全文获取类型
收费全文 | 87篇 |
免费 | 14篇 |
出版年
2021年 | 2篇 |
2019年 | 2篇 |
2016年 | 3篇 |
2015年 | 4篇 |
2014年 | 6篇 |
2013年 | 3篇 |
2012年 | 3篇 |
2011年 | 1篇 |
2010年 | 2篇 |
2009年 | 3篇 |
2008年 | 4篇 |
2007年 | 9篇 |
2006年 | 8篇 |
2005年 | 6篇 |
2004年 | 4篇 |
2003年 | 1篇 |
2002年 | 6篇 |
2001年 | 6篇 |
2000年 | 3篇 |
1999年 | 1篇 |
1998年 | 2篇 |
1997年 | 1篇 |
1996年 | 2篇 |
1994年 | 2篇 |
1993年 | 3篇 |
1992年 | 1篇 |
1991年 | 2篇 |
1990年 | 1篇 |
1989年 | 3篇 |
1988年 | 2篇 |
1987年 | 1篇 |
1985年 | 2篇 |
1977年 | 1篇 |
1975年 | 1篇 |
排序方式: 共有101条查询结果,搜索用时 15 毫秒
41.
42.
Ribosomal RNA secondary structure: compensatory mutations and implications for phylogenetic analysis 总被引:6,自引:0,他引:6
Using sequence data from the 28S ribosomal RNA (rRNA) genes of selected
vertebrates, we investigated the effects that constraints imposed by
secondary structure have on the phylogenetic analysis of rRNA sequence
data. Our analysis indicates that characters from both base-pairing regions
(stems) and non-base-pairing regions (loops) contain phylogenetic
information, as judged by the level of support of the phylogenetic results
compared with a well-established tree based on both morphological and
molecular data. The best results (the greatest level of support of
well-accepted nodes) were obtained when the complete data set was used.
However, some previously supported nodes were resolved using either the
stem or loop bases alone. Stem bases sustain a greater number of
compensatory mutations than would be expected at random, but the number is
< 40% of that expected under a hypothesis of perfect compensation to
maintain secondary structure. Therefore, we suggest that in phylogenetic
analyses, the weighting of stem characters be reduced by no more than 20%,
relative to that of loop characters. In contrast to previous suggestions,
we do not recommend weighting of stem positions by one-half, compared with
that of loop positions, because this overcompensates for the constraints
that selection imposes on the secondary structure of rRNA.
相似文献
43.
We address the questions, How do physicians adjust to and enjoy their retirement? What factors contribute to the well-being of retired physicians? A 60-item questionnaire mailed to 238 retired physicians in Los Angeles County with a 41.6% response rate assessed health, standard of living, relationships, activities, emotional difficulties, and general enjoyment. Health often improved after retirement, as did relationships with spouses and children. Standard of living was comfortable or better for most. Retired physicians engage in a wide range of interests and activities. Emotional difficulties are minimal and considerably reduced after retirement. Most physicians enjoy the freedom and activities of retirement and are happy. Fears of boredom and deterioration are unfounded. 相似文献
44.
W F Moo-Penn D C Swan T K Hine R M Baine D L Jue J M Benson M H Johnson D M Virshup W H Zinkham 《The Journal of biological chemistry》1989,264(36):21454-21457
Hb Catonsville is an unstable variant in which glutamic acid is inserted into the alpha-globin chain between Pro-37(C2) and Thr-38(C3). The peptide sequence data are consistent with the DNA sequence of the polymerase chain reaction-amplified fragment of the variant globin gene, which shows the insertion of the triplet codon--GAA--into the mutant alpha-globin gene. In the normal alpha-globin gene cluster the codon for glutamic acid is GAG rather than GAA. Thus, there are two features unique to Hb Catonsville, one the insertion of a single residue into the interior of the alpha-globin chain, and two the presence of the alternate codon for glutamic acid. The experimental evidence suggests that Hb Catonsville may be an example of nonhomologous nonallelic gene conversion, an observation not previously reported in this gene family. The mutation occurs in the critical alpha 1 beta 2 interface of the hemoglobin tetramer and leads to a variant with high oxygen affinity, a reduced cooperativity, and Bohr effect. 相似文献
45.
46.
Clara Correia‐Melo Francisco DM Marques Rhys Anderson Graeme Hewitt Rachael Hewitt John Cole Bernadette M Carroll Satomi Miwa Jodie Birch Alina Merz Michael D Rushton Michelle Charles Diana Jurk Stephen WG Tait Rafal Czapiewski Laura Greaves Glyn Nelson Mohammad Bohlooly‐Y Sergio Rodriguez‐Cuenca Antonio Vidal‐Puig Derek Mann Gabriele Saretzki Giovanni Quarato Douglas R Green Peter D Adams Thomas von Zglinicki Viktor I Korolchuk João F Passos 《The EMBO journal》2016,35(7):724-742
47.
PTEN, a phosphoinositide-3-phosphatase, serves dual roles as a tumor suppressor and regulator of cellular anabolic/catabolic metabolism. Adaptation of a redox-sensitive cysteinyl thiol in PTEN for signal transduction by hydrogen peroxide may have superimposed a vulnerability to other mediators of oxidative stress and inflammation, especially reactive carbonyl species, which are commonly occurring by-products of arachidonic acid peroxidation. Using MCF7 and HEK-293 cells, we report that several reactive aldehydes and ketones, e.g. electrophilic α,β-enals (acrolein, 4-hydroxy-2-nonenal) and α,β-enones (prostaglandin A(2), Δ12-prostaglandin J(2) and 15-deoxy-Δ-12,14-prostaglandin J(2)) covalently modify and inactivate cellular PTEN, with ensuing activation of PKB/Akt kinase; phosphorylation of Akt substrates; increased cell proliferation; and increased nuclear β-catenin signaling. Alkylation of PTEN by α,β-enals/enones and interference with its restraint of cellular PKB/Akt signaling may accentuate hyperplastic and neoplastic disorders associated with chronic inflammation, oxidative stress, or aging. 相似文献
48.
Margolis SS Perry JA Forester CM Nutt LK Guo Y Jardim MJ Thomenius MJ Freel CD Darbandi R Ahn JH Arroyo JD Wang XF Shenolikar S Nairn AC Dunphy WG Hahn WC Virshup DM Kornbluth S 《Cell》2006,127(4):759-773
DNA-responsive checkpoints prevent cell-cycle progression following DNA damage or replication inhibition. The mitotic activator Cdc25 is suppressed by checkpoints through inhibitory phosphorylation at Ser287 (Xenopus numbering) and docking of 14-3-3. Ser287 phosphorylation is a major locus of G2/M checkpoint control, although several checkpoint-independent kinases can phosphorylate this site. We reported previously that mitotic entry requires 14-3-3 removal and Ser287 dephosphorylation. We show here that DNA-responsive checkpoints also activate PP2A/B56delta phosphatase complexes to dephosphorylate Cdc25 at a site distinct from Ser287 (T138), the phosphorylation of which is required for 14-3-3 release. However, phosphorylation of T138 is not sufficient for 14-3-3 release from Cdc25. Our data suggest that creation of a 14-3-3 "sink," consisting of phosphorylated 14-3-3 binding intermediate filament proteins, including keratins, coupled with reduced Cdc25-14-3-3 affinity, contribute to Cdc25 activation. These observations identify PP2A/B56delta as a central checkpoint effector and suggest a mechanism for controlling 14-3-3 interactions to promote mitosis. 相似文献
49.