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981.
Many daily biological rhythms are governed by an innate timekeeping mechanism or clock. Endogenous, temperature-compensated circadian clocks have been localized to discrete sites within the nervous systems of a number of organisms. In mammals, the master circadian pacemaker is the bilaterally paired suprachiasmatic nucleus (SCN) in the anterior hypothalamus. The SCN is composed of multiple single cell oscillators that must synchronize to each other and the environmental light schedule. Other tissues, including those outside the nervous system, have also been shown to express autonomous circadian periodicities. This review examines 1) how intracellular regulatory molecules function in the oscillatory mechanism and in its entrainment to environmental cycles; 2) how individual SCN cells interact to create an integrated tissue pacemaker with coherent metabolic, electrical, and secretory rhythms; and 3) how such clock outputs are converted into temporal programs for the whole organism. 相似文献
982.
983.
Isabelle Nilsson Hans Jürg Monstein Erik Lindstr?m Rolf H?kanson Samuel Svensson 《Regulatory peptides》2002,103(1):29-37
A series of CCK(2) receptor ligands were analysed with respect to their interaction with binding sites in the membranes of COS-7 cells and SK-N-MC cells transiently expressing the human CCK(2) receptor (short isoform). The ligands were YF476, YM022, AG041R, L-740,093, JB93182, PD134308, and PD136450. Their binding was analysed by radioligand competition using [3H]L-365,260 as the labelled ligand. Saturation binding analysis indicated that [3H]L-365,260 interacted with a single class of binding sites. In competition binding experiments using COS-7-cell membranes, all seven ligands were incubated together with 2 nM [3H]L-365,260. The data for four of the compounds fitted a one-site model (pK(i) values: YM022: 9.2+/-0.02; YF476: 9.6+/-0.04; L-740,093: 9.2+/-0.01; and AG041R: 8.3+/-0.06), while the data for the three others fitted a two-site model (pK(i) values: JB93182: 8.8+/-0.04 and 6.0+/-0.15; PD134308: 9.0+/-0.04 and 6.1+/-0.15; and PD136450: 9.0+/-0.02 and 5.4+/-0.41). SK-N-MC cell membranes and 2 nM [3H]L-365,260 were incubated together with YM022, YF476, JB93182, and PD134308. The data for YM022 and YF476 fitted a one-site model (pK(i) values: YM022: 9.3+/-0.06; YF476: 9.4+/-0.02), while the data for JB93182 and PD134308 fitted a two-site model (pK(i) values: JB93182: 8.7+/-0.06 and 6.2+/-0.06; PD134308: 9.1+/-0.06 and 7.0+/-0.17). Competition binding experiments in the presence of the GTP-analogue guanylylimidodiphosphate, using either of the two cell types, produced similar binding data for PD134308 and JB93182 as in the absence of GTP-analogue. The human receptor seems to exist in a low and/or high affinity state. The shift from low to high affinity does not seem to reflect the degree of G protein coupling. 相似文献
984.
The NBS-LRR (nucleotide-binding site plus leucine-rich repeat) genes represent the major class of disease resistance genes in flowering plants and comprise 166 genes in the ecotype Col-0 of Arabidopsis thaliana. NBS-LRR genes are organized in single-gene loci, clusters, and superclusters. Phylogenetic analysis reveals nine monophyletic clades and a few phylogenetic orphans. Most clusters contain only genes from the same phylogenetic lineage, reflecting their origin from the exchange of sequence blocks as a result of intralocus recombination. Multiple duplications increased the number of NBS-LRR genes in the progenitors of Arabidopsis, suggesting that the present complexity in Col-0 may derive from as few as 17 progenitors. The combination of physical and phylogenetic analyses of the NBS-LRR genes makes it possible to detect relatively recent gene rearrangements, which increased the number of NBS-LRR genes by about 50, but which are almost never associated with large segmental duplications. The identification of 10 heterogeneous clusters containing members from different clades demonstrates that sequence sampling between different resistance gene loci and clades has occurred. Such events may have taken place early during flowering plant evolution, but they generated modules that have been duplicated and remobilized also more recently. 相似文献
985.
Elisabetta Giuffra Anna Törnsten Stefan Marklund Erik Bongcam-Rudloff Patrick Chardon James M.H. Kijas Susan I. Anderson Alan L. Archibald Leif Andersson 《Mammalian genome》2002,13(10):569-577
The Dominant White (I/KIT) locus is one of the major coat color loci in the pig. Previous studies showed that the Dominant
White (I) and Patch (IP) alleles are both associated with a duplication including the entire KIT coding sequence. We have
now constructed a BAC contig spanning the three closely linked tyrosine kinase receptor genes PDGFRA–KIT–KDR. The size of
the duplication was estimated at about 450 kb and includes KIT, but not PDGFRA and KDR. Sequence analysis revealed that the
duplication arose by unequal homologous recombination between two LINE elements flanking KIT. The same unique duplication
breakpoint was identified in animals carrying the I and IP alleles across breeds, implying that Dominant White and Patch alleles
are descendants of a single duplication event. An unexpected finding was that Piétrain pigs carry the KIT duplication, since
this breed was previously assumed to be wild type at this locus. Comparative sequence analysis indicated that the distinct
phenotypic effect of the duplication occurs because the duplicated copy lacks some regulatory elements located more than 150
kb upstream of KIT exon 1 and necessary for normal KIT expression. 相似文献
986.
Subha R Das Stewart W Schneller Jan Balzarini Erik De Clercq 《Bioorganic & medicinal chemistry》2002,10(2):457-460
5'-Noraristeromycin and its enantiomer have been found to possess a wide range of antiviral effects. In the search for analogues of and with improved activity, the synthesis of both enantiomers of 5'-mercapto-5'-deoxy-5'-noraristeromycin ( and ) has been accomplished. While (+)-7 was inactive, (-)- did show marginal activity against vaccinia virus, but not any other virus. 相似文献
987.
988.
Ami Klein Sharon Ramcharitar Nevena Christeff Erik Nisbett-Brown Emmanuel Nunez Aaron Malkin 《In vitro cellular & developmental biology. Animal》1991,27(4):307-311
Summary These authors attempted to test the effect of anticoagulants on lymphocytes viability by reproducing the procedure used for
lymphocyte isolation for various immunologic tests in which blood specimens are allowed to stay at room temperature for 2
h before lymphocytes are isolated. Blood was obtained with three different anticoagulants i.e. heparin, citrate, and CPDA
(citrate, phosphate, dextrose, and adenine). Plasma was lyophilized and extracted with ethanol. Dried ethanol extracts were
suspended in medium (RPMI 1640+10% fetal bovine serum) and incubated with a lymphocyte cell line (MOLT-4). After 24 h of incubation
the viability of cells was examined. The following death rates of the cells were observed: heparin −63±4.6% (mean±SEM), citrate
−27±6.7%, and CPDA 6.2±0.6% (P<0.0005). A significant correlation was found between these results and changes in the concentrations of free fatty acids
in the extracts. These results emphasize the importance of choosing the right anticoagulant when the viability of lymphocytes
is obligatory. 相似文献
989.
990.
Christopher A. Reed Christopher N. Mayhew A. Kathleen McClendon Erik S. Knudsen 《The Journal of biological chemistry》2010,285(2):1089-1096
The retinoblastoma (RB) tumor suppressor pathway is disrupted at high frequency in hepatocellular carcinoma. However, the mechanisms through which RB modulates physiological responses in the liver remain poorly defined. Despite the well established role of RB in cell cycle control, the deletion of RB had no impact on the kinetics of cell cycle entry or the restoration of quiescence during the course of liver regeneration. Although these findings indicated compensatory effects from the RB-related proteins p107 and p130, even the dual deletion of RB with p107 or p130 failed to deregulate hepatic proliferation. Furthermore, although these findings suggested a modest role for the RB-pathway in the context of proliferative control, RB loss had striking effects on response to the genotoxic hepatocarcinogen diethylnitrosamine. With diethylnitrosamine, RB deletion resulted in inappropriate cell cycle entry that facilitated secondary genetic damage and further uncoupling of DNA replication with mitotic entry. Analysis of the mechanism underlying the differential impact of RB status on liver biology revealed that, while liver regeneration is associated with the conventional induction of cyclin D1 expression, the RB-dependent cell cycle entry, occurring with diethylnitrosamine treatment, was independent of cyclin D1 levels and associated with the specific induction of E2F1. Combined, these studies demonstrate that RB loss has disparate effects on the response to unique tumorigenic stresses, which is reflective of distinct mechanisms of cell cycle entry. 相似文献