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151.
Actin polymerization promoted by a heptapeptide, an analog of the actin-binding S site on myosin head 总被引:3,自引:0,他引:3
M Eto F Morita N Nishi S Tokura T Ito K Takahashi 《The Journal of biological chemistry》1991,266(27):18233-18236
Polymerization of G-actin to F-actin was indicated by an increase in light-scattering intensity after the addition of a heptapeptide (Ile-Arg-Ile-Cys(MT)-Arg-Lys-Gly-OEt), an analog of the actin-binding S-site on S-1 heavy chain. The half-maximal concentration of the heptapeptide which induced an increase in the light-scattering intensity at 25 degrees C was about 110 microM, which was in the range of the dissociation constant of this peptide with F-actin. The polymerization of G-actin to F-actin by binding of the heptapeptide was further demonstrated by ultracentrifugal separation, Pi liberation, and electron microscopy. The polymerization of G-actin was induced only by the heptapeptide, but not by fragments of the heptapeptide. The well known acceleration of polymerization of G-actin by the myosin head may be due to the binding of G-actin with the S-site on the myosin head. 相似文献
152.
Oda S Oda T Nishi K Takabuchi S Wakamatsu T Tanaka T Adachi T Fukuda K Semenza GL Hirota K 《PloS one》2008,3(5):e2215
Background
Macrophage migration inhibitory factor (MIF) is not only a cytokine which has a critical role in several inflammatory conditions but also has endocrine and enzymatic functions. MIF is identified as an intracellular signaling molecule and is implicated in the process of tumor progression, and also strongly enhances neovascularization. Overexpression of MIF has been observed in tumors from various organs. MIF is one of the genes induced by hypoxia in an hypoxia-inducible factor 1 (HIF-1)-dependent manner.Methods/Principal Findings
The effect of MIF on HIF-1 activity was investigated in human breast cancer MCF-7 and MDA-MB-231 cells, and osteosarcoma Saos-2 cells. We demonstrate that intracellular overexpression or extracellular administration of MIF enhances activation of HIF-1 under hypoxic conditions in MCF-7 cells. Mutagenesis analysis of MIF and knockdown of 53 demonstrates that the activation is not dependent on redox activity of MIF but on wild-type p53. We also indicate that the MIF receptor CD74 is involved in HIF-1 activation by MIF at least when MIF is administrated extracellularly.Conclusion/Significance
MIF regulates HIF-1 activity in a p53-dependent manner. In addition to MIF''s potent effects on the immune system, MIF is linked to fundamental processes conferring cell proliferation, cell survival, angiogenesis, and tumor invasiveness. This functional interdependence between MIF and HIF-1α protein stabilization and transactivation activity provide a molecular mechanism for promotion of tumorigenesis by MIF. 相似文献153.
154.
Nishi H Senoo M Nishi KH Murphy B Rikiyama T Matsumura Y Habu S Johnson AC 《The Journal of biological chemistry》2001,276(45):41717-41724
155.
When pheromone-pretreated cells of an inducible a strain of Saccharomyces cerevisiae carrying the inducible gene saa1 were incubated in a growth medium at 28°C, induction of sexual agglutinability began after a 10 min lag period. If the cells were incubated at 38°C during the lag period, no induction occurred even after incubation at 28°C. Contrary to this, if the cells were incubated at 28°C during the lag period, almost complete induction occurred, even after transfer to 38°C. Temperature shift experiments revealed that 5 min incubation at 28°C was necessary for the initiation of the temperature-sensitive period and further 5 min incubation for the completion of the period. The temperature-sensitive period was sensitive to phenylmethylsulfonyl fluoride.Non-common abbreviations PBS
10-2 M phosphate buffer solution, pH 5.5
- PMSF
phenylmethylsulfonyl fluoride 相似文献
156.
Effects of tetrodotoxin on the action potential in Na-free media 总被引:2,自引:0,他引:2
157.
A temperature-sensitive mutant in the gene rplX for ribosomal protein L24 and its suppression by spontaneous mutations in a 23S rRNA gene of Escherichia coli. 总被引:2,自引:0,他引:2 下载免费PDF全文
A temperature-sensitive mutant with an altered ribosomal protein L24 was analysed. Revertant analysis showed that the temperature-sensitive growth was correlated with the altered protein. A DNA segment containing the mutant rplX gene was cloned and sequenced. The GGC codon for glycine at the amino acid position 84 of the protein was found to be altered to a GAC codon for aspartic acid. By transforming the rplX mutant with a plasmid carrying the rrnB operon and by selecting for temperature-resistant transformants we obtained two spontaneous suppressor mutants in the gene for 23S rRNA. DNA sequence analysis of the region corresponding to the 5' end of the 23S rRNA showed a C to T alteration at position 33 in both mutants and an additional A to G alteration at position 466 in one of them. The results suggest intimate interaction of protein L24 and the 5' end of 23S rRNA in vivo and support a secondary structure model of the 23S rRNA which brings these mutational points into a close contact. 相似文献
158.
Monitoring on the Lowveld reaches of the Olifants River, Limpopo River System, and its Steelpoort, Blyde, Klaserie and Selati tributaries was initiated in 2009. Analysis of the 2009–2015 data from four Olifants River sites showed deterioration in the river’s ecological condition between where it enters the Lowveld and where it enters the Kruger National Park, with a slight recovery within the Kruger National Park. Physico-chemical, aquatic macroinvertebrate and fish data collected in 2009–2015 at six sites on the Steelpoort, Blyde, Klaserie and Selati tributaries of the Olifants River corroborated the ecological condition of these tributaries. The Selati was the most polluted and was in a critically modified condition, whereas the Klaserie and Steelpoort were in fair condition and the Blyde was in good condition. The Selati appeared to have a significant negative impact on the water quality, macroinvertebrates and fish of the Olifants River within the Kruger National Park. 相似文献
159.
Tomoharu Tsukada Mizuki Takahashi Toshiyasu Takemoto Osamu Kanno Takahiro Yamane Sayako Kawamura Takahide Nishi 《Bioorganic & medicinal chemistry letters》2009,19(20):5909-5912
With the aim of discovering a novel class of fructose-1,6-bisphosphatase (FBPase) inhibitors, a series of compounds based on tricyclic scaffolds was synthesized. Extensive SAR studies led to the finding of 8l with an IC50 value of 0.013 μM against human FBPase. An X-ray crystallographic study revealed that 8l bound at AMP binding sites of human liver FBPase with hydrogen bonding interactions similar to AMP. 相似文献
160.
Chuanxi Cai Haruko Masumiya Noah Weisleder Zui Pan Miyuki Nishi Shinji Komazaki Hiroshi Takeshima Jianjie Ma 《The Journal of biological chemistry》2009,284(5):3314-3322
Membrane recycling and remodeling contribute to multiple cellular
functions, including cell fusion events during myogenesis. We have identified
a tripartite motif (TRIM72) family member protein named MG53 and defined its
role in mediating the dynamic process of membrane fusion and exocytosis in
striated muscle. MG53 is a muscle-specific protein that contains a TRIM motif
at the amino terminus and a SPRY motif at the carboxyl terminus. Live cell
imaging of green fluorescent protein-MG53 fusion construct in cultured
myoblasts showed that although MG53 contains no transmembrane segment it is
tightly associated with intracellular vesicles and sarcolemmal membrane. RNA
interference-mediated knockdown of MG53 expression impeded myoblast
differentiation, whereas overexpression of MG53 enhanced vesicle trafficking
to and budding from sarcolemmal membrane. Co-expression studies indicated that
MG53 activity is regulated by a functional interaction with caveolin-3. Our
data reveal a new function for TRIM family proteins in regulating membrane
trafficking and fusion in striated muscles.When myoblasts exit the cell cycle during myogenesis, dramatic changes in
membrane organization occur as myoblast fusion allows the formation of
multinucleated muscle fibers. In addition to cell fusion events,
differentiation of myotubes involves establishment of specialized membrane
structures (1,
2). The transverse tubular
invagination of sarcolemmal membrane and the intracellular membrane network
known as the sarcoplasmic reticulum are two highly organized membrane
architectures in cardiac and skeletal muscle. Establishment of these intricate
membrane compartments requires extensive remodeling of the immature myoblast
membranes. Dynamic membrane remodeling also contributes to many physiologic
processes in mature muscle, including Ca2+ signaling, trafficking
of glucose transporter (GLUT4), and other membrane internalization events
involving caveolae structures
(3-6).
Although defects in membrane integrity have been linked to various forms of
muscular dystrophy (7,
8), the molecular machinery
regulating these specific membrane recycling and remodeling events in striated
muscle is not well defined.The large tripartite motif
(TRIM)5 family of
proteins is involved in numerous cellular functions in a wide variety of cell
types. Members of this protein family contain signature motifs that include a
RING finger, a zinc binding moiety (B-box), and a
coiled coil structure (RBCC), which invariably comprise
the amino-terminal domain of TRIM family members
(9). The carboxyl-terminal
sequence of TRIM proteins is variable; in some cases a subfamily of TRIM
proteins contains a SPRY domain, a sequence first observed in the ryanodine
receptor Ca2+ channel in the sarcoplasmic reticulum membrane of
excitable cells (10).
Extensive studies have revealed that protein-protein interactions in the
cytosol mediate the defined functions of TRIM proteins. For example, the
ubiquitin E3 ligase enzymatic activity of several TRIM family members requires
the B-box motif (11,
12). Recent studies have also
indicated a role for TRIM proteins in defense against events involving
membrane penetration, such as protection against infection by various viruses,
including human immunodeficiency virus
(13-15).
Although most of the studies concentrate on the cytosolic action of TRIM,
limited reports have investigated the role of TRIM proteins in membrane
signaling or recycling.We have previously established an immunoproteomics approach that allows
definition of novel components involved in myogenesis, Ca2+
signaling, and maintenance of membrane integrity in striated muscle
(16). Using this approach, we
have shown that junctophilin is a structural protein that establishes
functional communication between sarcoplasmic reticulum and transverse tubule
membranes at triad and dyad junctions in striated muscle
(17-19).
Further studies identified mitsugumin 29, a synaptophysin-related protein that
is essential for biogenesis of triad membrane structures and Ca2+
signaling in skeletal muscle
(20,
21). Screening of this
immunoproteomics library led to the recent identification of MG53, a
muscle-specific TRIM family protein
(22). Domain homology analysis
revealed that MG53 contains the prototypical RBCC motifs plus a SPRY domain at
the carboxyl terminus. Genetic knock-out and functional studies reveal that
MG53 nucleates the assembly of the sarcolemmal membrane repair machinery to
restore cellular integrity following acute damage to the muscle fiber
(22).Here we present evidence illustrating that MG53, in contrast to other known
TRIM proteins, can localize to intracellular vesicles and the sarcolemmal
membrane. A functional interaction between MG53 and caveolin-3, another
muscle-specific protein, plays an essential role in regulating the dynamic
process of membrane budding and exocytosis in skeletal muscle. 相似文献