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41.
Christine A. Howell Julian K. Wood Mark D. Dettling Kenneth Griggs Codie C. Otte Linette Lina Thomas Gardali 《西北部美国博物学家》2011,70(1)
The Least Bell’s Vireo ( Vireo bellii pusillus ) was listed as state endangered in 1980 and federally endangered in 1986 in response to a sharp population decline and range reduction. This vireo commonly bred in riparian forests throughout the Central Valley of California, but prior to 2005, no nesting pairs had been confirmed in the region in over 50 years. On 29 June 2005, a Least Bell’s Vireo nest was located in a 3-year-old riparian restoration site at the San Joaquin River National Wildlife Refuge in Stanislaus County, California. In 2006, a Least Bell’s Vireo pair returned to the refuge to successfully breed, followed by an unsuccessful attempt in 2007 by an unpaired female. These records are approximately 350 km from the nearest known breeding population and appear to be part of a growing number of sightings outside of the species’ current southern California breeding range. These nesting attempts lend credence to the idea that extirpated species can recolonize restored habitat by long-distance dispersal. 相似文献
42.
M P Ollier M A Auger-Buendia L Hartmann 《Comptes rendus des séances de l'Académie des sciences. Série D, Sciences naturelles》1979,289(2):189-192
An original immunological two-dimensional technique with two different gels permits the protein analysis of 80 S cytoplasmic ribosomal murine particles and of their 60 S and 40 S subunits. The diagrams isolate and characterize a definite number of specific polypeptidic structures from each ribosomal particle. 相似文献
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44.
Epimutation of the telomeric imprinting center region on chromosome 11p15 in Silver-Russell syndrome
Gicquel C Rossignol S Cabrol S Houang M Steunou V Barbu V Danton F Thibaud N Le Merrer M Burglen L Bertrand AM Netchine I Le Bouc Y 《Nature genetics》2005,37(9):1003-1007
Silver-Russell syndrome (SRS, OMIM 180860) is a congenital disorder characterized by severe intrauterine and postnatal growth retardation, dysmorphic facial features and body asymmetry. SRS is genetically heterogenous with maternal uniparental disomy with respect to chromosome 7 occurring in approximately 10% of affected individuals. Given the crucial role of the 11p15 imprinted region in the control of fetal growth, we hypothesized that dysregulation of genes at 11p15 might be involved in syndromic intrauterine growth retardation. We identified an epimutation (demethylation) in the telomeric imprinting center region ICR1 of the 11p15 region in several individuals with clinically typical SRS. This epigenetic defect is associated with, and probably responsible for, relaxation of imprinting and biallelic expression of H19 and downregulation of IGF2. These findings provide new insight into the pathogenesis of SRS and strongly suggest that the 11p15 imprinted region, in addition to those of 7p11.2-p13 and 7q31-qter, is involved in SRS. 相似文献
45.
46.
Hillier LW Graves TA Fulton RS Fulton LA Pepin KH Minx P Wagner-McPherson C Layman D Wylie K Sekhon M Becker MC Fewell GA Delehaunty KD Miner TL Nash WE Kremitzki C Oddy L Du H Sun H Bradshaw-Cordum H Ali J Carter J Cordes M Harris A Isak A van Brunt A Nguyen C Du F Courtney L Kalicki J Ozersky P Abbott S Armstrong J Belter EA Caruso L Cedroni M Cotton M Davidson T Desai A Elliott G Erb T Fronick C Gaige T Haakenson W Haglund K Holmes A Harkins R Kim K Kruchowski SS Strong CM Grewal N Goyea E 《Nature》2005,434(7034):724-731
Human chromosome 2 is unique to the human lineage in being the product of a head-to-head fusion of two intermediate-sized ancestral chromosomes. Chromosome 4 has received attention primarily related to the search for the Huntington's disease gene, but also for genes associated with Wolf-Hirschhorn syndrome, polycystic kidney disease and a form of muscular dystrophy. Here we present approximately 237 million base pairs of sequence for chromosome 2, and 186 million base pairs for chromosome 4, representing more than 99.6% of their euchromatic sequences. Our initial analyses have identified 1,346 protein-coding genes and 1,239 pseudogenes on chromosome 2, and 796 protein-coding genes and 778 pseudogenes on chromosome 4. Extensive analyses confirm the underlying construction of the sequence, and expand our understanding of the structure and evolution of mammalian chromosomes, including gene deserts, segmental duplications and highly variant regions. 相似文献
47.
48.
Mechanism underlying the sleep-dream cycle 总被引:2,自引:0,他引:2
E Hartmann 《Nature》1966,212(5062):648-650
49.
J. Gillman Christine Gilbert E. Epstein J. C. Allan 《Cellular and molecular life sciences : CMLS》1958,14(2):79-80
Résumé Après ablation de la glande pituitaire, ledérèglement du du métabolisme des hydrates de carbone persiste, tandis que l'intense lipémie est abolie. L'administration de la cortisone aux babouins pancréas- et hypophysectomisés privés d'insuline, rétablit la lipémie mais non la cétonémie.Le dérèglement du métabolisme des hydrates de carbone dans les babouins diabétiques peut être dissocié de celui des lipides par un traitement approprié des glandes endocrines.La cétonémie des babouins pancréas- et hypophysectomisés, contrairement à la lipémie, n'est pas rétabli par l'administration de la cortisone, thyroxin ou par une combinaison de ces hormones. 相似文献
50.
Packaging of proteins from the endoplasmic reticulum into COPII vesicles is essential for secretion. In cells, most COPII vesicles are approximately 60-80?nm in diameter, yet some must increase their size to accommodate 300-400?nm procollagen fibres or chylomicrons. Impaired COPII function results in collagen deposition defects, cranio-lenticulo-sutural dysplasia, or chylomicron retention disease, but mechanisms to enlarge COPII coats have remained elusive. Here, we identified the ubiquitin ligase CUL3-KLHL12 as a regulator of COPII coat formation. CUL3-KLHL12 catalyses the monoubiquitylation of the COPII-component SEC31 and drives the assembly of large COPII coats. As a result, ubiquitylation by CUL3-KLHL12 is essential for collagen export, yet less important for the transport of small cargo. We conclude that monoubiquitylation controls the size and function of a vesicle coat. 相似文献