Disease relevance of ZNF143

• DNA binding domains of ZNF143 and ZNF76 produced in E. coli recognized CAE1 and CAE2 elements in electrophoretic mobility shift assay [1].
• METHODS: The Strategies of Treatment of Atrial Fibrillation (STAF) multicenter pilot trial randomized 200 patients (100 per group) with persistent AF to rhythm- or rate-control [2].
• Cutaneous and subcutaneous blood flow (CBF, SBF) were studied in non-lesional psoriatic skin (NLS) of 10 patients with only minimal psoriatic skin manifestations, using the local 133Xe washout method [3].
• By comparing the weight loss during corrosion in tris with that in the calcium and phosphate containing SBF, it is possible to establish whether the glass can induce apatite formation at its surface or not [4].
• The toxicity of SBF 8-MOP was then determined with and without UV-A irradiation in the diploid strain D7 of the yeast Saccharomyces cerevisiae which is suitable for the detection of lethal, mutagenic and recombinogenic events [5].

Psychiatry related information on ZNF143

• The sensitivity of SBF to T(re) was higher (P<0.05) for sleep deprivation than for normal sleep [6].
• Smokers in the EBF and QSC conditions showed reductions in depressive symptoms by 2 months, but smokers in the SBF condition did not [7].
• Smokers were randomized to one of three smoking-cessation interventions: minimal contact quit-smoking counseling (QSC), QSC + exposure biomarker feedback (EBF), and QSC + EBF + biomarker feedback about genetic susceptibility to lung cancer (SBF) [8].

High impact information on ZNF143

• It enabled us to identify 23 other snRNA and snRNA-type genes carrying potential Staf binding sites [9].
• Using recombinant Staf, we established that it mediates the activating properties of Staf-responsive elements on RNA polymerase II and III snRNA promoters in vivo [9].
• Lastly a 19 bp consensus sequence for the Staf binding site, YY(A/T)CCC(A/G)N(A/C)AT(G/C)C(A/C)YY-RCR, was derived by binding site selection [9].
• Seven highly conserved regions were detected between Staf and human ZNF76, a protein of unknown function, thereby aiding in predicting the locations of the functional domains of Staf [10].
• The 600 amino acid Staf protein contains seven zinc fingers and a separate acidic activation domain [10].

Chemical compound and disease context of ZNF143

• Clinical Trials Update: CAPRICORN, COPERNICUS, MIRACLE, STAF, RITZ-2, RECOVER and RENAISSANCE and cachexia and cholesterol in heart failure. Highlights of the Scientific Sessions of the American College of Cardiology, 2001 [11].
• Four hundred and twenty-seven smokers were randomized to 1 of 3 treatments: (a) QSC, (b) QSC + exposure biomarker feedback (EBF) about carbon monoxide in exhaled breath, or (b) QSC + EBF + biomarker feedback about genetic susceptibility to lung cancer (SBF) [7].
• It is concluded that acute ANG II blockade has no influence on the vascular resistance in the human forearm, but increases basal SBF in sodium depleted subjects and 'paralyses' the vasoconstrictor response to LBNP [12].

Biological context of ZNF143

• Thus, ZNF143 plays a key role in basal and tissue-specific expression of transaldolase and regulation of the metabolic network controlling cell survival and differentiation [13].
• Also, polypeptide sequences containing the seven zinc fingers of ZNF76 and ZNF143 could efficiently repress in vivo the activated transcription from an snRNA-type promoter [14].
• Transfection experiments in Drosophila cells showed that ZNF76 and ZNF143 can activate transcription from an mRNA promoter through the Staf binding site [14].
• ZNF143 activates gene expression in response to DNA damage and binds to cisplatin-modified DNA [15].
• Here we have used a combined in silico and biochemical approach to identify 1175 conserved hStaf/ZNF143-binding sites (SBS) distributed in 938 promoters of four mammalian genomes [16].

Anatomical context of ZNF143

• ZNF143 and transaldolase expression correlated in 21 different human tissues and were coordinately upregulated 14- and 34-fold, respectively, in lactating mammary glands compared with nonlactating ones [13].
• When the Sp binding site of the minimal promoter construct was mutated, promoter activity was completely abolished in both cell lines, whereas mutation of the common binding site of ZNF76 and ZNF143 resulted in a decrease of 53% in TGW-nu-I and 37% in HeLa cells [17].
• With the use of a novel expression assay in X.laevis oocytes we succeeded in demonstrating that Staf can activate the RNA polymerase III promoter of the tRNA(Sec) gene [10].
• The above films immersed in simulated body fluid solution (1.5 x SBF) for more than 5 days led to the nucleation of apatitic calcium phosphate phase all over the film surface [18].
• We compared the ability of a leukocyte depletion filter (RC-400; LDF) to a standard red blood cell filter (SBF) to remove tumor cells derived from urologic malignancies [19].

Associations of ZNF143 with chemical compounds

• ZNF143 is an inducible gene by other DNA damaging agents such as gamma-irradiation, etoposide and adriamycin [15].
• However, ZNF 143 expression is not induced by transplatin, which is clinically ineffective [15].
• New fluorescent Na+ indicators, SBFI (short for sodium-binding benzofuran isophthalate) and SBFP (short for sodium-binding benzofuran phthalate) (Minta, A., and Tsien, R [20].
• When pre-treated titanium is exposed to SBF, the alkali ions are released from the surface into the surrounding fluid [21].
• When immersed in 1.0 SBF, a carbonated hydroxyapatite was induced on the surfaces of the films oxidized at higher voltages (>450 V) after 28 days, which is closely related to the Ca- and P-containing phases [22].

Regulatory relationships of ZNF143

• ZNF 143 expression is induced by cisplatin but ZNF 76 expression is not [15].

Other interactions of ZNF143

• Chromatin immunoprecipitation studies confirm that ZNF143/73 associates with the transaldolase promoter in vivo [13].
• Taken together, these findings demonstrate that ZNF76 and ZNF143 are two members of a same family of transactivator proteins [14].
• Functional analysis of the MRP S11 promoter showed that a Staf binding site in the promoter is required for both basal promoter activity and cisplatin-inducible activity [15].
• Two of these-YB-1 and ZNF143-lack the high-mobility group (HMG) domain and can bind preferentially to cisplatin-modified DNA in addition to HMG domain proteins or DNA repair proteins, indicating that these transcription factors may also participate in DNA repair [23].
• Furthermore, we demonstrated that the presence of the SBS alone is sufficient to direct expression of a luciferase reporter gene, suggesting that hStaf/ZNF143 can recruit per se the transcription machinery [16].

Analytical, diagnostic and therapeutic context of ZNF143

• Northern blot analysis revealed that ZNF76 and ZNF143 mRNAs were expressed in all normal adult tissues examined [14].
• The relative changes in SBF from day to night at the postoperative examination did not differ from that of the control group, i.e., the normal 24-hour blood flow pattern had been obtained [24].
• CONCLUSIONS: The STAF pilot study showed no differences between the two treatment strategies in all end points except hospitalizations [2].
• In all subjects, foot skin blood flow was assessed by laser Doppler flowmetry in the horizontal (HBF) and sitting (SBF) positions [25].
• Intragroup differences between SBF and HBF were significant before and after angioplasty (P < .001) [25].

References