Disease relevance of DBP

• Using transient transfection assays in HepG2 hepatoma cells, we demonstrated the ability of HLF alone and in synergistic combination with the D-box binding protein (DBP), another proline and acidic-rich (PAR) protein family member, to transactivate these promoters [1].
• We have previously implicated the PAR domain D-site-binding protein (DBP) as well as an upstream element, site 5, as playing important roles in the phenotypic recovery of hemophilia B Leyden [2].
• Cloning of a cDNA encoding a DNA-binding protein TAXREB302 that is specific for the tax-responsive enhancer of HTLV-I [3].
• Hypertension was defined by SBP or DBP above the 90(th) percentile for height, age, and sex [4].
• Cardiovascular measures (heart period, HP; preejection period, PEP; respiratory sinus arrhythmia, RSA; cardiac output, CO; systolic blood pressure, SBP; diastolic blood pressure, DBP & total peripheral resistance, TPR) were recorded during 4-minute baseline and 4-minute stressor task periods [5].

Psychiatry related information on DBP

• RESULTS: Systolic BP (SBP) was linearly related significantly to BMI and alcohol consumption, whereas diastolic BP (DBP) was related to age [6].
• The UV/TiO(2)/glass process yielded a 75% degradation efficiency of DBP with initial concentration of 5mgL(-1) at 80min reaction time [7].

High impact information on DBP

• Synergy between transcription factors DBP and C/EBP compensates for a haemophilia B Leyden factor IX mutation [8].
• Now we summarize the role of basic region/leucine zipper protein family members and particularly the albumin D site-binding protein (DBP) and the CAAT/enhancer-binding proteins (C/EBPs) for their importance in liver-specific gene expression and their role in liver function and development [9].
• Liver-enriched transcription factors in liver function and development. Part II: the C/EBPs and D site-binding protein in cell cycle control, carcinogenesis, circadian gene regulation, liver regeneration, apoptosis, and liver-specific gene regulation [9].
• Plasmodium vivax invasion of human erythrocytes requires that the ligand domain of the Duffy-binding protein (DBP) recognize its cognate erythrocyte receptor, making DBP a potential target for therapy [10].
• The deletion mutant still stimulates initiation of DNA replication like the intact DBP [11].

Chemical compound and disease context of DBP

• The liver-enriched transcription factor D-site-binding protein activates the promoter of the phosphoenolpyruvate carboxykinase gene in hepatoma cells [12].
• Phosphoserine but not phosphothreonine was also identified in acid hydrolysates of another preparation of 32P-DBP labeled for 30 min, chased for 20 h, and then immunoprecipitated by adenovirus type 1-simian virus 40 antiserum [13].
• After 50 weeks of therapy with delapril/manidipine 30mg/10mg once daily, mean SBP/DBP was reduced by 22/14mm Hg in patients with mild to moderate hypertension (n = 309) [14].
• Evidence is presented here which indicates that the adenovirus DNA-binding protein (DBP) is phosphorylated at a tyrosine residue early in infection [15].
• Phthalate esters with short alkyl chains, such as di-ethyl (DEP), di-n-propyl (DPP), and di-butyl phthalate (DBP), have adjuvant effects on an FITC-induced contact hypersensitivity mouse model [16].

Biological context of DBP

• A naturally occurring variant of DBP (tDBP), lacking the transactivation domain, has been identified and shown to impede the formation of active TEF dimers in a competitive manner and to reduce the TEF-dependent induction of bcl-gS [17].
• TEF and DBP control elements have never been investigated in the insulin-secreting cells, but impairment of the circadian rhythm of the beta-cells might be involved in the development of diabetic state as type 2 diabetics have lost daily temporal variations of insulin secretion [18].
• These data confirmed by molecular genetic analysis highlight the novel association between the C677T MTHFR genotype with the Gc2 polymorphism of the DBP [19].
• In vitro, TEF and DBP bind the same DNA sequences [20].
• In this study, the functional role of DBP and C/EBP (which have several potential binding sites on the IGFBP-1 proximal promoter) have been investigated [21].

Anatomical context of DBP

• We investigated the expression pattern of TEF and DBP in insulin-secreting cells [18].
• TEF and DBP transcripts are expressed at extremely high levels in human pancreatic islets compared to other tissues, suggesting a potentially important circadian regulation of these cells [18].
• Both transcription factors albumin site d-binding protein (DBP) and thyrotroph embryonic factor (TEF) are elements of the "cell-clock". Their circadian accumulation in suprachiasmatic nucleus (SCN) and peripheral tissues such as liver, kidney and lung is thought to participate in controlling circadian regulation of downstream genes [18].
• In hepatocytes in primary culture, the strong transactivator is C/EBP while DBP is essentially inactive [22].
• These results indicate that fusion of granules with the plasma membrane forms HM that contains DBP binding sites [23].

Associations of DBP with chemical compounds

• Finally, these studies reaffirm the potential role of dimeric transcription factor complexes in mediating interactions with specific promoter elements, which, in the case of the Factor VIII promoter, results in dramatically enhanced binding of HLF-DBP heterodimers to two cis-acting sequences [1].
• D-site binding protein transactivation requires the proline- and acid-rich domain and involves the coactivator p300 [24].
• Seated systolic BP (SBP) and diastolic BP (DBP) were measured using a standard mercury sphygmomanometer [4].
• Di-n-butyl phthalate (DBP) is one of the most dominant phthalate esters and is widely distributed environmental contaminant [25].
• Moreover, neutrophils treated with LPS bound more avidity to immobilized DBP than sham-treated cells [23].

Physical interactions of DBP

• We have previously demonstrated that the Adenovirus 2 DNA Binding Protein (DBP) binds to SrCap and inhibits the transcription mediated by the carboxyl-terminal region of SrCap (amino acids 1275-2971) [26].
• We have used a 5' regulatory sequence fragment of the human parathyroid hormone-related peptide (PTHrP) gene to identify nuclear DNA-binding proteins (DBP), using South-Western analysis [27].
• We previously reported the isolation and functional characterization of seven adenovirus type 5 (Ad5) DNA-binding protein (DBP) point mutants (Quinn, C. O., and Kitchingman, G. R. (1986) J. Virol. 60, 653-661) [28].

Regulatory relationships of DBP

• In addition, DBP also inhibits the ability of SrCap to enhance Protein Kinase A (PKA) activated transcription of the enkaphalin promoter [26].

Other interactions of DBP

• Enhanced binding of HLF/DBP heterodimers represents one mechanism of PAR protein transactivation of the factor VIII and factor IX genes [1].
• The D-site binding protein (DBP) is a member of the proline- and acid-rich (PAR) domain subfamily of basic/leucine zipper proteins and is involved in transcriptional regulation in the liver [24].
• Furthermore, the AGTR1 L191 allele showed a SBP lowering effect in subjects with a high socioeconomic status (SES;p = .048) and a DBP lowering effect in AAs (p = .038) [29].
• These studies suggest that HNF-1 and C/EBP alpha help establish ADH gene family transcription in fetal liver and that LAP and DBP help maintain high-level ADH gene family transcription in postnatal liver [30].
• In patients, DBP decreased slightly and MBP dropped during the first 2 minutes, then increased [31].

Analytical, diagnostic and therapeutic context of DBP

• The six common genetic types of the group specific component/vitamin D-binding protein (GC/DBP) system are usually classified by isoelectric focusing in carrier ampholytes, followed by visualization of the GC proteins by immunoprinting with monospecific antiserum [32].
• Mean middle cerebral artery blood flow velocity (CBFV) was recorded with transcranial Doppler sonography, while systolic (SBP), diastolic (DBP), and mean (MBP) blood pressure and heart rate were measured in the supine position and after passive tilting [31].
• In a microinjection system, plasmids containing the DBP gene associated with both its early (map coordinate 75) and late (coordinate 72) promoters, or only with the early promoter, are inefficiently expressed, and the presence of E1A DNA is required for full expression [33].
• The association of purified DBP with RNA in vitro was demonstrated by using either a gel filtration or a filter binding assay [34].
• To define sequences involved in nuclear transport of DBP, a series of point and small deletion mutants were constructed via oligonucleotide-directed mutagenesis [35].

References