNA polymerase II at ...
NFKB1
... nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ... RELB, STAT3, STAT6, and TSC22D3. GRCh38: Ensembl release 89: ENSG00000109320 - Ensembl, May 2017 GRCm38: Ensembl release 89: ... NF-κB is a transcription factor that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free ... Bottex-Gauthier C, Pollet S, Favier A, Vidal DR (2002). "[The Rel/NF-kappa-B transcription factors: complex role in cell ...
NFKB2
Schreck R, Albermann K, Baeuerle PA (1993). "Nuclear factor kappa B: an oxidative stress-responsive transcription factor of ... NFKB2 has been shown to interact with: BCL3, BTRC, MAP3K8, NFKB1, NFKBIE, RELA, RELB, REL, and TSC22D3. NF-κB DAVID syndrome ... Bottex-Gauthier C, Pollet S, Favier A, Vidal DR (Apr 2002). "[The Rel/NF-kappa-B transcription factors: complex role in cell ... Garg A, Aggarwal BB (Jun 2002). "Nuclear transcription factor-kappaB as a target for cancer drug development". Leukemia. 16 (6 ...
Autoimmune regulator
AIRE is a transcription factor expressed in the medulla (inner part) of the thymus. It is part of the mechanism which ... July 2000). "RNA and protein expression of the murine autoimmune regulator gene (Aire) in normal, RelB-deficient and in NOD ... Other AIRE partners include positive transcription elongation factor b (P-TEFb) and DNA activated protein kinase (DNA-PK). DNA- ... like conventional transcription factors, AIRE engages in coordinated sequences that are performed by its multimolecular ...
Soumen Basak
Extracellular cues engage discrete cell signaling pathways to control dynamically specific sets of transcription factors, which ... "Non-canonical NF-kB mutations reinforce pro-survival TNF response in multiple myeloma through an autoregulatory RelB:p50 NF-kB ... "Non-canonical NFκB mutations reinforce pro-survival TNF response in multiple myeloma through an autoregulatory RelB:p50 NFκB ...
Lymphotoxin alpha
As years progressed, its name was changed to tumor necrosis factor-beta (TNF-β). Later discovery of LT-β and LT-α1-β2 complex ... Yilmaz ZB, Weih DS, Sivakumar V, Weih F (January 2003). "RelB is required for Peyer's patch development: differential ... Copeland KF (December 2005). "Modulation of HIV-1 transcription by cytokines and chemokines". Mini Reviews in Medicinal ... Lymphotoxin-alpha (LT-α) formerly known as tumor necrosis factor-beta (TNF-β) is a protein that in humans is encoded by the LTA ...
MALT1
It has an important role in the activation of the transcription factor NF-κB, in the production of interleukin-2 (IL-2) and in ... "Malt1-dependent RelB cleavage promotes canonical NF-kappaB activation in lymphocytes and lymphoma cell lines". Proc Natl Acad ... "MALT1 auto-proteolysis is essential for NF-κB-dependent gene transcription in activated lymphocytes". PLOS ONE. 9 (8): e103774 ...
NFKBIB
"A cytokine-responsive IkappaB kinase that activates the transcription factor NF-kappaB". Nature. 388 (6642): 548-54. Bibcode: ... NFKB1 (MIM 164011) or NFKB2 (MIM 164012) is bound to REL (MIM 164910), RELA (MIM 164014), or RELB (MIM 604758) to form the NFKB ... "Entrez Gene: NFKBIB nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, beta". Woronicz JD, Gao X, ... Page M, Tuckerman EM, Li TC, Laird SM (2002). "Expression of nuclear factor kappa B components in human endometrium". J. Reprod ...
RelA and RelBTranslocationProteinsDimersProteinHeterodimericPathwayInducesNfkb2DifferentiationGenesNFKB1PathwaysNFkBNucleusDimeric transcriptionTranscriptionalStimulationCytokinesActivatesRegulationResponsesUbiquitousNuclear factorTumorPromoterAcuteActivationImmunityMechanismsLymphocyteQuantitativeTumorigenesisCellsExpressionInflammationActivityRoleAutoimmuneCellFamilyControl
RelA and RelB4
- These analyses suggest that an integrated NF-κB system network underlies activation of both RelA and RelB containing dimer and that a malfunctioning canonical pathway will lead to an aberrant cellular response also through the non-canonical pathway. (wikipedia.org)
- Furthermore, the introduction of Peyers areas in RelA and RelB can be clogged (Yilmaz et al. (cancerhappens.com)
- 2002). Because of this insufficiency it isn't possible to review the part of RelA and RelB in the FAE as well as the M cells within it using RelA- or RelB-deficient mice given that they absence Peyers areas. (cancerhappens.com)
- To examine NF-κB RelB signaling in DCs inside a quantitative way we created a numerical model that identifies the development and rules of RelA and RelB dimers with regards to mass actions kinetics (Supplementary Records). (buyresearchchemicalss.net)
Translocation5
- Stimulation of TLRs (Toll-Like Receptors) by a pathogen induces activation of signal transduction cascades, which leads to translocation of nuclear factor-κB (NF-κB) to the nucleus [ 1 ], activation of interferon regulatory factors 3/7 (IRF3/7) and/or activator protein-1 (AP-1), which cooperate to induce transcription of various cytokines such as alpha/beta interferon (IFN-α/β) to counteract infection [ 2 - 4 ]. (biomedcentral.com)
- ultimately, this results in nuclear translocation of p52 and RelB in NDCs. (bvsalud.org)
- It is also known as Transcription factor p65 and is a REL-associated protein involved in NF-κB heterodimer formation, nuclear translocation and activation. (antibodyguide.com)
- NIK phosphorylates and activates IKKα, which in turn phosphorylates p100, triggering p100 processing, and leading to the generation of p52 and the nuclear translocation of p52 and RELB. (creative-proteomics.com)
- Preliminary data indicate that chronic but not acute TNF stimulation also induces RelB nuclear translocation and DNA binding. (biomedcentral.com)
Proteins5
- NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. (abcam.com)
- In addition to increasing the transcription of cytokines and adhesion proteins, NF-κB also increases the transcription of IκB, thus leading to its own inactivation and subsequent termination of the response. (soton.ac.uk)
- The first subfamily of proteins (c-Rel, RelB, p65/RelA) contains a C-terminal transactivation domain. (oncotarget.com)
- In mammals, there are five members of the transcription factor NF-κB family: RELA (p65), RELB and c-REL, and the precursor proteins NF-κB1 (p105) and NF-κB2 (p100), which are processed into p50 and p52, respectively. (creative-proteomics.com)
- Results Proteins involved in maintenance DNA methylation and R-loop resolution/prevention are decreased on nascent DNA in the absence of CDCA7 We hypothesized that the CDCA7/HELLS complex could 21-Hydroxypregnenolone play a role in facilitating maintenance DNA methylation at pericentromeric repeats by recruiting DNA methylation maintenance factors. (cell-signaling-pathways.com)
Dimers2
- Moreover, generation of canonical and non-canonical dimers, viz RelA:p50 and RelB:p52, within the cellular milieu are mechanistically interlinked. (wikipedia.org)
- NF-κB transcription factors bind as dimers to κB sites in promoters and enhancers of a variety of genes and induce or repress transcription. (creative-proteomics.com)
Protein8
- Transcription factor RelB is a protein that in humans is encoded by the RELB gene. (wikipedia.org)
- In resting cells, RelB is sequestered by the NF-κB precursor protein p100 in the cytoplasm. (wikipedia.org)
- The nuclear transcription factor NF-κB is a dimer composed of Rel protein family members. (xcessbio.com)
- The NF-κB protein RelB controls dendritic cell (DC) maturation and could be targeted therapeutically to manipulate T cell responses in disease. (buyresearchchemicalss.net)
- Shape 1 A MEF-based kinetic model will not take into account RelB rules in DCs To adjust the model to DCs we 1st measured the manifestation of crucial NF-κB protein in bone tissue marrow-derived DCs (BMDCs) compared to mouse embryonic fibroblasts (MEFs) and bone tissue marrow-derived macrophages (BMDMs). (buyresearchchemicalss.net)
- A central adaptor protein of the noncanonical NF-κB pathway is NF-κB-inducing kinase (NIK), which activates the downstream kinase IKKα to process p100 to p52, thereby forming the RelB/p52 heterodimer to initiate the expression of target genes. (xiahepublishing.com)
- 1 MYC is a basic helix-loop-helix-leucine zipper transcription factor that dimerizes with the related protein MAX. (ashpublications.org)
- Not only does LPS set the start for the comorbidities that increase the risk associated with SARS-CoV-2 infection, Gianna Petruk and colleagues show that LPS works synergistically with the spike protein from the SARS-CoV-2 virus to further increase inflammation through an increase in nuclear factor-κB (NF-κB) transcription, activation, and pro-longed signaling. (anoasisofhealing.com)
Heterodimeric2
- NF-kappa-B heterodimeric p65-p50 and RelB-p50 complexes are transcriptional activators. (hmdb.ca)
- The NF-kappa-B heterodimeric RelB-p52 complex is a transcriptional activator. (cusabio.com)
Pathway12
- In this pathway, NIK stimulates the processing of p100 into p52, which in association with RelB appears in the nucleus as RelB:p52 NF-κB heterodimers. (wikipedia.org)
- For example, syntheses of the constituents of the non-canonical pathway, viz RelB and p52, are controlled by canonical IKK2-IκB-RelA:p50 signalling. (wikipedia.org)
- Our findings demonstrated that BMSCs promote remyelination in the spinal cord of HD-exposed rats via TNFα/RelB-Hes1 pathway, providing novel insights for evaluating and further exploring the therapeutical effect of BMSCs on demyelinating neurodegenerative disease. (biomedcentral.com)
- Forkhead box G1 (FOXG1, also known as BF1), a member of the FOX family and an inhibitor of TGF-ß signaling pathway, is a nucleocytoplasmic transcription factor that is essential for forebrain development. (bvsalud.org)
- RelB was also found to be rapidly triggered in DCs by canonical pathway stimuli TNF and lipopolysaccharide (LPS)16-19 and the canonical signaling pathway component TRAF6 was shown to be essential9. (buyresearchchemicalss.net)
- We used a Systems Biology approach of iterative computational modeling and quantitative experimental analyses of the NF-κB signaling network in DCs to reveal that RelB activity was limited by classical IκBs IκBα and IκBε and regulated via the canonical pathway. (buyresearchchemicalss.net)
- Modeling studies identified two DC-specific control points that render RelB subject to regulation by the canonical pathway and we demonstrated their sufficiency by engineering MEFs accordingly to produce Cyclo (-RGDfK) DC-like RelB control. (buyresearchchemicalss.net)
- Finally gene expression profiling revealed that RelB-dependent gene expression programs regulated by the canonical pathway activity control DC-orchestrated immune responses. (buyresearchchemicalss.net)
- The non-canonical pathway involving the kinases NIK and IKK1 triggers processing of p100 to p52 and generation of the RelB-p52 transcription factor which is implicated in cell survival and maturation. (buyresearchchemicalss.net)
- Our data reveal that DC differentiation requires not only improved manifestation of RelB but also raised constitutive activity of the non-canonical NF-κB signaling pathway. (buyresearchchemicalss.net)
- The NF-kB signaling pathway is a family of mammalian transcription factors NF-kB, composed of P50, P52, REL, REL-A and REL-B, and is widely used in the processing of tumor necrosis and lymphotoxin receptor activator. (creative-proteomics.com)
- In a non-canonical activation pathway, the MAP3K14-activated CHUK/IKKA homodimer phosphorylates NFKB2/p100 associated with RelB, inducing its proteolytic processing to NFKB2/p52 and the formation of NF-kappa-B RelB-p52 complexes. (cusabio.com)
Induces1
- A variety of cell stimuli activate NF-B transcription factors which in-turn induces the transcription of multiple target genes (May and Ghosh, 1998). (cancerhappens.com)
Nfkb22
- RELB has been shown to interact with NFKB2, NFKB1, and C22orf25. (wikipedia.org)
- NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. (nih.gov)
Differentiation7
- This control of cDC homeostasis is mediated by a number of factors that drive cDC differentiation, proliferation, and survival or apoptosis ( 4 ). (frontiersin.org)
- NF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. (abcam.com)
- The expressional changes of Hes1, a transcription factor negatively regulating OPC-differentiation, were studied. (biomedcentral.com)
- In vitro cultured OPCs showed more differentiation after incubation with BMSC-CM. Hes1 expression was found to be significantly increased by HD and decreased by BMSC or BMSC-CM. The change of Hes1 was found, however, independent of Notch1 activation, but dependent on TNFα/RelB signaling. (biomedcentral.com)
- 2015). The fate and terminal differentiation of distinct intestinal epithelial cell lineages from their uncommitted precursors is dependent on their intrinsic expression of one or more specific transcription factors during their development. (cancerhappens.com)
- NF-κB transcription factors are critical regulators of immunity, stress responses, apoptosis and differentiation. (creative-proteomics.com)
- NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. (cusabio.com)
Genes12
- Upon degradation of the inhibitor, NF-kappa-B moves to the nucleus and activates transcription of specific genes. (nih.gov)
- Our in silico findings report that there is cross-regulation between both pathways at the level of gene transcription regulation, mediated by the presence of binding sites for both factors in promoters of genes essential for these pathways. (biomedcentral.com)
- In this paper we examine evidence for a direct crosstalk of the NF-κB and IRF3 signaling pathways at the lowest level, between main transcription factors and genes coding for these transcription factors. (biomedcentral.com)
- We analyzed respective gene promoters' sequences using in silico methods for identification of transcription binding sites, mainly in the NF-κB- and IRF-coding genes. (biomedcentral.com)
- The NF-κB transcription factor complex plays a key role in the expression of genes involved in immune responses. (johnshopkins.edu)
- 2013). Analysis of the transcription factor binding site motifs in the promoter regions within this cluster of genes indicated that they shared a transcriptional programme, and suggested that motifs for the nuclear factor-B (NF-B) family of transcription factors were significantly enriched (Kobayashi et al. (cancerhappens.com)
- Like its homolog Bcl3, IκBζ can regulate the transcription of a set of inflamatory genes through its association with the p50 or p52 subunits of NF-κB. (oncotarget.com)
- 2 , 3 These NF-κB subunits form various homodimers or heterodimers that bind to κB enhancers of target genes and regulate their transcription. (xiahepublishing.com)
- To do so, MYC controls transcription of multiple genes involved in cell growth and metabolism, vasculogenesis, cell adhesion, and genomic stability. (ashpublications.org)
- MYC/MAX heterodimers bind to specific DNA elements, designated as E-boxes, located in the promoter regions of target genes mediating either activation or repression of transcription. (ashpublications.org)
- By interrogation of extended fragments of genomic sequence from 66 TNF-induced genes, we have mapped the DNA binding consensus sequence sites for different transcription factors. (biomedcentral.com)
- Precursor of the p52 subunit of the nuclear factor NF-kappa-B, which binds to the kappa-B consensus sequence 5'-GGRNNYYCC-3', located in the enhancer region of genes involved in immune response and acute phase reactions. (affbiotech.com)
NFKB11
- or RELB (MIM 604758) to form the NFKB complex.The p50 (NFKB1)/p65 (RELA) heterodimer is the most abundant form of NFKB. (bioinf.org)
Pathways3
- The upstream Notch1 and TNFα/RelB pathways were studied, and some key signaling molecules were measured. (biomedcentral.com)
- In contrast, regulation of breast cancer CSCs (BCSCs) occurs by CD44 standard splice isoform (CD44s)-activated platelet-derived growth factor receptor b (PDGFRb)/signal transducer and activator of transcription 3 (STAT3), forkhead box C1 (FOXC1)-activated sonic hedgehog (SHH), and sphingosine-1-phosphate (S1P)/S1PR3-activated NOTCH pathways [ 10 - 13 ] . (oaepublish.com)
- To provide insight into the mechanisms whereby sustained tumour necrosis factor (TNF) stimulation promotes chronic inflammatory responses, we have examined TNF-R signalling pathways in murine T-cell hybridomas. (biomedcentral.com)
NFkB1
- NFkB-p100 a transcription factor of the nuclear factor-kappaB ( NFkB) group. (affbiotech.com)
Nucleus1
- To investigate tumor necrosis factor α (TNF α) and interleukin-1β (IL-1 β) regulation of CCL3 expression in nucleus pulposus (NP) cells and in macrophage migration. (shu.ac.uk)
Dimeric transcription1
- NF-B is usually a widely studied dimeric transcription factor induced by several stimuli including inflammatory cytokines, lipopolysaccharides, and others [19]. (medicalconsultingcenter.com)
Transcriptional1
- In concert with RELB, regulates the circadian clock by repressing the transcriptional activator activity of the CLOCK-ARNTL/BMAL1 heterodimer. (cusabio.com)
Stimulation1
- However, with continued stimulation RelB completely disappeared from anti-Ig-stimulated κB binding material, but remained a component of CD40L-induced NF-κB. (johnshopkins.edu)
Cytokines1
- The atherosclerotic process is accelerated by a myriad of factors, such as the release of inflammatory chemokines and cytokines, the generation of reactive oxygen species (ROS), growth factors, and the proliferation of vascular smooth muscle cells. (hindawi.com)
Activates1
- RelB:p52 activates the expression homeostatic lymphokines, which instruct lymphoid organogenesis and determine the trafficking of naive lymphocytes in the secondary lymphoid organs. (wikipedia.org)
Regulation2
- We conclude that members of the NF-κB family may directly impact regulation of IRF family, while IRF members impact regulation of NF-κB family rather indirectly, via other transcription factors such as AP-1 and SP1. (biomedcentral.com)
- The loss of DNA-binding RelB from anti-Ig-induced NF-κB did not result from depletion of RelB from B cell nuclei, suggesting specific regulation of RelB function which is not directly attributed to IκB function. (johnshopkins.edu)
Responses1
- Here we report that when mice lacking the RelA subunit of NF-κB are brought to term by breeding onto a tumor necrosis factor receptor (TNFR)1-deficient background, the mice that are born lack lymph nodes, Peyer's patches, and an organized splenic microarchitecture, and have a profound defect in T cell-dependent antigen responses. (rupress.org)
Ubiquitous2
- NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. (nih.gov)
- NF-κB ( Nuclear Factor kappa B ) is a ubiquitous family of transcription factors involved in biological processes such as inflammation, immunity, proliferation and apoptosis [ 1 - 3 ]. (oncotarget.com)
Nuclear factor2
- The transcription factor nuclear factor (NF)-κB has been suggested to be a key mediator of the development of lymph nodes and Peyer's patches. (rupress.org)
- Each alone, SARS-CoV-2 infection or LPS metabolic endotoxemia, can create problems, but collectively, cause significantly more systemic havoc through pro-longed nuclear factor-κB (NF-κB) transcription. (anoasisofhealing.com)
Tumor3
- Herein, we engineered attenuated Salmonella typhimurium VNP20009 with gene circuits to synthetize granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 7 (IL-7) within tumors, which recruited dendritic cells (DCs) and enhanced T cell priming to elicit anti-tumor response. (bvsalud.org)
- The c-MYC (MYC) transcription factor has been implicated in the control of many aspects of tumor cell biology. (ashpublications.org)
- The NF-κB transcription factor is also linked to tumor initiation and progression. (ashpublications.org)
Promoter1
- In contrast, c-Rel and RelB had little effect on promoter activity. (shu.ac.uk)
Acute1
- Controlling these factors reduces the risk of acute vascular complications and death from CVD [ 1 , 7 ]. (hindawi.com)
Activation5
- Cardiovascular (CV) risk factors such as hypercholesterolemia, hyperglycaemia, obesity, hypertension, smoking, and aging promote vascular inflammation and endothelial activation [ 7 - 9 ]. (hindawi.com)
- Using a mAb specific for the activated form of NF-κB, immunocytochemistry, confocal microscopy, and gel shift assays have been used in conjunction to localize this transcription factor to human lung mast cells and to study its activation. (soton.ac.uk)
- Activation of mast cells with stem cell factor (10 ng/ml) and anti-IgE (1 μg/ml) induced maximal activation of NF-κB at 4 and 2 h, respectively. (soton.ac.uk)
- it recapitulates well-documented NF-κB control in MEFs20-22 such as for example fast LPS-induced RelA activation and postponed lymphotoxin β-mediated RelB activation (Fig. Cyclo (-RGDfK) 1b). (buyresearchchemicalss.net)
- Notably, the activation of MT1-MMP and the pro-invasive effects of NIK persist in the absence of the downstream NF-kappaB transcription factors RelA/p65 and RelB. (tamu.edu)
Immunity1
- Inflammation and immunity are key factors for the development and complications of atherosclerosis, and therefore, the whole atherosclerotic process is a target for diagnosis and treatment. (hindawi.com)
Mechanisms2
- In DCs the molecular control mechanisms must provide for constitutive RelB expression to enable rapid and decisive induction of maturation programs following exposure to pathogens or PAMPs but must limit spontaneous maturation of DCs in their absence. (buyresearchchemicalss.net)
- In this study we elucidated the molecular mechanisms responsible for regulating RelB in DCs. (buyresearchchemicalss.net)
Lymphocyte1
- Most intriguingly, a recent study identified that TNF-induced canonical signalling subverts non-canonical RelB:p52 activity in the inflamed lymphoid tissues limiting lymphocyte ingress. (wikipedia.org)
Quantitative1
- Quantitative reverse transcription polymerase chain reaction and immunohistochemistry were used to measure CCL3 expression in NP cells. (shu.ac.uk)
Tumorigenesis1
- There are many known risk factors involved in the tumorigenesis and progression of BC, such as obesity, genetic factors, family history, and endocrine factors. (aging-us.com)
Cells4
- 2003). The NF-B subunits RelB and RelA perform a crucial part in the introduction of supplementary lymphoid cells, including Peyers areas. (cancerhappens.com)
- The aggressive invasion of GBM cells into healthy brain tissue is a major factor contributing to the therapy resistance and poor prognosis of this malignancy. (tamu.edu)
- 3 In resting cells, the NF-κB dimer is inactive and is sequestered in the cytoplasm by binding to members of the κB inhibitory factor (IκB) family. (xiahepublishing.com)
- We demonstrated that abnormal transcription from hypomethylated pericentromeric satellite repeats and the formation of aberrant DNA:RNA hybrids occur in ICF mutant cells and presumably trigger DNA damage. (cell-signaling-pathways.com)
Expression3
- NF-κB also controls expression of the downstream IFN auto-amplification loop through STAT1, IRF-1, −5, and −7 transcription factors. (biomedcentral.com)
- HD was found to increase TNFα, RelB and Hes1 expression, and BMSCs were found to have the opposite effect. (biomedcentral.com)
- Addition of recombinant TNFα to OPCs or RelB overexpression similarly caused upregulation of Hes1 expression. (biomedcentral.com)
Inflammation2
- The NF-κB and IRF transcription factor families are major players in inflammation and antiviral response and act as two major effectors of the innate immune response (IIR). (biomedcentral.com)
- NF-κB is a transcription factor that plays a key role in regulating the immune response to infection and inflammation. (antibodyguide.com)
Activity1
- these together potently accumulated unprocessed p100, which attenuated the RelB activity. (wikipedia.org)
Role1
- As a result, growing evidence support the role of this transcription factor in the pathogenesis number of human hematological and solid malignancies. (oncotarget.com)
Autoimmune1
- A single nucleotide polymorphism, PTPN22 R620W , is one of the strongest genetic risk factors for multiple autoantibody associated human autoimmune diseases. (frontiersin.org)
Cell1
- These domains are found in cell surface receptors such as Met and Ron as well as in intracellular transcription factors where it is involved in DNA binding. (embl.de)
Family1
- 2013). The NF-B family of transcription factors consists of five members: NF-B1 (p50), NF-B2 (p52), RelA (p65), RelB and c-Rel. (cancerhappens.com)
Control4
- The control of the risk factors is the main cost-effective available measure for preventing major events associated to CVD [ 10 ]. (hindawi.com)
- These reports suggest that RelB control in DCs may be different than what has been described in MEFs. (buyresearchchemicalss.net)
- ß-catenin engages IKZF factors to control lymphopoiesis. (ucsf.edu)
- ssvQC: an integrated CUT&RUN quality control workflow for histone modifications and transcription factors. (ucsf.edu)