Transcription Factor CHOP
Endoplasmic Reticulum
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
Transcription Factors
Unfolded Protein Response
A cellular response to environmental insults that cause disruptions in PROTEIN FOLDING and/or accumulation of defectively folded protein in the ENDOPLASMIC RETICULUM. It consists of a group of regulatory cascades that are triggered as a response to altered levels of calcium and/or the redox state of the endoplasmic reticulum. Persistent activation of the unfolded protein response leads to the induction of APOPTOSIS.
Transcription, Genetic
CCAAT-Enhancer-Binding Proteins
A class of proteins that were originally identified by their ability to bind the DNA sequence CCAAT. The typical CCAAT-enhancer binding protein forms dimers and consists of an activation domain, a DNA-binding basic region, and a leucine-rich dimerization domain (LEUCINE ZIPPERS). CCAAT-BINDING FACTOR is structurally distinct type of CCAAT-enhancer binding protein consisting of a trimer of three different subunits.
Endoplasmic Reticulum Stress
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
Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)-ATF composite site to regulate Gadd153 expression during the stress response. (1/701)
Gadd153, also known as chop, encodes a member of the CCAAT/enhancer-binding protein (C/EBP) transcription factor family and is transcriptionally activated by cellular stress signals. We recently demonstrated that arsenite treatment of rat pheochromocytoma PC12 cells results in the biphasic induction of Gadd153 mRNA expression, controlled in part through binding of C/EBPbeta and two uncharacterized protein complexes to the C/EBP-ATF (activating transcription factor) composite site in the Gadd153 promoter. In this report, we identified components of these additional complexes as two ATF/CREB (cAMP-responsive-element-binding protein) transcription factors having differential binding activities dependent upon the time of arsenite exposure. During arsenite treatment of PC12 cells, we observed enhanced binding of ATF4 to the C/EBP-ATF site at 2 h as Gadd153 mRNA levels increased, and enhanced binding of ATF3 complexes at 6 h as Gadd153 expression declined. We further demonstrated that ATF4 activates, while ATF3 represses, Gadd153 promoter activity through the C/EBP-ATF site. ATF3 also repressed ATF4-mediated transactivation and arsenite-induced activation of the Gadd153 promoter. Our results suggest that numerous members of the ATF/CREB family are involved in the cellular stress response, and that regulation of stress-induced biphasic Gadd153 expression in PC12 cells involves the ordered, sequential binding of multiple transcription factor complexes to the C/EBP-ATF composite site. (+info)Amino acid limitation regulates CHOP expression through a specific pathway independent of the unfolded protein response. (2/701)
The gene encoding CHOP (C/EBP-homologous protein) is transcriptionally activated by many stimuli and by amino acid deprivation. CHOP induction was considered to be due to an accumulation of unfolded protein into the ER (unfolded protein response (UPR)). We investigate the role of the UPR in the induction of CHOP by amino acid deprivation and show that this induction is not correlated with BiP expression (an UPR marker). Moreover, amino acid deprivation and UPR inducers regulate the CHOP promoter activity using distinct cis elements. We conclude that amino acid deprivation does not activate the UPR and regulates CHOP expression through a pathway that is independent of the UPR. (+info)Induction of a secreted protein by the myxoid liposarcoma oncogene. (3/701)
The TLS-CHOP oncoprotein, found in the majority of human myxoid liposarcomas, consists of a fusion between the transcription factor CHOP/GADD153 and the N terminus of an RNA-binding protein TLS/FUS. Clinical correlation and in vitro transformation assays indicate that the N terminus of TLS plays an important role in oncogenesis by TLS-CHOP. Until now, however, the only activity attributed to the oncoprotein is that of inhibiting the binding of transcription factors of the C/EBP class to certain adipogenic target genes, a function that TLS-CHOP shares with the nononcogenic CHOP protein. Here we report the isolation of a gene, DOL54, that is activated in primary fibroblasts by the expression of TLS-CHOP. DOL54 is expressed in the neoplastic component of human myxoid liposarcomas and increases the tumorigenicity of cells injected in nude mice. Activation of DOL54 requires an intact DNA-binding and dimerization domain in TLS-CHOP, a suitable cellular dimerization partner, and depends on the TLS N terminus. Normal adipocytic differentiation is associated with an early and transient expression of DOL54, and the gene encodes a secreted protein that is tightly associated with the cell surface or extracellular matrix. TLS-CHOP thus leads to the unscheduled expression of a gene that is normally associated with adipocytic differentiation. (+info)Regulated expression and functional role of the transcription factor CHOP (GADD153) in erythroid growth and differentiation. (4/701)
The hematopoietic growth factor erythropoietin (Epo) triggers changes in the expression of genes that encode important regulators of erythroid cell growth and differentiation. We now report that Epo markedly upregulates chop (gadd153) expression and that this transcription factor plays a role in erythropoiesis. Using a differential hybridization assay, we isolated a full-length cDNA of chop as an Epo upregulated gene in Rauscher murine erythroleukemia cells. RNase protection assays demonstrated that Epo or dimethyl sulfoxide induction increased steady-state mRNA levels 10- to 20-fold after 24 to 48 hours. Western blot analysis confirmed a marked increase in CHOP protein. Among the other c/ebp family members, only c/ebp beta was also upregulated during erythroid differentiation. Among normal hematopoietic cells examined, steady-state mRNA levels were highest in erythroid cells, with levels peaking during terminal differentiation. Transient overexpression of chop in Rauscher cells resulted in a significant increase in Epo- or dimethyl sulfoxide (DMSO)-induced hemoglobinization, further linking chop upregulation to erythroid differentiation. Artificial downregulation of chop in normal murine bone marrow cells with antisense oligodeoxynucleotides inhibited colony-forming unit-erythroid (CFU-E)-derived colony growth in a concentration-dependent manner. Burst-forming unit-erythroid (BFU-E)-derived colony growth was not affected. Using a Far Western type of analysis, we detected several potential CHOP binding partners among the nuclear proteins of Rauscher cells. Importantly, the number and relative abundance of these proteins changed with differentiation. The results strongly suggest that CHOP plays a role in erythropoiesis, possibly through interactions with both C/EBP and non-C/EBP family members. (+info)Urea-associated oxidative stress and Gadd153/CHOP induction. (5/701)
Urea treatment (100-300 mM) increased expression of the oxidative stress-responsive transcription factor, Gadd153/CHOP, at the mRNA and protein levels (at >/=4 h) in renal medullary mIMCD3 cells in culture, whereas other solutes did not. Expression of the related protein, CCAAT/enhancer-binding protein (C/EBP-beta), was not affected, nor was expression of the sensor of endoplasmic reticulum stress, grp78. Urea modestly increased Gadd153 transcription by reporter gene analysis but failed to influence Gadd153 mRNA stability. Importantly, upregulation of Gadd153 mRNA and protein expression by urea was antioxidant sensitive. Accordingly, urea treatment was associated with oxidative stress, as quantitated by intracellular reduced glutathione content in mIMCD3 cells. In addition, antioxidant treatment partially inhibited the ability of urea to activate transcription of an Egr-1 luciferase reporter gene. Therefore oxidative stress represents a novel solute-signaling pathway in the kidney medulla and, potentially, in other tissues. (+info)Induction of gadd153 mRNA by nutrient deprivation is overcome by glutamine. (6/701)
The growth arrest and DNA damage-inducible (gadd) genes are co-ordinately activated by a variety of genotoxic agents and/or growth-cessation signals. The regulation of gadd153 mRNA was investigated in renal proximal tubular epithelial cells (LLC-PK1) cultured in a nutrient- and serum-deprived medium. The addition of glutamine alone to LLC-PK1 cells cultured in Earl's balanced salt solution (EBSS) is sufficient to suppress gadd153 mRNA expression, and the removal of only glutamine from Dulbecco's modified Eagle's medium (DMEM) is also sufficient to induce gadd153 mRNA expression. Consistent with these findings, the inhibition of glutamine utilization with acivicin and 6-diazo-5-oxo-l-norleucine (DON) in cells grown in a glutamine-containing medium effectively induces gadd153 expression. Glutamine can be used as an energy source in cultured mammalian cells. However, it is unlikely that deficits in cellular energy stores (ATP) are coupled to gadd153 mRNA expression, because concentrations of ATP, UTP and GTP are all elevated in EBSS-exposed cells, and the addition of alpha-oxoglutarate to cells grown in EBSS has no effect on gadd153 mRNA expression. In contrast, concentrations of CTP decline substantially in EBSS and glutamine-deprived DMEM-cultured cells. Glutamine also serves as a precursor for the synthesis of protein and DNA. The addition of glutamine to cells grown in EBSS partly restores CTP concentrations. The addition of pyrimidine ribonucleosides (cytidine and uridine) to LLC-PK1 cells also restores CTP concentrations, in a manner commensurate with their relative abilities to overcome gadd153 expression. Finally, glutamine does not completely suppress DNA damage-induced gadd153 expression, suggesting that multiple signalling pathways lead to the expression of gadd153 mRNA under conditions of nutrient deprivation and DNA damage. (+info)Homocysteine-induced endoplasmic reticulum stress and growth arrest leads to specific changes in gene expression in human vascular endothelial cells. (7/701)
Alterations in the cellular redox potential by homocysteine promote endothelial cell (EC) dysfunction, an early event in the progression of atherothrombotic disease. In this study, we demonstrate that homocysteine causes endoplasmic reticulum (ER) stress and growth arrest in human umbilical vein endothelial cells (HUVEC). To determine if these effects reflect specific changes in gene expression, cDNA microarrays were screened using radiolabeled cDNA probes generated from mRNA derived from HUVEC, cultured in the absence or presence of homocysteine. Good correlation was observed between expression profiles determined by this method and by Northern blotting. Consistent with its adverse effects on the ER, homocysteine alters the expression of genes sensitive to ER stress (ie, GADD45, GADD153, ATF-4, YY1). Several other genes observed to be differentially expressed by homocysteine are known to mediate cell growth and differentiation (ie, GADD45, GADD153, Id-1, cyclin D1, FRA-2), a finding that supports the observation that homocysteine causes a dose-dependent decrease in DNA synthesis in HUVEC. Additional gene profiles also show that homocysteine decreases cellular antioxidant potential (glutathione peroxidase, NKEF-B PAG, superoxide dismutase, clusterin), which could potentially enhance the cytotoxic effects of agents or conditions known to cause oxidative damage. These results successfully demonstrate the use of cDNA microarrays in identifying homocysteine-respondent genes and indicate that homocysteine-induced ER stress and growth arrest reflect specific changes in gene expression in human vascular EC. (+info)Quantitation of the change in GADD153 messenger RNA level as a molecular marker of tumor response in head and neck cancer. (8/701)
Cells injured by exposure to cisplatin (cDDP) undergo a cellular injury response that shares characteristics with responses produced by many other injurious agents. We sought to determine whether the increase of the message of the "growth arrest and DNA damage-inducible" gene, GADD153, could be used to assess the extent of the cellular injury response in model systems and in patients with head and neck cancer after treatment with cDDP. The mRNA levels of GADD153, a gene highly transcriptionally activated by cDDP damage, were increased in a transient, concentration-dependent manner by cDDP when human UMSCC10b head and neck carcinoma cells were treated with cDDP both in vitro and when grown as tumor xenografts in nude mice. There was a good correlation between the change in level of GADD153 mRNA and UMSCC10b cell kill by cDDP in vitro (r = 0.98). The magnitude of the increase was proportionally reduced in UMSCC10b sublines that were 3- or 6-fold resistant to cDDP. GADD153 mRNA levels were measured in biopsies obtained before and 24 h after treatment with cDDP from 32 patients with stage III/IV head and neck cancer. There was a relationship between the increase in GADD153 mRNA levels and the response rate. Seven of the 32 patients had no response and no increase in GADD153 mRNA level. Among the eight patients who attained a partial response, the increase in GADD153 message ranged from 0.7-2.5-fold. In contrast, 17 of 32 patients had a complete response, and this was accompanied by a 2-9-fold induction of GADD153. The mean increase in the complete responders (3.8+/-2.2-fold) differed significantly from that for the partial responders (1.6+/-0.9) and nonresponders (0.8+/-0.5; P <0.05); the difference between the partial responders and nonresponders was also significant (P <0.05). An increase of GADD153 mRNA of 1.75-fold or higher predicted a complete response, with a sensitivity of 94% and a specificity of 87%. We conclude that the magnitude of the increase in GADD153 mRNA is a promising candidate for service as an intermediate marker of head and neck tumor response to cDDP. The fact that the change in GADD153 mRNA reflects the actual extent of injury sustained by the tumor makes it particularly attractive as a potential marker. One strength of this approach is that it can provide a measure of the effectiveness of therapy as early as 24-48 h after the first dose of treatment. (+info)Transcription Factor CHOP, also known as GADD153 or DDIT3, is a protein involved in the regulation of gene expression, primarily functioning as a transcriptional activator that responds to endoplasmic reticulum stress and contributes to the development of apoptosis in cells.
Transcription Factor CHOP, also known as DNA Binding Protein C/EBP Homologous Protein or GADD153 (Growth Arrest and DNA Damage-inducible protein 153), is a transcription factor that is involved in the regulation of gene expression in response to various stress stimuli, such as endoplasmic reticulum (ER) stress, hypoxia, and DNA damage.
CHOP is a member of the C/EBP (CCAAT/enhancer-binding protein) family of transcription factors, which bind to specific DNA sequences called cis-acting elements in the promoter regions of target genes. CHOP can form heterodimers with other C/EBP family members and bind to their target DNA sequences, thereby regulating gene expression.
Under normal physiological conditions, CHOP is expressed at low levels. However, under stress conditions, such as ER stress, the expression of CHOP is upregulated through the activation of the unfolded protein response (UPR) signaling pathways. Once activated, CHOP can induce the transcription of genes involved in apoptosis, cell cycle arrest, and oxidative stress response, leading to programmed cell death or survival, depending on the severity and duration of the stress signal.
Therefore, CHOP plays a critical role in maintaining cellular homeostasis by regulating gene expression in response to various stress stimuli, and its dysregulation has been implicated in several pathological conditions, including neurodegenerative diseases, cancer, and metabolic disorders.
The endoplasmic reticulum (ER) is a complex network of interconnected tubules and sacs within the cell's cytoplasm, responsible for protein synthesis, folding, modification, and transport, as well as lipid metabolism and calcium homeostasis, functioning as a crucial organelle in the secretory pathway.
The endoplasmic reticulum (ER) is a network of interconnected tubules and sacs that are present in the cytoplasm of eukaryotic cells. It is a continuous membranous organelle that plays a crucial role in the synthesis, folding, modification, and transport of proteins and lipids.
The ER has two main types: rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER). RER is covered with ribosomes, which give it a rough appearance, and is responsible for protein synthesis. On the other hand, SER lacks ribosomes and is involved in lipid synthesis, drug detoxification, calcium homeostasis, and steroid hormone production.
In summary, the endoplasmic reticulum is a vital organelle that functions in various cellular processes, including protein and lipid metabolism, calcium regulation, and detoxification.
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.
The Unfolded Protein Response (UPR) is a cellular stress response pathway that becomes activated when the endoplasmic reticulum experiences an accumulation of misfolded or unfolded proteins, aiming to restore protein homeostasis by reducing protein load and enhancing protein folding capacity.
The Unfolded Protein Response (UPR) is a cellular stress response pathway that is activated when the endoplasmic reticulum (ER), an organelle responsible for protein folding and processing, becomes overwhelmed with misfolded or unfolded proteins. The UPR is initiated by three ER transmembrane sensors: IRE1, PERK, and ATF6. These sensors detect the accumulation of unfolded proteins in the ER lumen and transmit signals to the nucleus to induce a variety of adaptive responses aimed at restoring ER homeostasis.
These responses include:
* Transcriptional upregulation of genes encoding chaperones, folding enzymes, and components of the ER-associated degradation (ERAD) machinery to enhance protein folding capacity and promote the clearance of misfolded proteins.
* Attenuation of global protein synthesis to reduce the influx of new proteins into the ER.
* Activation of autophagy, a process that helps eliminate damaged organelles and aggregated proteins.
If these adaptive responses are insufficient to restore ER homeostasis, the UPR can also trigger apoptosis, or programmed cell death, as a last resort to eliminate damaged cells and prevent the spread of protein misfolding diseases such as neurodegenerative disorders.
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.
CCAAT-Enhancer-Binding Proteins (C/EBPs) are a family of transcription factors that bind to the CCAAT box motif in the promoter or enhancer regions of target genes, playing crucial roles in various biological processes including inflammation, immunity, differentiation, and metabolism.
CCAAT-Enhancer-Binding Proteins (C/EBPs) are a family of transcription factors that play crucial roles in the regulation of various biological processes, including cell growth, development, and differentiation. They bind to specific DNA sequences called CCAAT boxes, which are found in the promoter or enhancer regions of many genes.
The C/EBP family consists of several members, including C/EBPα, C/EBPβ, C/EBPγ, C/EBPδ, and C/EBPε. These proteins share a highly conserved basic region-leucine zipper (bZIP) domain, which is responsible for their DNA-binding and dimerization activities.
C/EBPs can form homodimers or heterodimers with other bZIP proteins, allowing them to regulate gene expression in a combinatorial manner. They are involved in the regulation of various physiological processes, such as inflammation, immune response, metabolism, and cell cycle control. Dysregulation of C/EBP function has been implicated in several diseases, including cancer, diabetes, and inflammatory disorders.
Endoplasmic Reticulum (ER) stress refers to the condition where the accumulation of misfolded or unfolded proteins in the ER lumen exceeds its folding capacity, leading to the activation of an evolutionarily conserved unfolded protein response (UPR).
Endoplasmic reticulum (ER) stress refers to a cellular condition characterized by the accumulation of misfolded or unfolded proteins within the ER lumen, leading to disruption of its normal functions. The ER is a membrane-bound organelle responsible for protein folding, modification, and transport, as well as lipid synthesis and calcium homeostasis. Various physiological and pathological conditions can cause an imbalance between the rate of protein entry into the ER and its folding capacity, resulting in ER stress.
To cope with this stress, cells have evolved a set of signaling pathways called the unfolded protein response (UPR). The UPR aims to restore ER homeostasis by reducing global protein synthesis, enhancing ER-associated degradation (ERAD) of misfolded proteins, and upregulating the expression of genes involved in protein folding, modification, and quality control.
The UPR is mediated by three major signaling branches:
1. Inositol-requiring enzyme 1α (IRE1α): IRE1α is an ER transmembrane protein with endoribonuclease activity that catalyzes the splicing of X-box binding protein 1 (XBP1) mRNA, leading to the expression of a potent transcription factor, spliced XBP1 (sXBP1). sXBP1 upregulates genes involved in ERAD and protein folding.
2. Activating transcription factor 6 (ATF6): ATF6 is an ER transmembrane protein that, upon ER stress, undergoes proteolytic cleavage to release its cytoplasmic domain, which acts as a potent transcription factor. ATF6 upregulates genes involved in protein folding and degradation.
3. Protein kinase R-like endoplasmic reticulum kinase (PERK): PERK is an ER transmembrane protein that phosphorylates the α subunit of eukaryotic initiation factor 2 (eIF2α) upon ER stress, leading to a global reduction in protein synthesis and preferential translation of activating transcription factor 4 (ATF4). ATF4 upregulates genes involved in amino acid metabolism, redox homeostasis, and apoptosis.
These three branches of the UPR work together to restore ER homeostasis by increasing protein folding capacity, reducing global protein synthesis, and promoting degradation of misfolded proteins. However, if the stress persists or becomes too severe, the UPR can trigger cell death through apoptosis.
In summary, the unfolded protein response (UPR) is a complex signaling network that helps maintain ER homeostasis by detecting and responding to the accumulation of misfolded proteins in the ER lumen. The UPR involves three main branches: IRE1α, ATF6, and PERK, which work together to restore ER homeostasis through increased protein folding capacity, reduced global protein synthesis, and enhanced degradation of misfolded proteins. Persistent or severe ER stress can lead to the activation of cell death pathways by the UPR.
'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.
Casein kinase 2, alpha 1
Ubeda M, Habener JF (October 2003). "CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional ... "Activation of mammalian ribosomal gene transcription requires phosphorylation of the nucleolar transcription factor UBF". ... Allende-Vega N, McKenzie L, Meek D (September 2008). "Transcription factor TAFII250 phosphorylates the acidic domain of Mdm2 ... "Casein kinase II interacts with the bZIP domains of several transcription factors". Nucleic Acids Res. 26 (16): 3854-61. doi: ...
FET protein family
"The oncogenic transcription factor FUS-CHOP can undergo nuclear liquid-liquid phase separation". Journal of Cell Science. 134 ( ... "FEV FEV transcription factor, ETS family member [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Durer, S.; Shaikh ... arm of chromosome 22 with part of the FLI1 ETS transcription factor family gene normally located on band 24 of the long arm of ... have tumor cells that express a fusion gene that merges part of a FET family gene with part of an ETS transcription factor ...
Myxoid liposarcoma
1993). "Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11)". Genes Chromosomes ... "The oncogenic transcription factor FUS-CHOP can undergo nuclear liquid-liquid phase separation". Journal of Cell Science. 134 ( ... Rabbitts TH, Forster A, Larson R, Nathan P (1993). "Fusion of the dominant negative transcription regulator CHOP with a novel ... arm of chromosome 16 with part of the DDIT3 ETS transcription factor family gene normally located at band 13.3 on the long (or ...
DNA damage-inducible transcript 3
... indicating that JNK activation is also involved in the modulation of CHOP levels. As a transcription factor, CHOP can regulate ... eukaryotic initiation factor 2α (eIF2α), and induction of a transcription factor, activation transcription factor 4 (ATF4), ... CHOP also interacts with the phosphorylated transcription factor JUN to form a complex that binds to the promoter region of DR4 ... June 2014). "The transcription factor CHOP, a central component of the transcriptional regulatory network induced upon CCl4 ...
Transcription factor Jun
Ubeda M, Vallejo M, Habener JF (November 1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 ... nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ... Transcription factor Jun is a protein that in humans is encoded by the JUN gene. c-Jun, in combination with protein c-Fos, ... c-jun was the first oncogenic transcription factor discovered. The proto-oncogene c-Jun is the cellular homolog of the viral ...
40S ribosomal protein S3a
Cui K, Coutts M, Stahl J, Sytkowski AJ (2000). "Novel interaction between the transcription factor CHOP (GADD153) and the ... "Novel interaction between the transcription factor CHOP (GADD153) and the ribosomal protein FTE/S3a modulates erythropoiesis". ... Transcript variants utilizing alternative transcription start sites have been described. This gene is co-transcribed with the ... 2003). "Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, ...
David Ron
He identified the transcription factor CHOP and discovered its role in deregulating adipose tissue development in liposarcoma. ...
Endoplasmic reticulum stress in beta cells
Hu, Hai; Tian, Mingxing; Ding, Chan; Yu, Shengqing (2019-01-04). "The C/EBP Homologous Protein (CHOP) Transcription Factor ... XBP1 mRNA cleavage leads to the translation of a transcription factor for genes that resolve ER stress. Measuring the rate at ... The UPR is also activated by cytokines ER-stress activates Apoptosis through C/EBP Homologous Protein (CHOP) ER Stress can be ... ER stress can be activated by a variety of factors. In experimental conditions, excessive lipid (which can happen following ...
KDELR1
A murine DCM study found an increase in apoptosis due to the high levels of CHOP expression. CHOP is a transcription factor ... Zinszner H, Kuroda M, Wang X, Batchvarova N, Lightfoot RT, Remotti H, Stevens JL, Ron D (April 1998). "CHOP is implicated in ... Increase pressure load/mechanical stress in KDEL D193N mice caused an even greater synthesis of BiP, CHOP and other proteins ...
Integrated stress response
ATF4 will work together with other transcription factors, such as CHOP and ATF3, by forming homodimers or heterodimers, ... The ATF4 transcription factor has the ability to form dimers with many different proteins that influence gene expression and ... The main intrinsic factor is endoplasmic reticulum stress due to the accumulation of unfolded proteins. It has also been ... On the other hand, ATF4 and CHOP work together to induce cell death, as well as regulating amino acid biosynthesis, transport ...
PEDF
Immediately upstream of the PEDF gene lies a 200bp promoter region with putative binding sites for the transcription factors ... HNF4, CHOP, and USF. The PEDF gene consists of 8 exons and 7 introns. The PEDF gene is present in vertebrates from human to ... In humans, pigment epithelium-derived factor is encoded by the SERPINF1 gene. Pigment epithelium-derived factor (PEDF) was ... "Down-regulation of vascular endothelial growth factor and up-regulation of pigment epithelium-derived factor: a possible ...
Trabectedin
Recently,[when?] it has been shown that trabectedin blocks DNA binding of the oncogenic transcription factor FUS-CHOP and ... By reversing the genetic program created by this transcription factor, trabectedin promotes differentiation and reverses the ... interferes directly with activated transcription, poisons the transcription-coupled nucleotide excision repair complex, ...
RNA-binding protein FUS
"The transcription factor Spi-1/PU.1 interacts with the potential splicing factor TLS". J. Biol. Chem. 273 (9): 4838-42. doi: ... Rabbitts TH, Forster A, Larson R, Nathan P (Sep 1993). "Fusion of the dominant negative transcription regulator CHOP with a ... "The transcription factor Spi-1/PU.1 interacts with the potential splicing factor TLS". J. Biol. Chem. 273 (9): 4838-42. doi: ... and with gene-specific transcription factors such as Spi-1/PU.1. or NF-κB. It also associates with the general transcriptional ...
Kinase
MAPK can regulate transcription factors directly or indirectly. Its major transcriptional targets include ATF-2, Chop, c-Jun, c ... For example, growth hormone, epidermal growth factor, platelet-derived growth factor, and insulin are all considered mitogenic ... While they are most known for their function in cell cycle control, CDKs also have roles in transcription, metabolism, and ... which can go on to regulate transcription and translation. Whereas RAF and MAPK are both serine/threonine kinases, MAPKK is a ...
PICALM
Ron D, Habener JF (1992). "CHOP, a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/ ... EBP and LAP and functions as a dominant-negative inhibitor of gene transcription". Genes Dev. 6 (3): 439-53. doi:10.1101/gad. ...
PCAF
"The p300/CBP-associated factor (PCAF) is a cofactor of ATF4 for amino acid-regulated transcription of CHOP". Nucleic Acids Res ... growth factor-beta regulates DNA binding activity of transcription factor Fli1 by p300/CREB-binding protein-associated factor- ... Korzus E, Torchia J, Rose DW, Xu L, Kurokawa R, McInerney EM, Mullen TM, Glass CK, Rosenfeld MG (1998). "Transcription factor- ... There are various protein targets of PCAF's acetyltransferase activity including transcription factors such as Fli1, p53 and ...
C20orf96
... has been found to bind to transcription factor binding sites AREB6, GATA-1, GATA-2, GATA-3, ATF6, c-Myc, Max, CHOP-10 ...
Amino acid response
2007). "The p300/CBP-associated factor (PCAF) is a cofactor of ATF4 for amino acid-regulated transcription of CHOP". Nucleic ... Membrane transporters Transcription factors from the basic region/leucine zipper (bZIP) superfamily Growth factors Metabolic ... Articles with short description, Short description matches Wikidata, Transcription factors). ... and results in an increase in activating transcription factor ATF4, which in turn affects many processes by sundry pathways to ...
Protein c-Fos
... nuclear factor-kappaB, and serum response factor as novel target molecules of the cancer-amplified transcription coactivator ... Ubeda M, Vallejo M, Habener JF (November 1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 ... c-Fos encodes a 62 kDa protein, which forms heterodimer with c-jun (part of Jun family of transcription factors), resulting in ... Glover JN, Harrison SC (January 1995). "Crystal structure of the heterodimeric bZIP transcription factor c-Fos-c-Jun bound to ...
Unfolded protein response
... activating transcription factor 4) and uniquely responsive to ER stress. CHOP causes downregulation of the anti-apoptotic ... ATF6 (activating transcription factor 6) is a basic leucine zipper transcription factor. Upon Grp78 dissociation, the entire ... The activated transcription factor upregulates UPR 'stress genes' by directly binding to stress element promoters in the ... These transcription factors then proceed to alter the expression of exercise-regulated muscle genes. PGC-1alpha, a ...
Mitochondrial unfolded protein response
... the transcription factor Chop and the kinases c-Jun N-terminal kinase (JNK) and the interferon-induced, double-stranded RNA- ... manages the unfolded proteins through heat shock factor 1 (HSF1). HSF-1 is a transcription factor that, upon increases in ... The appropriately named activating transcription factor associated with stress (ATFS-1) is one of the primary transcription ... The UPRmt progresses through the bZIP transcription factor ATFS-1 (in C. elegans; ATF5 in mammals). AFTS-1 is usually imported ...
CASS4
CHOP-10 (C/EBP homologous protein 10), POU3F1 (POU domain, class 3, transcription factor 1, aka Oct-6), Areb6 (ZEB1, Zinc ... nuclear factor, erythroid 2-like1), MAX1, C/EBPα, ...
MAPK14
... activating transcription factor 1 (ATF1), serum response factor (SRF), and mRNA-binding protein tristetraprolin (TTP) In ... via downstream targets STAT1, CHOP, FAK, SMAD, cytochrome c, NF-κB, PTEN, and p53. p38 MAPK can also target IRS-1 mediated AKT ... Janknecht R (Nov 2001). "Cell type-specific inhibition of the ETS transcription factor ER81 by mitogen-activated protein kinase ... Yang SH, Galanis A, Sharrocks AD (Jun 1999). "Targeting of p38 mitogen-activated protein kinases to MEF2 transcription factors ...
C5orf46
Histone nuclear factor P (HNFP) NKX homeodomain factors (NKXH) C/EBP homologous protein (CHOP) X-box binding factors (XBBF) ... The predictions included the following transcription factors: Sine oculis homeodomain factors (SIXF) p53 tumor suppressor (P53F ... Fork head domain factors (FKHD) RNA Polymerase II transcription factor II B (TF2B) TGF-beta induced apoptosis proteins (TAIP) ... A total of 428 transcription factor binding sites were predicted to be located within the predicted promoter sequence. ...
JunD
"Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143-52. doi: ... Ubeda M, Vallejo M, Habener JF (November 1999). "CHOP enhancement of gene transcription by interactions with Jun/Fos AP-1 ... "Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143-52. doi: ... Transcription factor JunD is a protein that in humans is encoded by the JUND gene. The protein encoded by this intronless gene ...
STAU1
... blocks cell migration and invasion through the degradation of metal regulatory transcription factor 1 (MTF1) and YY2 ... Elevated levels of STAU1 in neural cells have been shown to promote apoptosis by activating the PERK-CHOP pathway and lead to ... transcription factor (YY2) through SMD in glioma cell lines. In contrast, in RD cell lines, elevated STAU1 promotes cell ... SMD of transcriptional factor retina and anterior neural fold homobox2 (RAX2) transcript has shown to be required for the ...
Mir-708 microRNA precursor family
Upregulation of the DNA repair protein EYA3 in this tumour is mediated by the fusion protein transcription factor EWS/FLI1, ... Behrman S, Acosta-Alvear D, Walter P (March 2011). "A CHOP-regulated microRNA controls rhodopsin expression". The Journal of ... "Identification of novel stress-induced genes downstream of chop". The EMBO Journal. 17 (13): 3619-30. doi:10.1093/emboj/17.13. ...
List of MeSH codes (D12.776.930)
... transcription factor chop MeSH D12.776.930.127.124.937 - Y box binding protein 1 MeSH D12.776.930.127.500.061 - maf ... transcription factor brn-3b MeSH D12.776.930.632.625.875 - transcription factor brn-3c MeSH D12.776.930.635.600.100 - ets- ... mafg transcription factor MeSH D12.776.930.127.656.750.750 - mafk transcription factor MeSH D12.776.930.127.656.770 - nf-e2 ... mafg transcription factor MeSH D12.776.930.316.750.750.750 - mafk transcription factor MeSH D12.776.930.316.750.770 - nf-e2 ...
List of MeSH codes (D12.776.260)
... transcription factor chop MeSH D12.776.260.108.124.937 - Y box binding protein 1 MeSH D12.776.260.108.500.061 - maf ... nf-e2 transcription factor, p45 subunit MeSH D12.776.260.235.750.750 - maf transcription factors, small MeSH D12.776.260.235. ... transcription factor brn-3b MeSH D12.776.260.655.625.500 - transcription factor brn-3c MeSH D12.776.260.665.600.100 - ets- ... mafg transcription factor MeSH D12.776.260.235.750.750.750 - mafk transcription factor MeSH D12.776.260.235.750.770 - nf-e2 ...
ATF5
"Regulation of asparagine synthetase gene transcription by the basic region leucine zipper transcription factors ATF5 and CHOP ... ATF5 is a transcription factor that contains a bZip domain. Activating transcription factor ATF5 has been shown to interact ... biology and nomenclature of the activating transcription factor/cAMP responsive element binding family of transcription factors ... "Cyclin D3 interacts with human activating transcription factor 5 and potentiates its transcription activity". Biochem. Biophys ...
Peroxisome proliferator-activated receptor γ ligand troglitazone and TRAIL synergistically induce apoptosis
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to cause apoptosis in several types of malignant tumor ... Transcription Factor CHOP / biosynthesis * Transcription Factor CHOP / genetics * Transcription Factor CHOP / metabolism* ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to cause apoptosis in several types of malignant tumor ... TGZ elevated DR5 expression at the promoter level through the CCAAT/enhancer-binding protein homologous protein (CHOP) binding ...
Robust Endoplasmic Reticulum-Associated Degradation of Rhodopsin Precedes Retinal Degeneration
African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153<...
African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153. Journal of ... African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153. Christopher ... African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153. / Netherton ... title = "African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153", ...
Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11) | Make a difference for cancer
Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11) Author ... Rearrangement of the transcription factor gene CHOP in myxoid liposarcomas with t(12;16)(q13;p11) ... Using a cDNA probe that spans the CHOP coding region, we detected one rearranged and one wild type allele in nine of nine MLS ... We have used Southern blot technique to test whether a gene of the CCAAT/enhancer binding protein (C/EBP) family, CHOP, which ...
Frontiers | Therapeutic Potential of Ginsenosides as an Adjuvant Treatment for Diabetes
Forkhead transcription factor 1; GLP-1, lucagon-like peptide-1; CHOP, homologous protein; IDF, International Diabetes ... Forkhead transcription factor 1 (FOXO1) is another important factor in gluconeogenesis. AMPK can regulate FOXO1, which ... tumor necrosis factor-alpha; TNF-β, tumor necrosis factor-β; IL-2, interleukin-2; IL-6, interleukin-6; PPAR-γ, peroxisome ... This has become a factor limiting the development of TCMs. Since Tu You You invented artemisinin to treat malaria and won the ...
Casein kinase 2, alpha 1 - Wikipedia
Ubeda M, Habener JF (October 2003). "CHOP transcription factor phosphorylation by casein kinase 2 inhibits transcriptional ... "Activation of mammalian ribosomal gene transcription requires phosphorylation of the nucleolar transcription factor UBF". ... Allende-Vega N, McKenzie L, Meek D (September 2008). "Transcription factor TAFII250 phosphorylates the acidic domain of Mdm2 ... "Casein kinase II interacts with the bZIP domains of several transcription factors". Nucleic Acids Res. 26 (16): 3854-61. doi: ...
Targeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells,...
Services | PharmOptima LLC
... pro-apoptotic transcription factor Ddit3 (Chop), and reactive astrocyte marker Gfap demonstrates a robust response to injury ... qRT-PCR of Atf3, Sprr1a, Ddit3 (Chop), and Gfap from retinal RNA four days after optic nerve crush (ONC) compared to uninjured ... decreasing gene expression using anti-sense sequences to inhibit transcription or translation (e.g., Mipomersin inhibition of ... Pegaptinib inhibition of vascular endothelial growth factor, VEGF, in the treatment of macular degeneration). ...
A Complex Program of Striatal Gene Expression Induced by Dopaminergic Stimulation | Journal of Neuroscience
1992) CHOP, a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and ... and CHOP, which is an inhibitor/modulator of the transcription factor C/EBP (Ron and Habener, 1992). The induction of the mRNAs ... Other transcription factors may also be involved, because SKF38393 in lesioned striatum has been shown to increase AP-1 binding ... 5A,B). Because many of the most rapidly induced genes are transcription factors, they may be regulating some of the later genes ...
Liposarcoma: Practice Essentials, Background, Pathophysiology
The most common chromosomal translocation is the FUS-CHOP fusion gene, which encodes a transcription factor necessary for ... 15] The histologic grade of localized liposarcomas of the extremities may be the most important prognostic factor. [16] ... Wu J, Qian S, Jin L. Prognostic factors of patients with extremity myxoid liposarcomas after surgery. J Orthop Surg Res. 2019 ... Nishida Y, Tsukushi S, Nakashima H, Ishiguro N. Clinicopathologic Prognostic Factors of Pure Myxoid Liposarcoma of the ...
N-trans-Feruloyloctopamine Wakes Up BBC3, DDIT3, CDKN1A, and NOXA Signals to Accelerate HCC Cell Apoptosis
CHOP (DDIT3) is a member of the C/EBP transcription factor family, and its expression is related to endoplasmic reticulum ... CHOP functions as an upstream factor regulating BCL-2 family proteins, such as PUMA [28]. In addition, CHOP-mediated cell death ... Meanwhile, the upregulated CHOP might activate endoplasmic reticulum stress. Similarly, the elevating of CHOP also mediates the ... CHOP-forward: 5. -GGAAACAGAGTGGTCATTCCC-3. , reverse: 5. -CTGCTTGAGCCGTTCATTCTC-3. ; and GAPDH-forward: 5. - ...
GADD153/CHOP Overexpression Lysate (NBL1-09772): Novus Biologicals
GADD153/CHOP Overexpression Lysate. Tested Reactivity: Hu. Validated: WB. Backed by our 100% Guarantee. ... GADD153 encodes a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors. The protein functions ... Blogs on GADD153/CHOP. There are no specific blogs for GADD153/CHOP, but you can read our latest blog posts. ... GADD153/CHOP Overexpression Lysate Summary. Description. GADD153/CHOP Transient Overexpression Lysate. Expression Host: HEK293T ...
Purvalanol induces endoplasmic reticulum stress-mediated apoptosis and autophagy in a time-dependent manner in HCT116 colon...
CHOP) gene. CHOP is a transcription factor that regulates the expression of the Bcl-2 family members. Overexpression of CHOP ... CHOP, is a key ER stress-induced transcription factor and transcription activation is through ATF-6 and ATF-4 (29). Deficiency ... and activating transcription factor-6 (ATF-6). Activated and released IRE1α acts as an RNase to initiate transcription of XBP1 ... Haze K, Yoshida H, Yanagi H, Yura T and Mori K: Mammalian transcription factor ATF6 is synthesized as a transmembrane protein ...
XBP1 | Cancer Genetics Web
CHOP), glucose regulated protein 78 (GRP78), inositol-requiring enzyme 1 α (IRE1α), activating transcription factor-4 (ATF-4), ... This kind of genes is called transcription factor (TF) or sequence-specific DNA-binding factor. Transcription factors play ... sequence-specific DNA binding transcription factor activity - serotonin secretion, neurotransmission - transcription from RNA ... including the levels of activating transcription factor 4 (ATF4), C/EBPhomologous protein expression (CHOP), immunoglobulin- ...
HDNetDB: A Molecular Interaction Database for Network-Oriented Investigations into Huntington's Disease | Scientific Reports
The second gene, JUN, is a transcription factor and component of the AP-1 transcription complex that plays a key in role in ... also known as CHOP. Both are downstream of ERN1 and EIF2AK3. Additionally, BCL2-associated X protein (BAX) was included, which ... Migheli, A., Piva, R., Atzori, C., Troost, D. & Schiffer, D. c-Jun, JNK/SAPK kinases and transcription factor NF-kappa B are ... Besides the three key signaling components mentioned above (ERN1, EIF2AK3, ATF6), we selected transcription factors X-Box ...
CHOP Polyclonal Antibody (PA5-28956)
Invitrogen Anti-CHOP Polyclonal, Catalog # PA5-28956. Tested in Western Blot (WB) and Immunocytochemistry (ICC/IF) applications ... transcription factor activity, sequence-specific DNA binding transcription corepressor activity protein binding transcription ... CHOP Antibody (PA5-28956) in WB Western blot was performed using Anti-CHOP Polyclonal Antibody (Product # PA5-28956) and a ... GADD153 is a small nuclear protein that is capable of dimerizing with transcription factors C/EBP alpha and beta. Once ...
Cross Talk of Proteostasis and Mitostasis in Cellular Homeodynamics, Ageing, and Disease
X. Z. Wang and D. Ron, "Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP ... Another downstream component of HAF-1 is the bZip transcription factor ATFS-1 (Activating Transcription Factor associated with ... the nuclear factor-kappa beta (NF-κB), and the Hypoxia Inducible Factor 1α (HIF1α). The transcription factors NRF1 and NRF2 ... The PGC-1 family members potentiate the activity of other transcription factors and PGC-1α interacts with NRF1 and PPARα [299, ...
Leadership team | About | eLife
... that ONC201 induces TRAIL receptor DR5 through an integrated stress response involving ATF4 and CHOP transcription factors. ... One extension of this research was his discovery of a new family of transcription factors, the interferon regulatory factors ( ... lymphatic endothelial transcription factors. CAR T cell therapies. Experimental organism. human primary and cancer cells. ... cancer drugs with p53 pathway restoration and S-phase checkpoint targeting and recognizing ATF4 as a major transcription factor ...
Ongoing Molecular Research in the Science of Oncology-Leukemia - The ASCO Post
The transcription factor CHOP (CCAAT/enhancer-binding protein homology protein) accumulated in response to carfilzomib exposure ... with CHOP depletion conferring protection against cytotoxicity. Carfilzomib also induced accumulation of MCL-1 and Noxa, with ... and we identified the CHOP protein level as a biomarker that could predict sensitivity to carfilzomib in CLL." ...
FDA Grants Special Designation to Friedreich's Ataxia Treatment Based on Findings from Study Led by CHOP Neurologist | Children...
Omaveloxolone is an investigational, oral, once-daily, activator of Nrf2, a transcription factor that induces molecular ... FDA Grants Special Designation to Friedreichs Ataxia Treatment Based on Findings from Study Led by CHOP Neurologist. Published ... David Lynch, MD, PhD, Director of the Friedreichs Ataxia Program at Childrens Hospital of Philadelphia (CHOP), has been ...
Inhibition of p38 MAPK signaling promotes late stages of myogenesis | Journal of Cell Science | The Company of Biologists
Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase. Science ... Stress-induced phosphorylation and activation of the transcription factor CHOP (GADD153) by p38 MAP Kinase. Science ... Of particular importance has been the identification of two families of transcription factors: the myogenic regulatory factors ... CHOP10, a transcription factor, is a known target of p38α, whose phosphorylation by p38 is blocked by the SB203580 inhibitor in ...
JCI - Chop deletion reduces oxidative stress, improves β cell function, and promotes cell survival in multiple mouse models of...
... at least in part through the UPR-induced transcription factor C/EBP homologous protein (CHOP). We assessed the effect of Chop ... Chop mRNA was not detectable in Leprdb/+Chop-/- or Leprdb/dbChop-/- islets; n = 4-6 mice per condition. *P , 0.05, **P , 0.01 ... activating transcription factor 4; CHOP, C/EBP homologous protein; eIF2, eukaryotic translation initiation factor 2; GSIS, ... CHOP was identified as an ER stress-induced transcription factor that is a significant mediator of apoptosis in response to ER ...
Alexa Fluor® 647 Mouse Anti-p38 MAPK (pT180/pY182)
Amino acid starvation culture condition sensitizes EGFR-expressing cancer cell lines to gefitinib-mediated cytotoxicity by...
... acid-depleted culture conditions in these cell lines along with the upregulation of the pro-apoptotic transcription factor, ... CHOP/GADD153, although they exhibit no cytotoxicity in complete culture medium (18). Mammalian target of rapamycin (mTOR), is a ... Since epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors, including gefitinib (GEF) have been reported to ... Golden SH, Folsom AR, Coresh J, Sharrett AR, Szklo M and Brancati F: Risk factor groupings related to insulin resistance and ...
TNFα-dependent hepatic steatosis and liver degeneration caused by mutation of zebrafish s-adenosylhomocysteine hydrolase |...
Intranasal perillyl alcohol (POH)induces endoplasmic reticulum stress (ERS) in temozolomide sensitive and resistant malignant...
Deciphering the language of transcription factors | MIT News | Massachusetts Institute of Technology
A new method identifies the precise binding sites of transcription factors - proteins that regulate the production of other ... The leading method for determining how transcription factors behave in living cells is to chop up the DNA from millions of ... the transcription factor would bind, then compare those predictions to the experimental data on where the factor actually did ... For a single transcription factor, that role can vary according to both the type of cell in which its active and its ...
Myeloid-Derived Suppressor Cells | Cancer Immunology Research | American Association for Cancer Research
... including transcription factors sXBP1 and CHOP, and display an enlarged ER, one of the hallmarks of ER stress (30). ... The first group of signals is mostly driven by tumor-derived growth factors and involves such factors as STAT3, IRF8, C/EBPβ, ... Tumor-induced tolerance and immune suppression depend on the C/EBPbeta transcription factor ... Nrf2 is a transcription factor that plays an important role in cellular protection against free radical damage. Synthetic ...
Richard N. Kitsis - Publications - Albert Einstein College of Medicine
Jeffrey E. Pessin - Publications - Albert Einstein College of Medicine
Homologous protein6
- TGZ elevated DR5 expression at the promoter level through the CCAAT/enhancer-binding protein homologous protein (CHOP) binding site. (nih.gov)
- Chronic ER stress promotes apoptosis, at least in part through the UPR-induced transcription factor C/EBP homologous protein (CHOP). (jci.org)
- This agent induces cytotoxicity via ER stress pathway as shown by the increased expression of glucose-regulated protein-78 (GRP78), activating transcription factor 3 (ATF3), and C/EBP-homologous protein (CHOP). (cns.org)
- CHOP was identified as a C/EBP-homologous protein that inhibits C/EBP and LAP in a dominant-negative manner (1). (affbiotech.com)
- In addition, AMPK activation was shown to reduce the expression of ER stress markers, including C/EBP homologous protein (CHOP) and activating transcription factor 6 (ATF6). (diabetescompass.com)
- Treatment with BIMP increased the mRNA levels of the ER stress marker genes binding immunoglobulin protein (BiP) and the transcription factor C/EBP homologous protein (CHOP). (inra.fr)
Protein20
- We have used Southern blot technique to test whether a gene of the CCAAT/enhancer binding protein (C/EBP) family, CHOP, which maps to 12q13 and is assumed to be involved in adipocyte differentiation, could be the 12q gene in question. (lu.se)
- Increased cAMP can activate protein kinase A, which phosphorylates the transcription factor cAMP response element-binding protein (CREB). (jneurosci.org)
- Disclaimer note: The observed molecular weight of the protein may vary from the listed predicted molecular weight due to post translational modifications, post translation cleavages, relative charges, and other experimental factors. (novusbio.com)
- GADD153 encodes a member of the CCAAT/enhancer-binding protein (C/EBP) family of transcription factors. (novusbio.com)
- Activated and released IRE1α acts as an RNase to initiate transcription of XBP1 mRNA and it becomes a transcriptional activator for unfolded protein response (UPR) gene targets, such as BiP and calreticulin ( 10 ). (spandidos-publications.com)
- This gene product is a bZIP protein, which was also identified as a cellular transcription factor that binds to an enhancer in the promoter of the T cell leukemia virus type 1 promoter. (cancerindex.org)
- Here, we demonstrate that the endoplasmic reticulum stress sensor inositol-requiring enzyme 1 (IRE1α) and its substrate transcription factor X-box-binding protein 1 (XBP1) drive NK cell responses against viral infection and tumors in vivo. (cancerindex.org)
- GADD153 is a small nuclear protein that is capable of dimerizing with transcription factors C/EBP alpha and beta. (thermofisher.com)
- The transcription factor CHOP (CCAAT/enhancer-binding protein homology protein) accumulated in response to carfilzomib exposure, with CHOP depletion conferring protection against cytotoxicity. (ascopost.com)
- The investigators concluded: "Collectively, carfilzomib induced [endoplasmic reticulum] stress, culminating in activation of intrinsic and extrinsic caspase pathways, and we identified the CHOP protein level as a biomarker that could predict sensitivity to carfilzomib in CLL. (ascopost.com)
- These findings suggest that CHOP is a fundamental factor that links protein misfolding in the ER to oxidative stress and apoptosis in β cells under conditions of increased insulin demand. (jci.org)
- Transcription factors are proteins that bind to DNA to promote or suppress protein production. (mit.edu)
- Since almost all diseases involve disruption of the protein-production process, transcription factors are promising biological targets for drugs - and could even serve as drugs themselves. (mit.edu)
- The leading method for determining how transcription factors behave in living cells is to chop up the DNA from millions of cells and use protein antibodies to extract the fragments that have a particular transcription factor attached to them. (mit.edu)
- But determining transcription factors' precise binding sites is just the first step in understanding their role in protein production. (mit.edu)
- Protein expression of CHOP, BIP and IL-1beta remarkably reduced in caffeine treatment group compared with model group. (biomedcentral.com)
- The role of CHOP in the programmed cell death of ER-stressed cells is correlated with its role promoting protein synthesis and oxidative stress inside the ER (4). (affbiotech.com)
- This spliced form of XBP1 then translates into a transcription factor, which further translocates into the nucleus where it induces expression of a wide variety of genes including ER-associated chaperones and protein folding enzymes to increase ER size and folding capacity. (distantreader.org)
- eukaryotic translational initiation aspect-2 kinase 3 (Benefit), inositol-requiring enzyme 1 (IRE1) and activating transcription aspect 6 (ATF6) thus activating these protein. (cgp60474.com)
- Furthermore, BIMP increased the protein expressions and phosphorylation of BiP, CHOP, and protein kinase RNA-like ER kinase and the phosphorylation of eukaryotic translation initiation factor 2. (inra.fr)
Ddit31
- qRT-PCR of Atf3, Sprr1a, Ddit3 (Chop), and Gfap from retinal RNA four days after optic nerve crush (ONC) compared to uninjured contralateral control (CTL): upregulation of regeneration-associated genes Atf3 and Sprr1a, pro-apoptotic transcription factor Ddit3 (Chop), and reactive astrocyte marker Gfap demonstrates a robust response to injury following ONC. (pharmoptima.com)
CHOP102
- Overexpression of ATF-2 and CHOP10 in 3T3-L1 cells decreased Pgc-1 alpha transcription. (elsevierpure.com)
- Knockdown of Chop10 in 3T3-L1 cells using siRNA increased Pgc-1 alpha transcription, whereas siRNA against C/ebp beta in HIB-1B cells decreased Pgc-1 alpha and Ucp1 expression. (elsevierpure.com)
Encodes a transcription factor2
- This gene encodes a transcription factor that regulates MHC class II genes by binding to a promoter element referred to as an X box. (cancerindex.org)
- The most common chromosomal translocation is the FUS-CHOP fusion gene, which encodes a transcription factor necessary for adipocyte differentiation. (medscape.com)
ATF65
- Furthermore, we identify activating transcription factor 6 (ATF6), a key chaperone of endoplasmic reticulum stress, as a functional downstream effector of PCDH20. (biomedcentral.com)
- By administering a selective ATF6 activator, the impairment of intestinal barrier integrity and dysregulation of CHOP/β-catenin/p-p120-catenin pathway was reversed in Pcdh20 -ablated mice with colitis and PCDH20 -deficient colonic cell lines. (biomedcentral.com)
- Specifically, PCDH20 helps to protect against colitis by tightening adherens junctions through the ATF6/CHOP/β-catenin/p-p120-catenin axis. (biomedcentral.com)
- Specifically, the loss of PCDH20 impairs intestinal barrier function by unzipping adherens junctions in mice with colitis via targeting the ATF6/CHOP/β-catenin/p120-catenin axis. (biomedcentral.com)
- Activated ATF6 mediates transcription of genes encoding ER chaperone proteins also. (cgp60474.com)
GADD1532
- Netherton, CL, Parsley, JC & Wileman, TE 2004, ' African swine fever virus inhibits induction of the stress-induced proapoptotic transcription factor CHOP/GADD153 ', Journal of Virology , vol. 78, no. 19, pp. 10825-10828. (uea.ac.uk)
- Right -Over-expression Lysate for CHOP/GADD153. (novusbio.com)
Genes4
- Some of the induced genes, such as CREM, CHOP, and MAP kinase phosphatase-1, may be components of a homeostatic response to excessive stimulation. (jneurosci.org)
- The isoform encoded by the unspliced mRNA, XBP1(U), is constitutively expressed, and thought to function as a negative feedback regulator of XBP1(S), which shuts off transcription of target genes during the recovery phase of ER stress. (cancerindex.org)
- In addition, we found that isolated islets from Chop -/- mice displayed increased expression of UPR and oxidative stress response genes and reduced levels of oxidative damage. (jci.org)
- Acts as a dominant-negative regulator of C/EBP-induced transcription: dimerizes with members of the C/EBP family, impairs their association with C/EBP binding sites in the promoter regions, and inhibits the expression of C/EBP regulated genes. (affbiotech.com)
Kinase2
- inositol-requiring enzyme 1 (IRE1α), PRKR-like ER kinase (PERK) and activating transcription factor-6 (ATF-6). (spandidos-publications.com)
- Since epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors, including gefitinib (GEF) have been reported to induce the apoptosis of several cancer cell lines, in the present study, we examined whether the cytotoxic effects of GEF are further enhanced under amino acid starvation (AAS) culture conditions. (spandidos-publications.com)
Atf31
- Detection of elevated ER tension marker appearance including ATF3, Bip and CHOP in mouse islets subjected to raised lipids and high blood sugar and in -cells of type 2 diabetics supports the participation of ER tension in the pathogenesis of Type 2 diabetes [12]C[14]. (cgp60474.com)
MRNA4
- The resulting loss of 26 nt from the spliced mRNA causes a frame-shift and an isoform XBP1(S), which is the functionally active transcription factor. (cancerindex.org)
- Unexpectedly, there are few strongly downregulated proteins, despite expression of the pro-apoptotic transcription factor CHOP, suggesting that IRE1-dependent mRNA decay (RIDD) has a limited contribution to ER stress-mediated cell death in our system. (torvergata.it)
- JNK1 shRNA expressing INS1 cells demonstrated elevated apoptosis and cleaved caspase 9 and 3 in comparison to nonsense shRNA expressing control INS1 cells when subjected to palmitate and high blood sugar associated with elevated CHOP appearance, ROS development and mRNA appearance. (cgp60474.com)
- Dynamic IRE1 splices X-box binding proteins-1 (Xbp)-1 mRNA, translating into a dynamic transcription aspect sXbp-1 that induces ER chaperones and ER-associated proteins degradation. (cgp60474.com)
Proteins2
- A new method identifies the precise binding sites of transcription factors - proteins that regulate the production of other proteins - with 10 times the accuracy of its predecessors. (mit.edu)
- ATF4 activates the transcription of C/EBP homologous proteins (CHOP), considered to mediate palmitate-induced -cell loss of life [10], [11]. (cgp60474.com)
Mediates1
- Studies also found that CHOP mediates the activation of GADD34 and Ero1-Lα expression during ER stress. (affbiotech.com)
SiRNA1
- Compared to BIMP treatment alone, pretreatment with the CHOP siRNA, siCHOP, decreased BIMP-dependent CHOP expression and improved CCF-STTG1 cell viability. (inra.fr)
Induces1
- Omaveloxolone is an investigational, oral, once-daily, activator of Nrf2, a transcription factor that induces molecular pathways that promote the resolution of neuroinflammation by restoring mitochondrial function, reducing oxidative stress, and inhibiting pro-inflammatory signaling. (chop.edu)
Intron1
- Using PCR generated, site-specific probes corresponding to the non-coding exons 1 and 2 and intron 2 of CHOP, rearrangements in five of seven tumors mapped to the 2.4 and 1.6 kbp PstI fragments that contain the first two exons and introns of the gene and the upstream promoter region. (lu.se)
Ultrastructure1
- In both genetic and diet-induced models of insulin resistance, CHOP deficiency improved β cell ultrastructure and promoted cell survival. (jci.org)
Binds1
- While the DNA sequence that a transcription factor binds to consists of only about six to 12 DNA letters, the fragment extracted by the antibody could be a couple of hundred letters long. (mit.edu)
Pathways1
- 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)
Efficacy2
- David Lynch, MD, PhD, Director of the Friedreich's Ataxia Program at Children's Hospital of Philadelphia (CHOP), has been studying the efficacy of omaveloxolone for years in collaboration with others around the world and with Reata Pharmaceutical, a clinical-stage biopharmaceutical company. (chop.edu)
- Efficacy and safety of zanubrutinib plus R-CHOP in treatment of non-GCB DLBCL with extranodal involvement. (cdc.gov)
Mitochondria1
- In addition, the subcellular distribution of mitochondria can affect the cellular transcriptome and transcription rates. (hindawi.com)
Cellular2
- CHOP expression is induced by certain cellular stresses including starvation and the induced CHOP suppresses cell cycle progression from G1 to S phase (2). (affbiotech.com)
- It is also a major site of cellular stress, which can be caused by a variety of factors, including oxidative stress. (diabetescompass.com)
Liver1
- Current treatment modalities for liver fibrosis mainly focus on eliminating the risk factors that are known to progressively develop into end-stage liver fibrosis, and treatment of end-stage liver fibrosis mainly involves liver transplantation, which carries the risk of trauma and rejection. (biomedcentral.com)
Mice1
- We assessed the effect of Chop deletion in multiple mouse models of type 2 diabetes and found that Chop -/- mice had improved glycemic control and expanded β cell mass in all conditions analyzed. (jci.org)
Catalog1
- The following product was used in this experiment: CHOP Polyclonal Antibody from Thermo Fisher Scientific, catalog # PA5-28956, RRID AB_2546432. (thermofisher.com)
Tumor2
- Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to cause apoptosis in several types of malignant tumor cells through its interaction with the death domain-containing receptor, death receptor 5 (DR5). (nih.gov)
- In contrast to the findings in MLS, no tumor without a t(12;16) exhibited aberrant CHOP restriction digest patterns. (lu.se)
Enhancer1
- Of particular importance has been the identification of two families of transcription factors: the myogenic regulatory factors (MRFs) and the myocyte enhancer factors (MEFs). (biologists.com)
Regulatory1
- Dr. Liao pioneered the zebrafish model to investigate the developmental basis of craniofacial anomalies, elucidated the role of transcription factor IRF6 and the downstream regulatory pathway operating in the embryonic epithelium to regulate craniofacial development and orofacial cleft pathogenesis. (chop.edu)
Expression2
- We conclude that the increased cAMP stimulation of Pgc-1 alpha expression is regulated by the combinatorial effect of transcription factors acting at the CRE on the proximal Pgc-1 alpha promoter. (elsevierpure.com)
- Later it was shown that, during ER stress, the level of CHOP expression is elevated and CHOP functions to mediate programmed cell death (3). (affbiotech.com)
Accumulation1
- Oxidized low-density lipoprotein (oxLDL) is a major risk factor for the development of atherosclerosis, and its accumulation in the vascular wall can lead to ER stress. (diabetescompass.com)
Roles1
- As a consequence, the researchers were able to infer previously unknown relationships among transcription factors, which could provide clues to the roles they play in biological processes. (mit.edu)
Response1
- Multifunctional transcription factor in ER stress response. (affbiotech.com)
Predict1
- They then use that initial, rough guess about common sequences to predict where, throughout the entire genome, the transcription factor would bind, then compare those predictions to the experimental data on where the factor actually did bind. (mit.edu)
Product1
- Western blot was performed using Anti-CHOP Polyclonal Antibody (Product # PA5-28956) and a 21kDa band corresponding to CHOP was observed across the cell lines tested. (thermofisher.com)
Role1
- For a single transcription factor, that role can vary according to both the type of cell in which it's active and its interactions with other transcription factors. (mit.edu)
Type1
- Using a cDNA probe that spans the CHOP coding region, we detected one rearranged and one wild type allele in nine of nine MLS with t(12;16). (lu.se)
