Disease relevance of Usf1

• Elimination of an upstream Sp1 element reduced expression threefold, whereas elimination of an adenovirus upstream stimulatory factor element had little effect [1].
• Promoter sequences of varicella-zoster virus glycoprotein I targeted by cellular transactivating factors Sp1 and USF determine virulence in skin and T cells in SCIDhu mice in vivo [2].

High impact information on Usf1

• The B2 pol II promoters can be bound and stimulated by the transcription factor USF (for upstream stimulatory factor), as shown by transient transfection experiments [3].
• The major late transcription factor binds to and activates the mouse metallothionein I promoter [4].
• The results suggest that activation of Usf-1 by p38 at a wide variety of viral and cellular promoters will provide a link between stimuli as diverse as UV irradiation, glucose, viral infection and pro-inflammatory cytokines, and the changes in gene expression associated with the stress response [5].
• We reported that upstream stimulatory factor binding to the -65 E-box is required for induction of the FAS transcription by insulin in 3T3-L1 adipocytes [6].
• By using a formaldehyde crosslinking procedure and Gal4 fusion proteins, we have analyzed the timing and functional consequences of binding of Myc and upstream stimulatory factor (USF)1 to endogenous cellular genes [7].

Biological context of Usf1

• Upstream stimulatory factor (USF) is a basic helix-loop-helix-leucine zipper transcription factor that plays an important role in transcriptional activation and cell proliferation [8].
• More subtle changes also occurred in the constitutive genomic footprint at the composite major late transcription factor/antioxidant response element [9].
• In vitro protein-DNA binding assays and in vivo transient transfection assays indicated that members of both the upstream stimulatory factor and Sp families of transcription factors bound to and trans-activated the DOR promoter via the E box and GC box, respectively [10].
• Cotransfection of the upstream stimulatory factor and various FAS promoter-luciferase constructs as well as in vitro binding studies suggest a function for the upstream stimulatory factor at both the -65 and -332 E-box sequences [11].
• The roles of the bHLH-Zip protein, upstream stimulatory factor (USF), in mouse metallothionein-I (MT-I) gene expression were examined [12].

Anatomical context of Usf1

• The transcription factors MTF-1 and USF1 cooperate to regulate mouse metallothionein-I expression in response to the essential metal zinc in visceral endoderm cells during early development [13].
• Transcriptional regulation of mouse delta-opioid receptor gene. Ikaros-2 and upstream stimulatory factor synergize in trans-activating mouse delta-opioid receptor gene in T cells [14].
• Osteopontin transcription in aortic vascular smooth muscle cells is controlled by glucose-regulated upstream stimulatory factor and activator protein-1 activities [15].
• It is not until the levels of BSAP decrease during the antigen-driven stages of B cell development that both USF and B-MEF2 are able to bind to their respective promoter elements and activate J chain transcription [16].
• Finally, an USF-1 binding site that was necessary for activation of FiRE in keratinocytes was not needed in fibroblasts [17].

Associations of Usf1 with chemical compounds

• Similarly, dexamethasone treatment does not affect the upstream stimulatory factor activity of P1798 cells [18].
• The basic region/helix-loop-helix/leucine repeat transcription factor USF interferes with Ras transformation [19].
• Recognition of the E-C4 element from the C4 complement gene promoter by the upstream stimulatory factor-1 transcription factor [20].
• An indirect role for upstream stimulatory factor in glucose-mediated induction of pyruvate kinase and S14 gene expression [21].
• Synergistic role of specificity proteins and upstream stimulatory factor 1 in transactivation of the mouse carboxylesterase 2/microsomal acylcarnitine hydrolase gene promoter [22].

Physical interactions of Usf1

• Upstream stimulatory factor binding to the E-box at -65 is required for insulin regulation of the fatty acid synthase promoter [23].
• An oligonucleotide spanning the rat PGS-2 E-box bound two specific protein complexes which were supershifted in the presence of antibody specific for the upstream stimulatory factor [24].
• These results demonstrated that USF binding to the E-box at -893/-888 serves to trans-repress basal expression and IL-1beta induction of the iNOS promoter [25].

Regulatory relationships of Usf1

• Furthermore, we have demonstrated that Ik-2 and upstream stimulatory factor synergize in trans-activating the dor promoter via the putative Ik-binding site and the E box, respectively [14].

Other interactions of Usf1

• Mxi1, Usf1, and Usf2 have been mapped previously by in situ hybridization, but their positions on the meiotic linkage map had not been determined [26].
• Insulin regulation of fatty acid synthase gene transcription: roles of USF and SREBP-1c [27].
• Regulation of the murine Ddelta2 promoter by upstream stimulatory factor 1, Runx1, and c-Myb [28].
• Of these, upstream stimulatory factor 1, Runx1, and c-Myb appear necessary for full promoter activity in transiently transfected cells [28].
• Domains of USF2 encoded by exon 4, exon 5 and the USF-specific region are important for maximum activation of the Cox5b Inr [8].

Analytical, diagnostic and therapeutic context of Usf1

• Gel mobility shift assays showed that only USF-1 and USF-2 supershifted the USF protein-DNA complexes [25].
• We also show that a functional relationship exists between USF and a second J chain positive-regulating factor, B-MEF2, using co-immunoprecipitation assays and transfections [16].
• More interestingly, during liver regeneration after partial hepatectomy, a process which activates the HGF gene, we noted that the binding activity of USF to the HGF promoter element increased while that of NF1 decreased [29].

References