全文获取类型
收费全文 | 149篇 |
免费 | 8篇 |
出版年
2021年 | 1篇 |
2019年 | 1篇 |
2018年 | 4篇 |
2016年 | 4篇 |
2015年 | 7篇 |
2014年 | 10篇 |
2013年 | 4篇 |
2012年 | 6篇 |
2011年 | 18篇 |
2010年 | 7篇 |
2009年 | 7篇 |
2008年 | 8篇 |
2007年 | 8篇 |
2006年 | 15篇 |
2005年 | 12篇 |
2004年 | 7篇 |
2003年 | 8篇 |
2002年 | 9篇 |
1999年 | 1篇 |
1998年 | 1篇 |
1997年 | 6篇 |
1996年 | 2篇 |
1995年 | 1篇 |
1994年 | 1篇 |
1993年 | 1篇 |
1992年 | 1篇 |
1989年 | 1篇 |
1988年 | 1篇 |
1983年 | 1篇 |
1981年 | 1篇 |
1980年 | 2篇 |
1977年 | 1篇 |
排序方式: 共有157条查询结果,搜索用时 296 毫秒
1.
Yoshinao Nakagawa Manabu Totsuka Tomoaki Sato Yoshiro Fukuda Koichi Hirota 《European journal of applied physiology and occupational physiology》1989,59(3):239-242
We examined the influence exerted, through disuse of the hindlimb, on the collagen fibres of the achilles tendon in rats. With disuse the body mass decreased by 28%, and the mass of soleus muscle decreased by 20%. A decrease in the surface area and diameter was observed in the experimental group when compared to the control group. A histogram of the collagen fibres showed a decrease of the thick fibres in the experimental group. The maximum surface area of collagen fibres in the experimental group was seen to be only 43% of that of the control group. These results showed a decrease in the thickness of the collagen fibres of the achilles tendon through disuse. This seemed to suggest that resistance to tension is decreased by disuse. 相似文献
2.
Toshinobu Tokumoto Masakane Yamashita Mika Tokumoto Yoshinao Katsu Ryo Horiguchi Hiroko Kajiura Yoshitaka Nagahama 《The Journal of cell biology》1997,138(6):1313-1322
Immediately before the transition from metaphase to anaphase, the protein kinase activity of maturation or M-phase promoting factor (MPF) is inactivated by a mechanism that involves the degradation of its regulatory subunit, cyclin B. The availability of biologically active goldfish cyclin B produced in Escherichia coli and purified goldfish proteasomes (a nonlysosomal large protease) has allowed the role of proteasomes in the regulation of cyclin degradation to be examined for the first time. The 26S, but not the 20S proteasome, digested recombinant 49-kD cyclin B at lysine 57 (K57), producing a 42-kD truncated form. The 42-kD cyclin was also produced by the digestion of native cyclin B forming a complex with cdc2, a catalytic subunit of MPF, and a fragment transiently appeared during cyclin degradation when eggs were released from metaphase II arrest by egg activation. Mutant cyclin at K57 was resistant to both digestion by the 26S proteasome and degradation at metaphase/anaphase transition in Xenopus egg extracts. The results of this study indicate that the destruction of cyclin B is initiated by the ATP-dependent and ubiquitin-independent proteolytic activity of 26S proteasome through the first cutting in the NH2 terminus of cyclin (at K57 in the case of goldfish cyclin B). We also surmise that this cut allows the cyclin to be ubiquitinated for further destruction by ubiquitin-dependent activity of the 26S proteasome that leads to MPF inactivation. 相似文献
3.
4.
Katsura Kakoki Haruka Kamiyama Mai Izumida Yuka Yashima Hideki Hayashi Naoki Yamamoto Toshifumi Matsuyama Tsukasa Igawa Hideki Sakai Yoshinao Kubo 《Biochemical and biophysical research communications》2014
Xenotropic murine leukemia virus-related virus (XMRV) is a novel gammaretrovirus that was originally isolated from human prostate cancer. It is now believed that XMRV is not the etiologic agent of prostate cancer. An analysis of murine leukemia virus (MLV) infection in various human cell lines revealed that prostate cancer cell lines are preferentially infected by XMRV, and this suggested that XMRV infection may confer some sort of growth advantage to prostate cancer cell lines. To examine this hypothesis, androgen-dependent LNCaP cells were infected with XMRV and tested for changes in certain cell growth properties. We found that XMRV-infected LNCaP cells can proliferate in the absence of the androgen dihydrotestosterone. Moreover, androgen receptor expression is significantly reduced in XMRV-infected LNCaP cells. Such alterations were not observed in uninfected and amphotropic MLV-infected LNCaP cells. This finding explains why prostate cancer cell lines are preferentially infected with XMRV. 相似文献
5.
6.
Hirobe T Abe H Wakamatsu K Ito S Kawa Y Soma Y Mizoguchi M 《European journal of cell biology》2007,86(6):315-330
The murine recessive yellow (Mc1r(e)) is a loss-of-function mutation in the receptor for alpha-melanocyte-stimulating hormone, melanocortin receptor 1 (Mc1r) and produces yellow coats by inducing pheomelanin synthesis in hair follicular melanocytes. However, it is not known whether the Mc1r(e) mutation affects the proliferation and differentiation of melanocytes. In this study, the proliferation and differentiation of recessive yellow epidermal melanocytes cultured in dibutyryl cyclic AMP-supplemented serum-free medium were investigated in detail. The melanocytes produced mainly eumelanin in this culture system. The proliferation of recessive yellow melanocytes was decreased compared with that of wild-type at the e-locus, black melanocytes. The differentiation of melanocytes was also delayed and inhibited in recessive yellow mice. Tyrosinase (TYR) activity and TYR-related protein 1 (TRP1) and TRP2 (dopachrome tautomerase, DCT) expressions were decreased and, in addition, the maturation of stage IV melanosomes was inhibited. Excess l-tyrosine (l-Tyr) added to the culture media rescued the reduced activity of proliferation of melanocytes. l-Tyr also stimulated TYR activity and TRP1 and TRP2 expressions as well as the maturation of stage IV melanosomes and pigmentation. These results suggest that the Mc1r(e) mutation affects the proliferation and differentiation of melanocytes and l-Tyr rescues the reduced proliferative and differentiative activities by stimulating TYR activity and TRP1 and TRP2 expressions as well as melanosome maturation. 相似文献
7.
Fujita N Horiike S Sugimoto R Tanaka H Iwasa M Kobayashi Y Hasegawa K Ma N Kawanishi S Adachi Y Kaito M 《Free radical biology & medicine》2007,42(3):353-362
Hepatic oxidative stress occurs in chronic hepatitis C (CH-C), but little is known about its producing mechanisms and precise role in the pathogenesis of the disease. To determine the relevance of hepatic oxidatively generated DNA damage in CH-C, 8-hydroxy-2'-deoxyguanosine (8-OHdG) adducts were quantified in liver biopsy specimens by immunohistochemical staining, and its relationship with clinical, biochemical, and histological parameters, and treatment response was assessed in 40 CH-C patients. Hepatic 8-OHdG counts were significantly correlated with serum transaminase levels (r=0.560, p=0.0005) and histological grading activity (p=0.0013). Remarkably, 8-OHdG levels were also significantly related to body and hepatic iron storage markers (vs serum ferritin, r=0.565, p=0.0004; vs hepatic total iron score, r=0.403, p=0.0119; vs hepatic hepcidin messenger RNA, r=0.516, p=0.0013). Baseline hepatic oxidative stress was more prominent in nonsustained virological responder (non-SVR) than in SVR to interferon (IFN)/ribavirin treatment (50.8 vs 32.7 cells/10(5) microm2, p=0.0086). After phlebotomy, hepatic 8-OHdG levels were significantly reduced from 53.4 to 21.1 cells/10(5) microm2 (p=0.0125) with concomitant reductions of serum transaminase and iron-related markers in CH-C patients. In conclusion, this study showed that hepatic oxidatively generated DNA damage frequently occurs and is strongly associated with increased iron deposition and hepatic inflammation in CH-C patients, suggesting that iron overload is an important mediator of hepatic oxidative stress and disease progression in chronic HCV infection. 相似文献
8.
Minenosuke Matsutani Kohei Ito Yoshinao Azuma Hidetaka Ogino Mutsunori Shirai Toshiharu Yakushi Kazunobu Matsushita 《Applied microbiology and biotechnology》2015,99(17):7229-7240
Gluconacetobacter xylinus (formerly Acetobacter xylinum and presently Komagataeibacter medellinensis) is known to produce cellulose as a stable pellicle. However, it is also well known to lose this ability very easily. We investigated the on and off mechanisms of cellulose producibility in two independent cellulose-producing strains, R1 and R2. Both these strains were isolated through a repetitive static culture of a non-cellulose-producing K. medellinensis NBRC 3288 parental strain. Two cellulose synthase operons, types I and II, of this strain are truncated by the frameshift mutation in the bcsBI gene and transposon insertion in the bcsCII gene, respectively. The draft genome sequencing of R1 and R2 strains revealed that in both strains the bcsBI gene was restored by deletion of a nucleotide in its C-rich region. This result suggests that the mutations in the bcsBI gene are responsible for the on and off mechanism of cellulose producibility. When we looked at the genomic DNA sequences of other Komagataeibacter species, several non-cellulose-producing strains were found to contain similar defects in the type I and/or type II cellulose synthase operons. Furthermore, the phylogenetic relationship among cellulose synthase genes conserved in other bacterial species was analyzed. We observed that the cellulose genes in the Komagataeibacter shared sequence similarities with the γ-proteobacterial species but not with the α-proteobacteria and that the type I and type II operons could be diverged from a same ancestor in Komagataeibacter. 相似文献
9.
Yutaka Nakamura Atsushi Asano Yoshinao Hosaka Takashi Takeuchi Toshihiko Iwanaga Yoshiaki Yamano 《Experimental Animals》2015,64(4):415-424
Membrane trafficking in male germ cells contributes to their development
via cell morphological changes and acrosome formation. TBC family
proteins work as Rab GTPase accelerating proteins (GAPs), which negatively regulate Rab
proteins, to mediate membrane trafficking. In this study, we analyzed the expression of a
Rab GAP, TBC1D9, in mouse organs and the intracellular localization of the gene products.
Tbc1d9 showed abundant expression in adult mice testis. We found that
the Tbc1d9 mRNA was expressed in primary and secondary spermatocytes, and
that the TBC1D9 protein was expressed in spermatocytes and round spermatids. In 293T
cells, TBC1D9-GFP proteins were localized in the endosome and Golgi apparatus.
Compartments that were positive for the constitutive active mutants of Rab7 and Rab9 were
also positive for TBC1D9 isoform 1. In addition, TBC1D9 proteins were associated with Rab7
and Rab9, respectively. These results indicate that TBC1D9 is expressed mainly in
spermatocytes, and suggest that TBC1D9 regulates membrane trafficking pathways related to
Rab9- or Rab7-positive vesicles. 相似文献
10.