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排序方式: 共有186条查询结果,搜索用时 0 毫秒
181.
Yan Chao Cui Yu Sheng Qiu Qiong Wu Gang Bu Amira Peli Seoh Wei Teh Kok Pian Ang Narcisse MS Joseph Avin Ee-Hwan Koh Aisha Farhana Badr Alzahrani Mohammed Safwan Ali Khan Antony V Samrot Pooi Ling Mok Suresh Kumar Subbiah 《Experimental biology and medicine (Maywood, N.J.)》2021,246(10):1177
Osteoblasts play an important role in bone regeneration and repair. The hypoxia condition in bone occurs when bone undergoes fracture, and this will trigger a series of biochemical and mechanical changes to enable bone repair. Hence, it is interesting to observe the metabolites and metabolism changes when osteoblasts are exposed to hypoxic condition. This study has looked into the response of human osteoblast hFOB 1.19 under normoxic and hypoxic conditions by observing the cell growth and utilization of metabolites via Phenotype MicroArrays™ under these two different oxygen concentrations. The cell growth of hFOB 1.19 under hypoxic condition showed better growth compared to hFOB 1.19 under normal condition. In this study, osteoblast used glycolysis as the main pathway to produce energy as hFOB 1.19 in both hypoxic and normoxic conditions showed cell growth in well containing dextrin, glycogen, maltotriose, D-maltose, D-glucose-6-phospate, D-glucose, D-mannose, D-Turanose, D-fructose-6-phosphate, D-galactose, uridine, adenosine, inosine and α-keto-glutaric acid. In hypoxia, the cells have utilized additional metabolites such as α-D-glucose-1-phosphate and D-fructose, indicating possible activation of glycogen synthesis and glycogenolysis to metabolize α-D-glucose-1-phosphate. Meanwhile, during normoxia, D-L-α-glycerol phosphate was used, and this implies that the osteoblast may use glycerol-3-phosphate shuttle and oxidative phosphorylation to metabolize glycerol-3-phosphate. 相似文献
182.
Neville S. Gilhooly Carolina Carrasco Benjamin Gollnick Martin Wilkinson Dale B. Wigley Fernando Moreno-Herrero Mark S. Dillingham 《Nucleic acids research》2016,44(6):2727-2741
In bacteria, the repair of double-stranded DNA breaks is modulated by Chi sequences. These are recognised by helicase-nuclease complexes that process DNA ends for homologous recombination. Chi activates recombination by changing the biochemical properties of the helicase-nuclease, transforming it from a destructive exonuclease into a recombination-promoting repair enzyme. This transition is thought to be controlled by the Chi-dependent opening of a molecular latch, which enables part of the DNA substrate to evade degradation beyond Chi. Here, we show that disruption of the latch improves Chi recognition efficiency and stabilizes the interaction of AddAB with Chi, even in mutants that are impaired for Chi binding. Chi recognition elicits a structural change in AddAB that maps to a region of AddB which resembles a helicase domain, and which harbours both the Chi recognition locus and the latch. Mutation of the latch potentiates the change and moderately reduces the duration of a translocation pause at Chi. However, this mutant displays properties of Chi-modified AddAB even in the complete absence of bona fide hotspot sequences. The results are used to develop a model for AddAB regulation in which allosteric communication between Chi binding and latch opening ensures quality control during recombination hotspot recognition. 相似文献
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185.
MS Nandhu Jes Paul Korah P Kuruvilla Anitha Malat Chinthu Romeo CS Paulose 《Journal of biomedical science》2011,18(1):5
Parkinson's disease is characterized by progressive cell death in the substantia nigra pars compacta, which leads to dopamine
depletion in the striatum and indirectly to cortical dysfunction. Increased glutamatergic transmission in the basal ganglia
is implicated in the pathophysiology of Parkinson's disease and glutamate receptor mediated excitotoxicity has been suggested
to be one of the possible causes of the neuronal degeneration. In the present study, the effects of serotonin, gamma-aminobutyric
acid and bone marrow cells infused intranigrally to substantia nigra individually and in combination on unilateral 6-hydroxydopamine
induced Parkinson's rat model was analyzed. Scatchard analysis of total glutamate and NMDA receptor binding parameters showed
a significant increase in Bmax (P < 0.001) in the cerebral cortex of 6-hydroxydopamine infused rat compared to control. Real Time PCR amplification of NMDA2B,
mGluR5, bax, and ubiquitin carboxy-terminal hydrolase were up regulated in cerebral cortex of 6-hydroxydopamine infused rats
compared to control. Gene expression studies of GLAST, ά-Synuclien and Cyclic AMP response element-binding protein showed
a significant (P < 0.001) down regulation in 6-OHDA infused rats compared to control. Behavioural studies were carried out
to confirm the biochemical and molecular studies. Serotonin and GABA along with bone marrow cells in combination showed reversal
of glutamate receptors and behaviour abnormality shown in the Parkinson's rat model. The therapeutic significance in Parkinson's
disease is of prominence. 相似文献
186.
DNA binding mediates conformational changes and metal ion coordination in the active site of PcrA helicase. 总被引:1,自引:0,他引:1
P Soultanas M S Dillingham S S Velankar D B Wigley 《Journal of molecular biology》1999,290(1):137-148
Based upon the crystal structures of PcrA helicase, we have made and characterised mutations in a number of conserved helicase signature motifs around the ATPase active site. We have also determined structures of complexes of wild-type PcrA with ADPNP and of a mutant PcrA complexed with ADPNP and Mn2+. The kinetic and structural data define roles for a number of different residues in and around the ATP binding site. More importantly, our results also show that there are two functionally distinct conformations of ATP in the active site. In one conformation, ATP is hydrolysed poorly whereas in the other (activated) conformation, ATP is hydrolysed much more rapidly. We propose a mechanism to explain how the stimulation of ATPase activity afforded by binding of single-stranded DNA stabilises the activated conformation favouring Mg2+binding and a consequent repositioning of the gamma-phosphate group which promotes ATP hydrolysis. A part of the associated conformational change in the protein forces the side-chain of K37 to vacate the Mg2+binding site, allowing the cation to bind and interact with ATP. 相似文献