Ets-related protein Elk-1 is homologous to the c-fos regulatory factor p62TCF.

A key event in the response of cells to proliferative signals is the rapid, transient induction of the c-fos proto-oncogene, which is mediated through the serum response element (SRE) in the fos promoter. Genomic footprinting and transfection experiments suggest that this activation occurs through a ternary complex that includes the serum response factor (SRF) and the ternary complex factor p62. Interaction of p62TCF with the SRF-SRE binary complex requires a CAGGA tract immediately upstream of the SRE. Proteins of the ets proto-oncogene family bind to similar sequences and we have found that a member of this family, Elk-1, forms SRF-dependent ternary complexes with the SRE. Elk-1 and p62TCF have the same DNA sequence requirements and antibodies against Elk-1 block the binding of both proteins. Furthermore, we show that like p62TCF, Elk-1 forms complexes with the yeast SRF-homologue MCM1 but not with yeast ARG80. But ARG80 mutants that convey interaction with p62TCF can also form complexes with Elk-1. The similarity, or even identity, between Elk-1 and p62TCF suggests a novel regulatory role for Ets proteins that is effected through interaction with other proteins, such as SRF. Furthermore, the possible involvement of an Ets protein in the control of c-fos has interesting implications for proto-oncogene cooperation in cellular growth control.     

Characterization of dolochar wastes generated by the sponge iron industry

Solid wastes generated by the metallurgical industry contribute significantly towards the enhancement of environmental pollution. The handling, utilization, and safe disposal of these solid wastes are major concerns for the world. Dolochar is such a solid waste generated by the sponge iron industry. Investigations were carried out on the physical, mineralogical, and chemical characteristics for the efficient utilization of dolochar. The detailed studies on physico-chemical properties and petrography were carried out by optical microscopy, X-ray diffraction (XRD), and scanning electron microscopy (SEM). Characterization studies revealed that the dolochar consists of quartz (free as well as locked), free lime, Fe particles, and Ca or Mg and/or Ca+Mg+Fe oxide phases. The washability data of -300 μm dolochar samples indicated that clean coal with 41wt% ash at 18% yield can be produced from dolochar with 78wt% ash. The studies further suggested that the liberation of the dolochar is hard to achieve for clear separation. The dolochar is observed to have high ash fusion temperature and the unburned carbon can be best utilized for power generation.     

Rhodium-Catalyzed Asymmetric Reactions Using SelfAssembled Chiral Bidentate Ligands

We recently described a new combinatorial strategy for modular catalyst development, one using self-as-embly in the ligand scaffold-generating step to produce libraries of chiral self-assembled ligands. Metal-directed self-assembly of bifunetional subunits around a structural metal （typically zinc） can be used to form a heteroleptic complex in which a second set of ligating groups are suitably disposed to form a heterobimetallie cata- lyst system. See Fig. 1     

Nucleotide sequence of chicken c-myb complementary DNA and implications for myb oncogene activation

Avian myeloblastosis virus (AMV), like other acute transforming viruses, arose by recombination between its helper virus and host cellular sequences. The latter sequences, termed v-myb, are responsible for the oncogenic properties of the virus. AMV causes acute myeloblastic leukaemia in chickens and transforms a specific class of haematopoietic cells in vitro, but does not induce morphological transformation of cultured fibroblasts, suggesting that only a restricted target-cell population is responsive to its transforming gene product. The normal cellular counterpart of v-myb, c-myb, is highly conserved and is present in all vertebrate and some invertebrate species examined. DNA rearrangements and altered expression of the myb oncogene have been reported in mouse lymphoid tumours and human myeloid and colon tumours. The mechanism of activation of the cellular proto-oncogenes is thought to involve the structural alteration of the coding regions that result in either the synthesis of an altered gene product or the enhanced expression of a proto-oncogene caused by alterations in its regulatory elements. To distinguish between these two mechanisms, we have cloned and sequenced the chicken c-myb complementary DNA and compared it with that of v-myb sequences. We demonstrate that during the transduction of the cellular sequences and/or viral passage a substantial portion of the coding region of the c-myb gene has been lost from both the 5' and 3' ends, resulting in the generation of a truncated gene product that mediates the transforming function of the virus.     

Ethyl-α-p-chlorophenoxyisobutyrate induced hepatic microbody proliferation in rat liver and ubiquinone concentration

Zusammenfassung Verabreichung von körperfremdem Ubiquinon an Ratten verursacht keine vermehrte Aktivität der Leberkatalase, die mit derjenigen nach CPIB-Medikation vergleichbar wäre. Es wird angenommen, dass die hypocholemische Aktion von CPIB nicht von einer Steigerung der hepatischen Ubiquinon-Konzentration begleitet ist.     

X-ray study of the lithium complex of NAD.

The Li+-NAD+ complex exists as a 'dimer' of two molecules arranged head-to-tail with Li+ coordinated tetrahedrally to adenine N(7) and three pyrophosphate oxygens. Adenine is stacked intermolecularly on nicotinamide. The conformation of NAD+ is 'extended' and similar to that found in holoenzyme complexes. This is in contrast to the 'folded' structure proposed from spectroscopic studies.     

DNA helicase Srs2 disrupts the Rad51 presynaptic filament

Mutations in the Saccharomyces cerevisiae gene SRS2 result in the yeast's sensitivity to genotoxic agents, failure to recover or adapt from DNA damage checkpoint-mediated cell cycle arrest, slow growth, chromosome loss, and hyper-recombination. Furthermore, double mutant strains, with mutations in DNA helicase genes SRS2 and SGS1, show low viability that can be overcome by inactivating recombination, implying that untimely recombination is the cause of growth impairment. Here we clarify the role of SRS2 in recombination modulation by purifying its encoded product and examining its interactions with the Rad51 recombinase. Srs2 has a robust ATPase activity that is dependent on single-stranded DNA (ssDNA) and binds Rad51, but the addition of a catalytic quantity of Srs2 to Rad51-mediated recombination reactions causes severe inhibition of these reactions. We show that Srs2 acts by dislodging Rad51 from ssDNA. Thus, the attenuation of recombination efficiency by Srs2 stems primarily from its ability to dismantle the Rad51 presynaptic filament efficiently. Our findings have implications for the basis of Bloom's and Werner's syndromes, which are caused by mutations in DNA helicases and are characterized by increased frequencies of recombination and a predisposition to cancers and accelerated ageing.