Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The myeloid zinc finger gene 1, MZF1, encodes a transcription factor which is expressed in hematopoietic progenitor cells that are committed to myeloid lineage differentiation. MZF1 contains 13 C2H2 zinc fingers arranged in two domains which are separated by a short glycine- and proline-rich sequence. The first domain consists of zinc fingers 1 to 4, and the second domain is formed by zinc fingers 5 to 13. We have determined that both sets of zinc finger domains bind DNA. Purified, recombinant MZF1 proteins containing either the first set of zinc fingers or the second set were prepared and used to affinity select DNA sequences from a library of degenerate oligonucleotides by using successive rounds of gel shift followed by PCR amplification. Surprisingly, both DNA-binding domains of MZF1 selected similar DNA-binding consensus sequences containing a core of four or five guanine residues, reminiscent of an NF-kappa B half-site: 1-4, 5'-AGTGGGGA-3'; 5-13, 5'-CGGGnGAGGGGGAA-3'. The full-length MZF1 protein containing both sets of zinc finger DNA-binding domains recognizes synthetic oligonucleotides containing either the 1-4 or 5-13 consensus binding sites in gel shift assays. Thus, we have identified the core DNA consensus binding sites for each of the two DNA-binding domains of a myeloid-specific zinc finger transcription factor. Identification of these DNA-binding sites will allow us to identify target genes regulated by MZF1 and to assess the role of MZF1 as a transcriptional regulator of hematopoiesis.
Mol Cell Biol 1994 Mar
PMID:Characterization of the DNA-binding properties of the myeloid zinc finger protein MZF1: two independent DNA-binding domains recognize two DNA consensus sequences with a common G-rich core. 811 11

Phylogenetic trees were derived for the Alphaherpesvirinae subfamily of the Herpesviridae using molecular sequences. Sequences from the families of genes encoding glycoprotein B, thymidine kinase, S region protein kinase, immediate-early transcriptional regulator IE175 and ribonucleotide reductase large subunit were examined by means of both maximum parsimony and distance methods, and for both protein and DNA alignments. Trees obtained were evaluated by bootstrap analysis. A clear consensus tree was obtained, with most detail coming from 14 sequences in the glycoprotein B gene set. The tree showed two avian viruses branching first from the lineage leading to the mammalian alphaherpesviruses. The mammalian viruses were split into two groups, which corresponded to the Simplexvirus and Varicellovirus genera. A timescale for events in alphaherpesvirus evolution was tested, based on the proposition that most of the lineages arose by ancient cospeciation with hosts. The virus phylogenetic tree was unambiguously compatible with cospeciation for ten of the 12 mammalian viruses. The tree was also supported by demonstration of an approximate proportionality between magnitudes of pairwise divergences of viral sequences and times since lineages of corresponding pairs of hosts split. On the basis of this timescale it was estimated that the two mammalian alphaherpesvirus groups diverged around the period of the mammalian radiation, and that alphaherpesviral genome sequences have evolved faster than those of mammals by a factor of one to two orders of magnitude.
J Mol Biol 1994 Apr 22
PMID:Molecular phylogeny of the alphaherpesvirinae subfamily and a proposed evolutionary timescale. 814 60

The wilt-inducing phytopathogen Pseudomonas solanacearum produces several extracellular virulence factors, both polysaccharides (EPS I) and proteins (EXPs), which are independently regulated by a LysR-type transcriptional regulator, PhcA, and a histidine kinase sensor, VsrB. Here we characterize a third locus, vsrA, which is also required for normal production of EPS I, some EXPs and wilt disease. Analysis of eps::lacZ reporters in vsrA mutants showed that, like vsrB and phcA, vsrA is required for maximal expression (transcription) of eps, which contains some of the genes necessary for production of EPS I. Unlike vsrB and phcA mutants, however, eps transcription (and EPS I production) by vsrA mutants varies from 3 to 17% of wild-type levels, depending on growth conditions. Inactivation of vsrA also causes a dramatic reduction in production of three species of EXPs (28 kDa, 48 kDa, and 66 kDa), and an apparent increase in production of a few other EXPs. Unlike most other EPS-deficient P. solanacearum strains, vsrA mutants caused almost no disease symptoms when 10(4) cells were stem-inoculated into tomato plants. This correlated with a greater than 10-fold reduction in their ability to grow in planta. vsrA was cloned from a P. solanacearum genomic library by complementation of the vsrA mutant and was further subcloned on a 2.3 kb DNA fragment. PhoA fusion analysis and subcellular localization of the vsrA gene product in Escherichia coli maxicells suggest that it is a 53 kDa membrane-associated protein. Analysis of the nucleotide sequence of vsrA revealed a 502 residue open reading frame with homology to the histidine kinase domain of sensors in the two-component regulator family. This discovery shows that EPS I production by P. solanacearum is simultaneously controlled by dual two-component sensors.
Mol Microbiol 1994 Feb
PMID:VsrA, a second two-component sensor regulating virulence genes of Pseudomonas solanacearum. 815 73

The FHL1 gene was isolated by screening for high-copy-number suppressors of conditional RNA polymerase III mutations. This gene is unique on the yeast genome and was located close to RPC40 and PRE2 on the right arm of chromosome XVI. It codes for a 936-amino-acid protein containing a domain similar to the fork head DNA-binding domain, initially found in the developmental fork head protein of Drosophila melanogaster and in the HNF-3 family of hepatocyte mammalian transcription factors. Null mutations caused a severe reduction in growth rate and a lower rRNA content that resulted from defective rRNA processing. There was no detectable effect on mRNA splicing. Thus, the Fhl1p protein plays a key role in the control of rRNA processing, presumably by acting as a transcriptional regulator of genes specifically involved in that process. Moreover, mutants carrying the RNA polymerase III mutations were slightly defective in rRNA processing. This accounts for the isolation of FHL1 as a dosage-dependent suppressor and suggests that rRNA processing depends on a still-unidentified RNA polymerase III transcript.
Mol Cell Biol 1994 May
PMID:Suppression of yeast RNA polymerase III mutations by FHL1, a gene coding for a fork head protein involved in rRNA processing. 816 51

Secretion of the antidiuretic hormone (ADH) vasopressin is increased when body fluid homeostasis is disturbed by dehydration. Associated with this increased secretion is an elevation of vasopressin mRNA in magnocellular hypothalamic neurons projecting to the posterior pituitary. The proto-oncogene c-fos codes for a nuclear phospho-protein Fos which binds to specific DNA elements and acts as a transcriptional regulator coupling short-term extracellular stimuli to long-term responses by altering secondary target gene expression. This study in rats examined the time courses of dehydration induced c-fos expression and the change of vasopressin gene expression in the magnocellular neurons of the hypothalamus. Immunocytochemical and in situ hybridization study demonstrated that c-fos was induced by acute intracellular dehydration in the hypothalamic magnocellular nuclei of paraventricular (PVN), supraoptic (SON), and accessory groups such as nucleus circularis. Double-label immunocytochemical study co-localized Fos and vasopressin-neurophysin immunoreactivity in the same magnocellular neurons in the SON and PVN. In situ hybridization analysis after acute dehydration revealed a rapid and transient c-fos induction followed by a persistent increase in vasopressin mRNA for up to 2 days even after rehydration. Furthermore, prevention of c-fos translation by pretreatment with protein synthesis inhibitor cycloheximide attenuated this dehydration induced increase in vasopressin mRNA. This study demonstrated that an increase in vasopressin transcription after acute dehydration is dependent on an early phase of protein synthesis.
Brain Res Mol Brain Res 1994 Feb
PMID:Proto-oncogene c-fos and the regulation of vasopressin gene expression during dehydration. 817 Mar 49

The chromosomal ampC beta-lactamase in Citrobacter freundii and Enterobacter cloacae is inducible by beta-lactam antibiotics. When an inducible ampC gene is introduced on a plasmid into Escherichia coli together with its transcriptional regulator ampR, the plasmid-borne beta-lactamase is still inducible. We have isolated mutants, containing alterations in a novel E. coli gene, ampG, in which a cloned C. freundii ampC gene is unable to respond to beta-lactam inducers. The ampG gene was cloned, sequenced and mapped to minute 9.6 on the E. coli chromosome. The deduced amino acid sequence predicted AmpG to be a 53 kDa, transmembrane protein, which we propose acts as a signal transducer or permease in the beta-lactamase induction system. Immediately upstream of ampG there is another 579-base-pair-long open reading frame (ORF) encoding a putative lipoprotein shown to be non-essential for beta-lactamase induction. We have found that ampG and this ORF form an operon, whose promoter is located in front of the ORF. Located closely upstream of the putative promoter is the morphogene bolA, which is transcribed in the opposite orientation. However, using transcription fusions, we have found that the ampG transcription is not regulated by bolA. In addition, we show that transcription is probably not regulated by either the starvation specific sigma factor RpoS, which controls bolA, or by AmpD the negative regulator for ampC transcription.
Mol Microbiol 1993 Aug
PMID:AmpG, a signal transducer in chromosomal beta-lactamase induction. 823 4

The SUD1 gene was identified during a hunt for mutants that are able to express an sta1 gene (encoding an extracellular glucoamylase) lacking an upstream activation sequence (UAS) for transcription. A null allele of sud1 alleviated the transcriptional defect of the UAS-less sta1 and also suppressed mutations in trans-acting genes (GAM1/SNF2 and GAM3/ADR6) required for transcription of STA1. The mutation also increased expression from various core promoters (CYC1, CUP1, HIS3, PUT1, and PUT2), suggesting that the SUD1 protein is a global transcriptional regulator that plays a negative role at or near the TATA element. However, the SUD1 function was ineffective on promoters containing a UAS from either STA1 or GAL10 under derepressed conditions. The sud1 mutation suppressed the salt-sensitive cell growth phenotype caused by elevated levels of the TATA-binding protein (SPT15), further suggesting a transcriptional role for SUD1. sud1 cells showed additional pleiotropic phenotypes: temperature-sensitive (ts) growth, reduced efficiencies of sporulation, and sensitivity to heat shock and nitrogen starvation. The SUD1 gene is predicted to encode a 64 kDa, hydrophilic protein.
Mol Gen Genet 1993 Dec
PMID:Isolation and characterization of the SUD1 gene, which encodes a global repressor of core promoter activity in Saccharomyces cerevisiae. 826 36

The flagellar genes of the bacterium Caulobacter crescentus are organized into a regulatory hierarchy that consists of four classes or levels of genes, and expression of these genes is restricted to a discrete interval in the cell cycle that begins just prior to flagellum assembly. This paper summarizes data on the promoters and other cis-acting elements that are required for transcription of the level II gene fliF and the level III genes flaN and flbG. Regulated expression of flaN and flbG requires sigma 54 promoters, enhancer-like sequences called ftr, and sequences called ihf that conform to the consensus binding sequence for Escherichia coli integration host factor protein. The fliF regulatory region contains a new type of promoter sequence that is different from other known promoter motifs, and it has a sequence called ftr4 that is a site of negative regulation. ftr4 appears to function as part of a developmental switch that turns fliF transcription off at the correct time in the cell cycle. flbD, the last gene in the fliF operon is a negative regulator of fliF and an activator of both flaN and flbG expression. Evidence that FlbD protein plays a direct role as a transcriptional regulator comes from the finding that it has a DNA binding activity within its carboxy terminus that specifically recognizes ftr4 in fliF and four ftr elements in the flaN-flbG promoter region.
Cell Mol Biol Res 1993
PMID:Cis- and trans-acting elements required for regulation of flagellar gene transcription in the bacterium Caulobacter crescentus. 831 72

The Aspergillus nidulans brlA gene encodes a transcriptional regulator of central importance in controlling conidiophore development. I have determined the effects of mutations in other developmental regulatory genes on expression of a brlA-lacZ fusion gene. Deletion of brlA reduced beta-galactosidase levels by half and led to delocalization of enzyme accumulation. The medA26 and abaA2 developmental mutations led to overexpression of the fusion gene without altering spatial specificity. In contrast, the stuA1 mutation did not affect the timing or levels of brlA expression during induction, but instead resulted in spatial derangement of expression. These results and the phenotypes of the mutants suggest a model in which subsets of morphogenetic loci are controlled by differing levels and combinations of regulatory gene products, which are themselves determined by interactions among the regulatory genes.
Mol Microbiol 1993 Apr
PMID:Spatial and temporal controls of the Aspergillus brlA developmental regulatory gene. 831 75

Various Sarcophaga peregrina (flesh fly) defense protein genes were shown to be activated when NIH-Sape-4 cells were cultured with bacterial lipopolysaccharides or beta-1,3-glucan. The 5' upstream regions of the defense protein genes were found to have common motifs showing similarity to the mammalian NF-kappa B-binding consensus sequence. A protein with affinity to the NF-kappa B-binding motif of the Sarcophaga lectin promoter was identified and purified to near homogeneity. This 59-kDa protein also bound to the NF-kappa B-binding motifs of other defense protein genes, e.g., sarcotoxin I and sarcotoxin II genes. This protein was found in both the cytoplasmic and the nuclear fractions of the cells, and it appeared to migrate from the cytoplasm to the nucleus on treatment of the cells with lipopolysaccharides. This 59-kDa protein is probably a transcriptional regulator of the genes for defense proteins of S. peregrina.
Mol Cell Biol 1993 Jul
PMID:Purification and characterization of a 59-kilodalton protein that specifically binds to NF-kappa B-binding motifs of the defense protein genes of Sarcophaga peregrina (the flesh fly). 832 Dec 12


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>