BACKGROUND: Multiple sclerosis (MS) is a complex trait in which alleles at or near the class II loci HLA-DRB1 and HLA-DQB1 contribute significantly to genetic risk. The MHC class II transactivator (MHC2TA) is the master controller of expression of class II genes, and methylation of the promoter of this gene has been previously been shown to alter its function. In this study we sought to assess whether or not methylation of the MHC2TA promoter pIV could contribute to MS disease aetiology. METHODS: In DNA from peripheral blood mononuclear cells from a sample of 50 monozygotic disease discordant MS twins the MHC2TA promoter IV was sequenced and analysed by methylation specific PCR. RESULTS: No methylation or sequence variation of the MHC2TA promoter pIV was found. CONCLUSION: The results of this study cannot support the notion that methylation of the pIV promoter of MHC2TA contributes to MS disease risk, although tissue and timing specific epigenetic modifications cannot be ruled out.
STAT3 antibody (signal transducer and activator of transcription 3 (acute-phase response factor)) for ICC/IF, IHC-P, WB. Anti-STAT3 pAb (GTX50709) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
STAT5A (phospho Tyr694) antibody [5F6.F1] (signal transducer and activator of transcription 5A) for ELISA, ICC/IF, IHC-P, WB. Anti-STAT5A (phospho Tyr694) mAb (GTX48647) is tested in Human, Mouse, Rat samples. 100% Ab-Assurance.
Lapin STAT1 Polyclonal anticorps pTyr701 pour ELISA, WB. Publier en 3 références Pubmed. Order anti-STAT1 anticorps ABIN539531.
Abcam provides specific protocols for Anti-STAT6 antibody (ab88540) : Western blot protocols, Immunocytochemistry & immunofluorescence protocols
anti-STAT2, pAb is a polyclonal antibody that crossreacts with human protein. Works in WB. Important for Inflammation, Oxidative Stress, ROS, Immunology research.
Anti-STAT3 (phospho Y705) antibody [EP2147Y] (ab76315) has been cited in 56 publications. References for Human, Mouse, Rat in IHC, IHC-Fr, IHC-P, WB
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优异的STAT3兔单抗(ab76315)经WB, IP, IHC-P, ICC实验严格验证,可用于小鼠, 大鼠和人。被多篇文献引用并有多个独立的用户反馈。中国75%以上现货。
Polyclonal antibody for STAT1 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: WB. Reactive species: Human. STAT1 information: Molecular Weight: 87335 MW; Subcellular Localization: Cytoplasm . Nucleus . Translocated into the nucleus upon tyr
Polyclonal antibody for STAT2 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: WB. Reactive species: Human. STAT2 information: Molecular Weight: 97916 MW; Subcellular Localization: Cytoplasm. Nucleus. Translocated into the nucleus upon activ
Monoklonale und polyklonale STAT5B Antikörper für viele Methoden. Ausgesuchte Qualitäts-Hersteller für STAT5B Antikörper. Hier bestellen.
Mouse monoclonal STAT1 antibody [SM1] validated for WB, IP, IHC, Flow Cyt and tested in Human and Mouse. Referenced in 5 publications and 3 independent…
高い抗原親和性、特異性と安定した品質を兼ね備えたアブカムのウサギ・モノクローナル抗体 RabMAb® ab109320 交差種: Hu 適用: WB,IP,IHC-P,ICC,Flow Cyt
Looking for online definition of haematopoietic transcription factor PU.1 in the Medical Dictionary? haematopoietic transcription factor PU.1 explanation free. What is haematopoietic transcription factor PU.1? Meaning of haematopoietic transcription factor PU.1 medical term. What does haematopoietic transcription factor PU.1 mean?
Hepatitis B virus X protein targets the Bcl-2 protein CED-9 to induce intracellular Ca2+ increase and cell death in Caenorhabditis elegans Journal Article ...
Class II transactivator (CIITA) is a global transcriptional coactivator of human leukocyte antigen-D (HLA-D) genes. CIITA contains motifs similar to guanosine triphosphate (GTP)-binding proteins. This report shows that CIITA binds GTP, and mutations in these motifs decrease its GTP-binding and transactivation activity. Substitution of these motifs with analogous sequences from Ras restores CIITA function. CIITA exhibits little GTPase activity, yet mutations in CIITA that confer GTPase activity reduce transcriptional activity. GTP binding by CIITA correlates with nuclear import. Thus, unlike other GTP-binding proteins, CIITA is involved in transcriptional activation that uses GTP binding to facilitate its own nuclear import. ...
insulin promoter factor 1: PDX-1/IPF1/STF-1/IDX-1/IUF-1 is a homeodomain containing transcription factor; found in pancreatic beta-cells; RIPE3b1 was cloned and identified as the mammalian homologue of an avian regulator of cellular differentiation MafA/L-Maf; amino acid sequence in first source; RerSeq NM_008814 (mouse), NM_013311 (human), NM_022852
Please help populate SUNScholar with the full text of SU research output. Also - should you need this item urgently, please snd us the details and we will try to get hold of the full text as quick possible. E-mail to [email protected] Thank you.. ...
Rabbit Polyclonal Anti-Stat4 (phospho Tyr693) antibody (STJ90753). From Abcams OEM supplier St Johns Laboratory, validated in WB, IHC, ELISA. AntibodyPlus provides trial size antibody samples for antibody validation. Replacement to Abcam, Santa Cruz, Sigma and CST antibody.
The transcription factor PU.1 is often impaired in patients with acute myeloid leukemia (AML). Here, we used AML cells that already had low PU.1 levels and further inhibited PU.1 using either RNA interference or, to our knowledge, first-in-class small-molecule inhibitors of PU.1 that we developed specifically to allosterically interfere with PU.1-chromatin binding through interaction with the DNA minor groove that flanks PU.1-binding motifs. These small molecules of the heterocyclic diamidine family disrupted the interaction of PU.1 with target gene promoters and led to downregulation of canonical PU.1 transcriptional targets. shRNA or small-molecule inhibition of PU.1 in AML cells from either PU.1lo mutant mice or human patients with AML-inhibited cell growth and clonogenicity and induced apoptosis. In murine and human AML (xeno)transplantation models, treatment with our PU.1 inhibitors decreased tumor burden and resulted in increased survival. Thus, our study provides proof of concept that ...
RBMS1 overexpression lysate, 0.1 mg. Transient overexpression lysate of R binding motif, single stranded interacting protein 1 (RBMS1), transcript variant 2
TY - JOUR. T1 - The pancreatic duodenal homeobox-1 protein (Pdx-1) interacts with histone deacetylases Hdac-1 and Hdac-2 on low levels of glucose. AU - Mosley, Amber L.. AU - Özcan, Sabire. PY - 2004/12/24. Y1 - 2004/12/24. N2 - We have previously demonstrated that high concentrations of glucose stimulate insulin gene expression by causing hyperacetylation of histone H4 at the insulin gene promoter. Furthermore, we have shown that the glucose-mediated hyperacetylation of histone H4 depends on the recruitment of the histone acetyltransferase p300 by the beta cell-specific transcription factor Pdx-1. In this study, we demonstrate that the histone deacetylases Hdac-1 and Hdac-2 are rapidly recruited to the insulin promoter in the mouse insulinoma cell line MIN6 when cells are switched from high to low glucose media. Moreover, we demonstrate that the beta cell-specific homeodomain protein Pdx-1 interacts with histone deacetylases Hdac-1 and Hdac-2 at low levels of glucose. In vitro studies indicate ...
The role of hepatitis B virus (HBV) X protein (HBx) in the regulation of HBV replication remains controversial. In the present study, the role of HBx in regulating HBV replication was initially investigated in both HepG2 and Huh7 in vitro cell lines with a transient transfection system. Next, the regions of HBx responsible for transcriptional transactivation and promotion of HBV replication were mapped in an HBV replication mouse model by in vivo transfection of a series of HBx expression plasmids. In an in vitro setting, HBx deficiency had little effect on HBV replication in Huh7 cells, but impaired HBV replication in HepG2 cells. In an in vivo setting, HBx had a strong enhancing effect on HBV transcription and replication. For the C-terminal two-thirds of the protein (amino acids [aa] 51 to 154) was required for this function of HBx, and the regions spanning aa 52 to 72 and 88 to 154 were found to be important for the stimulatory function of HBx on HBV replication. In conclusion, the role of HBx in
The role of hepatitis B virus (HBV) X protein (HBx) in the regulation of HBV replication remains controversial. In the present study, the role of HBx in regulating HBV replication was initially investigated in both HepG2 and Huh7 in vitro cell lines with a transient transfection system. Next, the regions of HBx responsible for transcriptional transactivation and promotion of HBV replication were mapped in an HBV replication mouse model by in vivo transfection of a series of HBx expression plasmids. In an in vitro setting, HBx deficiency had little effect on HBV replication in Huh7 cells, but impaired HBV replication in HepG2 cells. In an in vivo setting, HBx had a strong enhancing effect on HBV transcription and replication. For the C-terminal two-thirds of the protein (amino acids [aa] 51 to 154) was required for this function of HBx, and the regions spanning aa 52 to 72 and 88 to 154 were found to be important for the stimulatory function of HBx on HBV replication. In conclusion, the role of HBx in
Background: A number of clinical trials using stem/progenitor cell transplantation in ischemic heart diseases are now on-going, however, aging-induced cell dysfunction may impair therapeutic efficacy. We tested the hypothesis that genetic modification of EPCs by sonic hedgehog (Shh), one of the embryonic morphogens, may ameliorate the loss of function in aged EPCs.. Methods and Results: Cultured EPCs were isolated from 3m.o. and 24m.o. mice and cell functions, including cytokine expression, were evaluated by real-time PCR. Proliferation, migration and adhesion activity were significantly decreased and apoptosis was increased in the 24m.o.-EPCs vs. 3m.o.-EPCs. The reduced expression of VEGF, eNOS, and IGF-1 were also observed in the 24m.o.-EPCs. We then evaluated the effect of Shh gene transfer to the 24m.o.-EPCs. Shh gene transfer significantly improved proliferation and anti-apoptosis activities in 24m.o.-EPCs vs. empty vector transfected (EV) 24m.o.-EPCs, up to a similar level of EV ...
J:117226 Wei K, Che N, Chen F, Myocardin-related transcription factor B is required for normal mouse vascular development and smooth muscle gene expression. Dev Dyn. 2007 Feb;236(2):416-25 ...
[ Hcc Chemistry Lab Manual ] - Boiling And Melting Points Study Questions Lab 3 Bioling And,Full Text Mir 663 Overexpression Induced By Endoplasmic Reticulum,Nuclear Expression Of Hepatitis B Virus X Protein Is Associated
Clone REA272 recognizes the N-terminus of the signal transducer and activator of transcription 1-α/β (STAT1) antigen, regardless of phosphorylation status. STAT1 is expressed in two alternatively spliced isoforms (91 kDa STAT1α and 84 kDa STAT1β) and clone REA272 recognizes both isoforms. STAT1 expression is found ubiquitously. It is involved in upregulating genes due to a signal by either type I, type II, or type III interferons. In response to interferon γ (IFN-γ) stimulation, the STAT1 subunits become tyrosine-phosphorylated at Y701, and the complex is translocated to the nucleus. STAT1 forms homodimers or heterodimers with STAT3 that bind to the IFN-γ activated sequence promoter element. In response to either IFN-α or IFN-β stimulation, STAT1 forms a heterodimer with STAT2 that can bind the interferon stimulated response promoter element. In either case, binding of the promoter element leads to an increased expression of interferon stimulated genes. Additional information: Clone REA272
The Ets-Related Gene (ERG) belongs to the Ets family of transcription factors and is critically important for maintenance of the hematopoietic stem cell population. A chromosomal translocation observed in the majority of human prostate cancers leads to the aberrant overexpression of ERG. We have identified regions flanking the ERG Ets domain responsible for autoinhibition of DNA binding and solved crystal structures of uninhibited, autoinhibited, and DNA-bound ERG. NMR-based measurements of backbone dynamics show that uninhibited ERG undergoes substantial dynamics on the millisecond-to-microsecond timescale but autoinhibited and DNA-bound ERG do not. We propose a mechanism whereby the allosteric basis of ERG autoinhibition is mediated predominantly by the regulation of Ets-domain dynamics with only modest structural changes. Structural and dynamic studies of the transcription factor ERG reveal DNA binding is allosterically autoinhibited.,Regan MC, Horanyi PS, Pryor EE Jr, Sarver JL, Cafiso DS, ...
Targeting of the tetracycline transactivator gene to the BF1 locus. The targeting construct was made by replacing thelacZ sequence in the BF1 targeting vector previously described (Xuan et al., 1995) with the sequence encoding the tetracycline transactivator (tTA) from pUHD 15-1 (Gossen and Bujard, 1992). The SalI site in the tTA sequence was eliminated by mutagenesis. The tTA sequence was inserted between aSalI-ApaI fragment containing the BF1promoter and an EcoRI-KpnI fragment containing an SV40 intron and poly(A) sequence (Hebert and McConnell, 2000). TheSalI-BamHI fragment was then inserted into theSalI-BamHI sites in the pHBL3 plasmid. Linearized targeting vector was electroporated into W9.5 embryonic stem (ES) cells. Targeted ES clones were identified by PCR and Southern blot as previously described. Three correctly targeted clones were injected into blastocysts to generate chimeric mice that were bred with C57/BL6 mice.. Generation and screening of tetO transgenic lines.IRES3lacZ was ...
Desert Hedgehog (Dhh) belongs to the highly conserved Hedgehog family of proteins which are involved in multiple developmental processes. Hedgehogs…
Regulation of gene transcription Ub conjugation affects gene transcription because many transcription factors become conjugated to Ub, and transcription activators are degraded by the proteasome [16 ...
cdna chromosome:GRCm38:10:23104763:23349887:-1 gene:ENSMUSG00000010461 gene_biotype:protein_coding transcript_biotype:protein_coding gene_symbol:Eya4 description:EYA transcriptional coactivator and phosphatase 4 [Source:MGI Symbol;Acc:MGI:1337104 ...
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TY - JOUR. T1 - Hepatitis B virus X protein represses LKB1 expression to promote tumor progression and poor postoperative outcome in hepatocellular carcinoma. AU - Wu, Cheng Chung. AU - Wu, De Wei. AU - Lin, Ying Yu. AU - Lin, Po Lin. AU - Lee, Huei. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Background: Hepatitis B virus X (HBx) protein plays critical roles in hepatitis B virus (HBV)-associated hepatocellular tumorigenesis through different molecular mechanisms, including inactivation of p53, a key transcription factor of liver kinase B1 (LKB1). We hypothesized that p53 inactivation by HBx protein could decrease LKB1 expression, thereby promoting tumor progression and poor outcomes in patients with HBV-associated hepatocellular carcinoma. Methods: Manipulation strategies for HBx protein and/or p53 were used to verify that loss of LKB1 could promote colony formation and invasiveness in HepG2 and Hep3B cells. The expressions of HBx protein and LKB1 in 93 hepatocellular carcinomas (HCC) were also ...
Hepatitis B virus x protein induces epithelial-mesenchymal transition of hepatocellular carcinoma cells by regulating long non-coding RNA. https://t.co/ewvzsLK8Xn https://t.co/18bd2tE7UL. ...
Hepatitis B virus (HBV) infections play an important role in the development of hepatocellular carcinoma (HCC). HBV X protein (HBx) is a multifunctional protein that can modulate various cellular processes and plays a crucial role in the pathogenesis of HCC. HBx is known to interact with DNA helicase components of TFIIH, a basal transcriptional factor and an integral component of DNA excision repair. In this study, the functional relevance of this association was further investigated in the context to DNA repair. By site-directed mutagenesis HBxs critical residues for interaction with TFIIH were identified. Similarly, TFIIH mutants lacking ATPase domain and the conserved carboxyl-terminal domain failed to interact with HBx. Yeast and mammalian cells expressing HBxwt conferred hypersensitivity to UV irradiation, which is interpreted as a basic deficiency in nucleotide excision repair. HBxmut120 (Glu to Val) was defective in binding to TFIIH and failed to respond to UV. We conclude that HBx may act as
The hepatitis B virus X gene encodes a transcription activator which stimulates the synthesis of RNAs from a variety of class II and III promoter elements. In this report, we present a mutational analysis which genetically demonstrates that the X gene actually encodes two, and possibly three, related polypeptides from a single mRNA using alternate translation initiation from any of three in-frame AUG codons. Genetic analysis shows that translation initiates at the 5 proximal AUG of X mRNA and produces a full-length 17-kDa X protein but in addition also likely initiates at either of two conserved, in-frame AUG codons, producing two amino-terminally truncated X proteins presumably of 8 and 6.6 kDa. Expression of mRNAs capable of encoding only one of each X protein all individually transactivate class III (RNA polymerase III)-transcribed promoters. However, class II (RNA polymerase II)-transcribed promoters displayed various requirements for the different X proteins. Expression of two X proteins, ...
Members of the CREB-binding protein/p300-interacting transactivator with ED-rich tail (CITED) family bind CREB-binding protein and p300 with high affinity and regulate gene transcription. Gene knockout studies indicate that CITED2 is required for neural crest and neural tube development and that it functions as a co-activator for transcription factor AP-2 (TFAP2). Here we describe human CITED4, a new member of this family, which is encoded by a single exon mapping to chromosome 1p34--1p35. CITED4 and p300/CREB-binding protein are present in endogenous naturally occurring complexes, indicating that they interact physiologically. The interaction occurs between the cysteine-histidine-rich domain 1 of p300 and the carboxyl terminus of CITED4. In keeping with this, CITED4 functions as a transactivator when artificially targeted to a promoter element. CITED4 physically interacts with all TFAP2 isoforms in vitro and strongly co-activates all TFAP2 isoforms in Hep3B cells. Co-activation of TFAP2 requires amino
Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.
The studies presented here clearly demonstrated that TGF-β1 triggers the nuclear translocation of MRTFs, which activates the two parallel pathways during EMT (Fig. 10 J). One pathway up-regulates the expression of EMT-regulating genes, such as slug, via MRTFs, Smad3, and GCCG-like motifs, leading to dissociation of cell-cell contacts. The other up-regulates the expression of actin cytoskeletal genes via MRTFs, SRF, and CArG box, resulting in remodeling of the actin cytoskeleton.. Recent studies demonstrate that MRTFs associate with monomeric G-actin through their RPEL motifs, which anchor MRTFs in the cytoplasm (Miralles et al., 2003; Posern et al., 2004). Activated Rho reduces the cytoplasmic G-actin pool by enhancing actin polymerization, and then triggers the dissociation of MRTFs from G-actin, resulting in the nuclear translocation of MRTFs. TGF-β1 stimulation enhances the Rho activity in many kinds of epithelial cell lines (Bhowmick et al., 2001, 2003; Tian et al., 2003). We demonstrated ...
Fig. 4. EBV lytic cycle genes activated by Rta alone or together with Z(S186A). Cells were either untreated (lane 1), chemically induced with TPA and sodium butyrate (lane 2), or transfected with 10 μg of plasmid DNA (lanes 3 to 10). In lanes 4, 6, and 8, cells received 5 μg of activator and 5 μg of empty vector. In lanes 3, 5, and 7, cells received only vector pRTS (lane 3), pBXG1 (lane 5), or pCMV (lane 7). In lanes 9 and 10, Rta was transfected with ZEBRA and the mutant Z(S186A), respectively. Total RNA prepared 30 h following transfection was analyzed by Northern blotting using probes for the indicated genes (see Materials and Methods). The blot was stripped between probes. Classification of the genes according to primary activator(s) is indicated to the right (see Discussion). The extra band above the expected size of the BRLF1 mRNA in lane 10 is most likely the result of an Rta-activated transcript from the Z(S186A) expression vector. ...
2390 Janus kinase 2 (JAK2) is a cytokine receptor associated tyrosine kinase. Binding of cytokines to their specific receptors leads to their dimerization and activation of associated JAKs. Activated JAKs phosphorylate specific tyrosine residues in the cytoplasmic chains of the receptor, which now act as docking sites for SH2 containing latent transcription factors known as STATs. Once bound to the receptor, STATs are activated by JAKs through phosphorylation of their tyrosine residues. Activated STATs form stable dimers and translocate to the nucleus, where they bind specific promoter sequences of their target genes involved in cell proliferation and survival, such as Bcl-xL, Bcl-2, c-myc and cyclin D1. Tumor cell lines and samples derived from hematopoetic malignancies (leukemia, lymphoma and multiple myeloma) and solid tumors (breast, head and neck, lung, prostrate and ovarian cancers) exhibit deregulated JAK-STAT signaling, which can be attributed to autocrine cytokine production or growth ...
PURPOSE: To study the effect of hepatitis B virus X protein binding protein (HBXIP) on proliferation, migration and invasion of adenoid cystic carcinoma cell line ACC-M, and the possible mechanism of PI3K/Akt signaling pathway. METHODS: HBXIP plasmid was transfected into ACC-M. The cells were divided into experimental group (transfected with plasmid pEGFP-N1-HBXIP) control group (non-transfected group) and blank control group (vector group, pEGFP-N1). RT-PCR was used to detect the expression HBXIP in ACC-M; MTT assay, transwell chamber experiments and scratches over the proliferation of HBXIP were utilized individually to evaluate the influence of HBXIP on ACC-M expression, migration and invasion; Western blotting was used to detect the protein expression of Akt, p-Akt, PI3K, p-PI3K and S100A4 after overexpression of HBXIP ...
Clone REA324 recognizes the signal transducer and activator of transcription 3 (STAT3) antigen phosphorylated at serine 727 (pS727). STAT3 expression is found ubiquitously. It is activated in response to various growth factors, hormones, and cytokines, and has an important role in their signaling. When these ligands bind to the specific transmembrane STAT3 receptor, STAT3 becomes activated by tyrosine phosphorylation of two important phosphorylation sites, pY705 and pS727. The dimeric STAT3 translocates to the nucleus, where it binds to consensus STAT3 binding sequences within the promoter region of target genes and thereby activates their transcription. The persistent activation of STAT3 also mediates tumor-promoting inflammation. STAT3 promotes pro-oncogenic inflammatory pathways in tumor inflammation and immunity, including nuclear factor-κB and interleukin-6-GP130-Janus kinase pathways, and by opposing STAT1- and NF-κB-mediated T helper 1 anti-tumor immune responses. Additional information: Clone
In the context of gene regulation: transactivation is the increased rate of gene expression triggered either by biological processes or by artificial means, through the expression of an intermediate transactivator protein. In the context of receptor signaling, transactivation occurs when one or more receptors activate yet another; receptor transactivation may result from the crosstalk of signaling cascades. Transactivation can be triggered either by endogenous cellular or viral proteins, also called transactivators. These protein factors act in trans (i.e., intermolecularly). HIV and HTLV are just two of the many viruses that encode transactivators to enhance viral gene expression. These transactivators can also be linked to cancer if they start interacting with, and increasing expression of, a cellular proto-oncogene. HTLV, for instance, has been associated with causing leukemia primarily through this process. Its transactivator, Tax, can interact with p40, inducing overexpression of ...
The results from this study show that control of a key developmental regulator through an optimized tetracycline-regulation system can be used to manipulate the formation of a compound gland during fetal organogenesis and the maintenance of glandular function in mature animals. We incorporated several modifications to help ensure that regulated expression of PDX1 from a transgene could compensate for the absence of both endogenous Pdx1 alleles. The correct timing of activation of the Pdx1 transgene was optimized by inserting the coding region of the tTA transcriptional activator into the Pdx1 locus to place tTA under control of the endogenous Pdx1 promoter. Sufficient tTA was produced to activate the Pdx1 transgene to an effective level. By screening multiple lines bearing the tetracycline-responsive Pdx1 transgene, we were able to identify several that could restore fetal pancreatic development in the absence of a functional endogenous Pdx1 allele.. The rescue of pancreatic development by the ...
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Interacting selectively and non-covalently with a activating transcription factor and also with the basal transcription machinery in order to increase the frequency, rate or extent of transcription. Cofactors generally do not bind DNA, but rather mediate …