CCAAT-Enhancer-Binding Protein-beta
CCAAT-Enhancer-Binding Proteins
CCAAT-Enhancer-Binding Protein-alpha
Promoter Regions, Genetic
CCAAT-Enhancer-Binding Protein-delta
Gene Expression Regulation
Transcriptional Activation
Binding Sites
DNA-Binding Proteins
Enhancer Elements, Genetic
Transcription Factors
Cells, Cultured
Transcription, Genetic
Nuclear Proteins
Transfection
Transcription Factor CHOP
Base Sequence
RNA, Messenger
Adipocytes
Molecular Sequence Data
Cell Differentiation
Protein Binding
Electrophoretic Mobility Shift Assay
3T3-L1 Cells
Response Elements
Cell Nucleus
Granulocytes
Gene Expression
3T3 Cells
PPAR gamma
Liver
Down-Regulation
Myelopoiesis
Signal Transduction
Chromatin Immunoprecipitation
GTP-Binding Protein beta Subunits
Blotting, Western
Genes, Reporter
Trans-Activators
DNA
Luciferases
Leucine Zippers
Mutation
Tumor Cells, Cultured
Up-Regulation
DNA Primers
Protein Isoforms
Mice, Knockout
Gene Expression Regulation, Enzymologic
Adipose Tissue
Regulatory Sequences, Nucleic Acid
Hepatocyte Nuclear Factor 3-beta
Endrin
Reverse Transcriptase Polymerase Chain Reaction
Cyclic AMP Response Element-Binding Protein
Acute-Phase Reaction
NF-kappa B p50 Subunit
HeLa Cells
Mice, Transgenic
Amino Acid Sequence
RNA Polymerase Sigma 54
Carrier Proteins
NF-kappa B
Phosphorylation
U937 Cells
C/EBPalpha regulates generation of C/EBPbeta isoforms through activation of specific proteolytic cleavage. (1/788)
C/EBPalpha and C/EBPbeta are intronless genes that can produce several N-terminally truncated isoforms through the process of alternative translation initiation at downstream AUG codons. C/EBPbeta has been reported to produce four isoforms: full-length 38-kDa C/EBPbeta, 35-kDa LAP (liver-enriched transcriptional activator protein), 21-kDa LIP (liver-enriched transcriptional inhibitory protein), and a 14-kDa isoform. In this report, we investigated the mechanisms by which C/EBPbeta isoforms are generated in the liver and in cultured cells. Using an in vitro translation system, we found that LIP can be generated by two mechanisms: alternative translation and a novel mechanism-specific proteolytic cleavage of full-length C/EBPbeta. Studies of mice in which the C/EBPalpha gene had been deleted (C/EBPalpha-/-) showed that the regulation of C/EBPbeta proteolysis is dependent on C/EBPalpha. The induction of C/EBPalpha in cultured cells leads to induced cleavage of C/EBPbeta to generate the LIP isoform. We characterized the cleavage activity in mouse liver extracts and found that the proteolytic cleavage activity is specific to prenatal and newborn livers, is sensitive to chymostatin, and is completely abolished in C/EBPalpha-/- animals. The lack of cleavage activity in the livers of C/EBPalpha-/- mice correlates with the decreased levels of LIP in the livers of these animals. Analysis of LIP production during liver regeneration showed that, in this system, the transient induction of LIP is dependent on the third AUG codon and most likely involves translational control. We propose that there are two mechanisms by which C/EBPbeta isoforms might be generated in the liver and in cultured cells: one that is determined by translation and a second that involves C/EBPalpha-dependent, specific proteolytic cleavage of full-length C/EBPbeta. The latter mechanism implicates C/EBPalpha in the regulation of posttranslational generation of the dominant negative C/EBPbeta isoform, LIP. (+info)CCAAT/enhancer-binding proteins are mediators in the protein kinase A-dependent activation of the decidual prolactin promoter. (2/788)
In the course of decidualization, human endometrial stromal cells (ESC) activate the alternative upstream promoter of the decidual prolactin (dPRL) gene. The dPRL promoter is induced by the protein kinase A pathway in a delayed fashion via the region -332/-270 which contains two overlapping consensus binding sequences, B and D, for CCAAT/enhancer-binding proteins (C/EBP). Here we show that sites B and D both bind C/EBPbeta and -delta from ESC nuclear extracts. When decidualization of cultured ESC was induced by treatment with 8-Br-cAMP, complex formation on sites B and D was enhanced. Western blot analysis revealed an elevation of both C/EBPbeta isoforms, liver-enriched activator protein and liver-enriched inhibitory protein, with a delayed onset between 8 and 24 h of cAMP treatment, while C/EBPdelta expression remained unaffected. Cyclic AMP-mediated activation of dPRL promoter construct dPRL-332/luc3 was abrogated by mutation of sites B and D at -310/-285. An expression vector for liver-enriched activator protein potently induced transcription of dPRL-332/luc3 and further enhanced cAMP-mediated induction, while liver-enriched inhibitory protein expression vector abolished the cAMP response, implying that C/EBPs serve as mediators in the delayed cAMP signal transduction to the dPRL promoter. The ratio between activating and repressing isoforms is likely to dictate the transcriptional output. (+info)CUG repeat binding protein (CUGBP1) interacts with the 5' region of C/EBPbeta mRNA and regulates translation of C/EBPbeta isoforms. (3/788)
The transcription factor CCAAT/enhancer binding protein beta, C/EBPbeta, plays a significant role in the regulation of hepatocyte growth and differentiation. A single mRNA coding for C/EBPbeta produces several protein isoforms. Two pathways for generation of low molecular weight C/EBPbeta isoforms have been described: specific proteolytic cleavage and initiation of translation from different AUG codons of C/EBPbeta mRNA. A truncated C/EBPbeta isoform, LIP, is induced in rat livers in response to partial hepatectomy (PH) via the alternative translation mechanism. Here we present evidence that CUG repeat binding protein, CUGBP1, interacts with the 5' region of C/EBPbeta mRNA and regulates translation of C/EBPbeta isoforms. Two binding sites for CUGBP1 are located side by side between the first and second AUG codons of C/EBPbeta mRNA. One binding site is observed in an out of frame short open reading frame (sORF) that has been previously shown to regulate initiation of translation from different AUG codons of C/EBPbeta mRNA. Analysis of cytoplasmic and polysomal proteins from rat liver after PH showed that CUGBP1 is associated with polysomes that translate low molecular weight isoforms of C/EBPbeta. The binding activity of CUGBP1 to the 5' region of C/EBPbeta mRNA shows increased association with these polysomal fractions after PH. Addition of CUGBP1 into a cell-free translation system leads to increased translation of low molecular weight isoforms of C/EBPbeta. Our data demonstrate that CUGBP1 protein is an important component for the regulation of initiation from different AUG codons of C/EBPbeta mRNA. (+info)The C/EBP bZIP domain can mediate lipopolysaccharide induction of the proinflammatory cytokines interleukin-6 and monocyte chemoattractant protein-1. (4/788)
C/EBPalpha, beta, and delta are all expressed by bone marrow-derived macrophages. Ectopic expression of any of these transcription factors is sufficient to confer lipopolysaccharide (LPS)-inducible expression of interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) to a B lymphoblast cell line, which normally lacks C/EBP factors and does not display LPS induction of proinflammatory cytokines. Thus, the activities of C/EBPalpha, beta, and delta are redundant in regard to expression of IL-6 and MCP-1. Surprisingly, the bZIP region of C/EBPbeta, which lacks any previously described activation domains, can also confer LPS-inducible expression of IL-6 and MCP-1 in stable transfectants. Transient transfections reveal that the bZIP regions of C/EBPbeta, C/EBPdelta, and, to a lesser extent, C/EBPalpha can activate the IL-6 promoter and augment its induction by LPS. Furthermore, the transdominant inhibitor, LIP, can activate expression from the IL-6 promoter. The ability of the C/EBPbeta bZIP region to activate the IL-6 promoter in transient transfections is completely dependent upon an intact NF-kappaB-binding site, supporting a model where the bZIP protein primarily functions to augment the activity of NF-kappaB. Replacement of the leucine zipper of C/EBPbeta with that of GCN4 yields a chimeric protein that can dimerize and specifically bind to a C/EBP consensus sequence, but shows a markedly reduced ability to activate IL-6 and MCP-1 expression. These results implicate the leucine zipper domain in some function other than dimerization with known C/EBP family members, and suggest that C/EBP redundancy in regulating cytokine expression may result from their highly related bZIP regions. (+info)Inflammatory versus proliferative processes in epidermis. Tumor necrosis factor alpha induces K6b keratin synthesis through a transcriptional complex containing NFkappa B and C/EBPbeta. (5/788)
Epidermal keratinocytes respond to injury by becoming activated, i.e. hyperproliferative, migratory, and proinflammatory. These processes are regulated by growth factors and cytokines. One of the markers of activated keratinocytes is keratin K6. We used a novel organ culture system to show that tumor necrosis factor alpha (TNFalpha) induces the expression of K6 protein and mRNA in human skin. Multiple isoforms of K6 are encoded by distinct genes and have distinct patterns of expression. By having shown previously that proliferative signals, such as epidermal growth factor (EGF), induce expression of the cytoskeletal protein keratin K6b, we here demonstrate that the same isoform, K6b, is also induced by TNFalpha, a proinflammatory cytokine. Specifically, TNFalpha induces the transcription of the K6b gene promoter. By using co-transfection, specific inhibitors, and antisense oligonucleotides, we have identified NFkappaB and C/EBPbeta as the transcription factors that convey the TNFalpha signal. Both transcription factors are necessary for the induction of K6b by TNFalpha and act as a complex, although only C/EBPbeta binds the K6b promoter DNA. By using transfection, site-directed mutagenesis, and footprinting, we have mapped the site that responds to TNFalpha, NFkappaB, and C/EBPbeta. This site is separate from the one responsive to EGF and AP1. Our results show that the proinflammatory (TNFalpha) and the proliferative (EGF) signals in epidermis separately and independently regulate the expression of the same K6b keratin isoform. Thus, the cytoskeletal responses in epidermal cells can be precisely tuned by separate proliferative and inflammatory signals to fit the nature of the injuries that caused them. (+info)NF-IL6 and CRE elements principally account for both basal and interleukin-1 beta-induced transcriptional activity of the proximal 528bp of the PGHS-2 promoter in amnion-derived AV3 cells: evidence for involvement of C/EBP beta. (6/788)
Prostaglandin H synthase (PGHS)-2 promoter fragments (-528 to +9 bp and 5' unidirectional deletions thereof) were cloned upstream of the chloramphenicol acetyl-transferase (CAT) reporter gene. These were transfected into amnion-derived AV3 cells. The region, -528 to -203, which includes NF-kappa B sites, had little influence on CAT expression. The region, -203 and -52, however, was responsible for most of the basal promoter activity and also conferred responsiveness to interleukin (IL)-1 beta (>3-times basal). Point mutations of NF-IL6 and cAMP response element (CRE) in this region reduced both basal and IL-1 beta-stimulated production of CAT; dual mutation eliminated IL-1 beta responsiveness. Factors in nuclear extracts from control or IL-1 beta-stimulated AV3 cells specifically complexed the NF-IL6 and CRE sequences. However, the NF-IL6 and CRE oligonucleotides cross-competed, suggesting a common factor. C/EBP beta was identified by supershift assay as interacting with both sequences. To a lesser extent C/EBP alpha and delta also interacted with the NF-IL6 site. However, CRE binding protein (CREB), was absent from the complex with the CRE. In conclusion, NF-IL6 and CRE elements principally account in AV3 amnion cells for basal and IL-1 beta-inducible transcriptional activity of the proximal 528 bp of the PGHS-2 promoter, while NF-kappa B elements play no substantial role. C/EBPs, particularly C/EBPbeta, are implicated in control of PGHS-2 transcription through the NF-IL6 and CRE sites. (+info)Multiple regulatory elements in the murine stromelysin-3 promoter. Evidence for direct control by CCAAT/enhancer-binding protein beta and thyroid and retinoid receptors. (7/788)
Stromelysin-3 (ST3) belongs to the matrix metalloproteinase (MMPs) family, a protease family involved in tissue remodeling. Although this family of enzymes is regulated by nuclear receptors, few hormone-responsive elements have been demonstrated in MMP promoters. In order to identify regulatory elements and/or factors that control the expression of the mouse st3 gene, we have analyzed genomic sequences encompassing 5 kilobase pairs of the ST3 promoter. Analysis of these sequences revealed several CCAAT/enhancer-binding proteins (C/EBP) and retinoic acid-responsive elements (RAREs), as well as one thyroid-responsive element. However, in contrast to most MMP promoters, no AP-1-binding sites were identified. Specific binding activities were demonstrated for all elements. Consistent with previous reports, retinoid X receptor is required for maximal binding to the ST3 RAREs and the TRE. The ST3-C/EBP element was shown to mediate dose-dependent promoter activation by C/EBPbeta. Among the RAREs, the proximal DR1-RARE was shown to be sufficient for ST3 promoter activation by ligand-bound retinoid receptors, whereas the two distal DR2-RAREs appear to be involved more in the control of base-line promoter activity. Accordingly, ST3 expression was induced by retinoic acid and was reduced in cells where specific retinoic acid receptors had been inactivated. The involvement of these conserved regulatory elements is discussed in the context of physiological or pathological situations associated with st3 expression. Our findings therefore assign to C/EBP, retinoids, and thyroid hormone important roles in the regulation of ST3 gene expression. (+info)ERK1 and ERK2 activate CCAAAT/enhancer-binding protein-beta-dependent gene transcription in response to interferon-gamma. (8/788)
Interferons (IFNs) regulate the expression of a number of cellular genes by activating the JAK-STAT pathway. We have recently discovered that CCAAAT/enhancer-binding protein-beta (C/EBP-beta) induces gene transcription through a novel IFN response element called the gamma-IFN-activated transcriptional element (Roy, S. K., Wachira, S. J., Weihua, X., Hu, J., and Kalvakolanu, D. V. (2000) J. Biol. Chem. 275, 12626-12632. Here, we describe a new IFN-gamma-stimulated pathway that operates C/EBP-beta-regulated gene expression independent of JAK1. We show that ERKs are activated by IFN-gamma to stimulate C/EBP-beta-dependent expression. Sustained ERK activation directly correlated with C/EBP-beta-dependent gene expression in response to IFN-gamma. Mutant MKK1, its inhibitors, and mutant ERK suppressed IFN-gamma-stimulated gene induction through the gamma-IFN-activated transcriptional element. Ras and Raf activation was not required for this process. Furthermore, Raf-1 phosphorylation negatively correlated with its activity. Interestingly, C/EBP-beta-induced gene expression required STAT1, but not JAK1. A C/EBP-beta mutant lacking the ERK phosphorylation site failed to promote IFN-stimulated gene expression. Thus, our data link C/EBP-beta to IFN-gamma signaling through ERKs. (+info)The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.
Some key components of an acute-phase reaction include:
1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.
CEBPB
WD Repeat and Coiled Coil Containing Protein
EHMT1
Myosatellite cell
Serum response factor
DNA damage-inducible transcript 3
Estrogen receptor alpha
CCDC85B
PCK1
SUMO3
SUMO2
NFE2L1
DLX3
CEBPD
ATF4
CEBPA
Branimir Ivan Sikic
CEBPG
MiR-155
Sp1 transcription factor
MicroRNA
RETNLB
Serdar Bulun
Liver X receptor alpha
Glucocorticoid receptor
ADH1C
RELA
PIAS4
C5orf46
PANO1
CUTL1
CAAT box
C1orf112
Glutamate-rich protein 4
ENO3
Adipogenesis
FOXA3
Multiple Epidermal Growth Factor-like Domains 8
Transmembrane protein 251
U7 small nuclear RNA
Transcription factor
Induced stem cells
PRKD3
CCDC180
TMEM128
The E3 ubiquitin ligase TRIM23 regulates adipocyte differentiation via stabilization of the adipogenic activator PPARγ | eLife
Pesquisa | Biblioteca Virtual em Saúde - BRASIL
Genatlas sheet
DeCS
Professor Dipak Ramji - People - Cardiff University
HIT-result
Transcription and enhancer profiling in human monocyte subsets | Blood | American Society of Hematology
Decidual expression and regulation of fatty acid desaturase 3 during mouse decidualization in: Reproduction Volume 156 Issue 5 ...
DeCS 2017 - December 21, 2017 version
Human Genome Epidemiology Literature Finder|Home|PHGKB
Hidrocortisona/farmacologia
anti-C/EBP-beta mouse monoclonal, EBP-333, purified | 691625
Neurotrophin/Trk receptor signaling mediates C/EBPalpha, -beta and NeuroD recruitment to immediate-early gene promoters in...
Development - Glucocorticoid receptor signaling Pathway Map - PrimePCR | Life Science | Bio-Rad
Glucose-6-Phosphatase | Profiles RNS
antibodies bind to - ELISA Strip
Human KLK11(Kallikrein 11) ELISA Kit - Dla Różnorodności Biologicznej - Life Sciences
The Heterogeneity of White Adipose Tissue | IntechOpen
磷脂氫麩胱甘肽過氧化酵素PHGPx抑制砷
Human PVRL1(Poliovirus Receptor Related Protein 1) ELISA Kit - Elisa kits Gentaur
Human AP2m1(Adaptor Related Protein Complex 2 Mu 1) ELISA Kit - Lotuskring Poeldijk
MedlinePlus: Genes: C
The shift in the balance between osteoblastogenesis and adipogenesis of mesenchymal stem cells mediated by glucocorticoid...
Taehoon Chun - Research output - Korea University
Metabolite and transcriptome analysis during fasting suggest a role for the p53-Ddit4 axis in major metabolic tissues | BMC...
Therapeutic potential of mesenchymal stem cells in regenerative medicine - GIOSTAR
Rat BMP-6(Bone Morphogenetic Protein 6) ELISA Kit - Rat BMP-6(Bone Morphogenetic Protein 6) ELISA Kit Exporter, Importer,...
MA RAT AGING DN
enzymes function
Detailed Information [JCRB1054]
Receptor6
- Other immunophilins or heat shock proteins (for example, HSP70 ) that are found associated with unliganded steroid receptors are likely to be involved in the maturation of the receptor to its hormone-binding conformation. (bio-rad.com)
- Neurotrophin/Trk receptor signaling mediates C/EBPalpha, -beta and NeuroD recruitment to immediate-early gene promoters in neuronal cells and requires C/EBPs to induce immediate-early gene transcription. (ox.ac.uk)
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Poliovirus Receptor Related Protein 1 (PVRL1) in Tissue homogenates, cell lysates and other biological fluids. (1elisakits.com)
- Description: A sandwich ELISA kit for detection of Poliovirus Receptor Related Protein 1 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (1elisakits.com)
- Glucocorticoids exert their function by binding to the glucocorticoid receptor (GR). Physiological concentrations of glucocorticoids stimulate osteoblast proliferation and promote osteogenic differentiation of MSCs. (biomedcentral.com)
- Cellular internalization and degradation of antithrombin III-thrombin, heparin cofactor II-thrombin, and alpha 1-antitrypsin-trypsin complexes is mediated by the low density lipoprotein receptor-related protein. (go.jp)
Antibodies2
- Do the antibodies contain any other proteins? (progen.com)
- The serum antibodies contain other proteins present in serum. (progen.com)
Factor1
- Hepatitis B virus HBx protein induces transcription factor AP-1 by activation of extracellular signal-regulated and c-Jun N-terminal mitogen-activated protein kinases. (go.jp)
Genes4
- This requires the activity of proteins called transcription factors that bind to DNA and switch on the expression of genes. (elifesciences.org)
- GCR mediates transactivation of target genes by binding glucocorticoid response elements in their promoter region. (bio-rad.com)
- CONCLUSION: We here identify three IE genes as targets for BDNF/TrkB signaling, show that C/EBPalpha and -beta are recruited along with NeuroD to target promoters, and that C/EBPs are essential mediators of Trk signaling in cortical neurons. (ox.ac.uk)
- The UPR restores ER homeostasis by attenuating protein synthesis or by inducing the expression of various genes encoding molecular chaperones and protein processing enzymes that promote protein folding and post-translational modification. (molcells.org)
ELISA KIT1
- Description: A sandwich ELISA kit for detection of Adaptor Related Protein Complex 2 Mu 1 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (lotuskringpoeldijk.nl)
Activator2
- GCR and corepressor NCOA2 inhibit Activator protein 1 ( AP-1 ) and so induce AP-1 -mediated gene expression, for example Matrix metallopeptidase 13 ( MMP-13 ). (bio-rad.com)
- Activator protein 1 activity is involved in the regulation of the cell type-specific expression from the proximal promoter of the human profilaggrin gene. (go.jp)
Dopamine2
- OBJECTIVE: 18F-FP-CIT positron emission tomography (PET) is known for its high sensitivity and specificity for evaluating striatal dopamine transporter (DAT) binding. (bvsalud.org)
- This drug also binds to dopamine D2 receptors in the corpus striatum, thereby mimicking the actions of dopamine on motor control. (blogspot.com)
Transmembrane1
- These transmembrane proteins are major transducers of the UPR in mammals and mediate multiple distinct signals from the ER to the cytosol. (molcells.org)
Inhibitor1
- Upon administration, C3-targeted complement inhibitor APL-2 selectively binds to C3 and blocks the cleavage of C3 into C3a and C3b by C3 convertase. (blogspot.com)
Intracellular2
- The GR is an intracellular protein that is ubiquitously expressed in almost every cell of the organism and interacts with chromatin to modulate the activity of numerous transcription factors in a cell type-specific manner. (biomedcentral.com)
- Biochemical characterization and intracellular localization of the Menkes disease protein. (go.jp)
Mediates1
- Here, we show that a novel ubiquitin E3 ligase, tripartite motif protein 23 (TRIM23), stabilizes PPARγ protein and mediates atypical polyubiquitin conjugation. (elifesciences.org)
Receptors1
- Due to the structural similarity to adenosine, caffeine binds to and blocks adenosine receptors, thereby preventing the inhibitory effects of adenosine on nerve cells. (blogspot.com)
Glucocorticoid1
- GCR can interact productively with the POU class 2 homeobox 1 and 2 ( Oct-1 and Oct-2 ) proteins to recruit them to DNA and this contributes to activation of transcription by Oct from glucocorticoid-responsive promoters [ 17 ], [ 18 ]. (bio-rad.com)
Inhibits1
- Although the exact mode of action through which cadazolid exerts its effect has yet to be fully elucidated, upon administration, this agent inhibits bacterial protein synthesis and leads to bacterial cell death. (blogspot.com)
Cells5
- analyzed this process in mouse cells and identified a protein called TRIM23 that is produced in precursor cells. (elifesciences.org)
- Adipose tissue not only stores energy, but also controls metabolism through secretion of hormones, cytokines, proteins, and microRNAs that affect the function of cells and tissues throughout the body. (intechopen.com)
- Adenovirus early region 4 34-kilodalton protein directs the nuclear localization of the early region 1B 55-kilodalton protein in primate cells. (go.jp)
- The alpha-isoform of the CCAAT/enhancer-binding protein is required for mediating cAMP responsiveness of the phosphoenolpyruvate carboxykinase promoter in hepatoma cells. (go.jp)
- Stratified squamous epithelial-specific expression in cultured cells is mediated by binding of Sp1 and ets transcription factors to a proximal promoter element. (go.jp)
Cytoplasmic2
- Unligated cytoplasmic GCR exists as a heteromeric complex that contains a dimer of HSP90 , an immunophilin protein of the FK506 binding protein family (for example, FK506 binding protein 4, 59kDa ( FKBP4 )), and Prostaglandin E synthase 3 ( p23 co-chaperone ). (bio-rad.com)
- Alpha L beta 2 integrin/LFA-1 binding to ICAM-1 induced by cytohesin-1, a cytoplasmic regulatory molecule. (go.jp)
Variants2
- CCAAT/enhancer binding protein alpha, beta and delta gene variants: associations with obesity related phenotypes in the Leeds Family Study. (cdc.gov)
- The GCR gene encodes two splicing variants, GCR-alpha and GCR-beta [ 1 ], [ 2 ]. (bio-rad.com)
Calcium1
- The endoplasmic reticulum (ER) is a critical organelle for protein synthesis, folding and modification, and lipid synthesis and calcium storage. (molcells.org)
Chaperone1
- The GCR must be bound to the protein chaperone Heat shock protein 90kDa ( HSP90 ) in order to acquire the high affinity steroid binding conformation [ 3 ]. (bio-rad.com)
Complex2
- Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Adaptor Related Protein Complex 2 Mu 1 (AP2m1) in Tissue homogenates and other biological fluids. (lotuskringpoeldijk.nl)
- Protein quality control is monitored by a complex system that modulates ER function to resolve ER stress and dysfunction. (molcells.org)
Stabilizes1
- Cabazitaxel binds to and stabilizes tubulin, resulting in the inhibition of microtubule depolymerization and cell division, cell cycle arrest in the G2/M phase, and the inhibition of tumor cell proliferation. (blogspot.com)
Alpha1
- GCR-alpha binding to NF-kB leads to inactivation of both proteins [ 13 ]. (bio-rad.com)
Regions2
- These enhancer regions are subsequently inherited by late enhanceosomes. (elifesciences.org)
- We found that C/EBPalpha/beta and NeuroD formed complexes in vitro and in vivo, and were recruited to all three homologous promoter regions. (ox.ac.uk)
Molecular2
- It is known from previous work that TRIM23 belongs to a family of enzymes that attach a small molecular tag called ubiquitin onto other proteins. (elifesciences.org)
- This ubiquitin tag typically marks these proteins for rapid destruction by a large molecular machine called the proteasome. (elifesciences.org)
Gene expression2
- If the amount of PPARγ bound to DNA is too low, then it is unable to activate gene expression. (elifesciences.org)
- Significant decreases were observed in the levels of hematocrit, hemoglobin, erythrocytes, triglycerides and total protein and catalase, H+-ATPase, and GpX gene expression. (bvsalud.org)
Leads1
- Dysregulation of ER functions leads to the accumulation of misfolded- or unfolded-protein in the ER lumen, and this triggers the unfolded protein response (UPR), which restores ER homeostasis. (molcells.org)
Early2
- TRIM23 knockdown caused a marked decrease in PPARγ protein abundance during preadipocyte differentiation, resulting in a severe defect in late adipogenic differentiation, whereas it did not affect the formation of early enhanceosomes. (elifesciences.org)
- Our results suggest that TRIM23 plays a critical role in the switching from early to late adipogenic enhanceosomes by stabilizing PPARγ protein possibly via atypical polyubiquitin conjugation. (elifesciences.org)