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Zhu  Zhu  Zhang  Luoyan  Gao  Lexuan  Tang  Shaoqing  Zhao  Yao  Yang  Ji 《Tree Genetics & Genomes》2016,12(1):1-10
Tree Genetics &; Genomes - To breed a new variety of coffee (Coffea arabica) requires approximately 25&;nbsp;years due to the long generation time (5–6&;nbsp;years) of this perennial...  相似文献   
74.
A series of new thienopyrimidine derivatives has been discovered as potent PI3K inhibitors. The systematic SAR studies for these analogues are described. Among them, 8a and 9a exhibit nanomolar enzymatic potencies and sub-micromolar cellular anti-proliferative activities. 8a displays favorable pharmacokinetic profiles, while 9a easily undergoes deacetylation to yield a major metabolite 8a. Furthermore, 8a and 9a potently inhibit tumor growth in a dose-dependent manner in the NCI-H460 xenograft model with an acceptable safety profile.  相似文献   
75.
Alzheimer’s disease (AD) is characterized by an excessive accumulation of toxic amyloid beta (Aβ) plaques and memory dysfunction. The onset of AD is influenced by age, genetic background, and impaired glucose metabolism in the brain. Several studies have demonstrated that diabetes involving insulin resistance and glucose tolerance could lead to AD, ultimately resulting in cognitive dysfunction. Even though the relationship between diabetes and AD was indicated by significant evidences, the critical mechanisms and metabolic alterations in diabetes induced AD are not clear until now. Recently, iron metabolism has been shown to play multiple roles in the central nervous system (CNS). Iron deficiency and overload are associated with neurodegenerative diseases. Iron binds to Aβ and subsequently regulates Aβ toxicity in the CNS. In addition, previous studies have shown that iron is involved in the aggravation of insulin resistance. Considering these effects of iron metabolism in CNS, we expect that iron metabolism may play crucial roles in diabetic AD brain. Thus, we review the recent evidence regarding the relationship between diabetes-induced AD and iron metabolism.  相似文献   
76.
Chalcone synthase (CHS) is a key enzyme in the biosynthesis of flavonoids, which are important for the pigmentation of flowers and act as attractants to the pollinators. Genes encoding CHS constitute a multigene family in which the copy number varies among plant species and functional divergence appears to have occurred repeatedly. Plants of the Dendranthema genus have white, yellow, and pink flowers, exhibiting considerable variation in flower color. In this article, 18 CHS genes from six Dendranthema species were sequenced. Two of them were found to be pseudogenes. The functional Dendranthema CHS genes formed three well-supported subfamilies: SF1, SF2, and SF3. The inferred phylogeny of the CHS genes of Dendranthema and Gerbera suggests that those genes originated as a result of duplications before divergence of these two genera, and the function of Dendranthema CHS genes have diverged in a similar fashion to the Gerbera CHS genes; i.e., the genes of SF1 and SF3 code for typical CHS enzymes expressed during different stages of development, whereas the genes of SF2 code for another enzyme that is different from CHS in substrate specificity and reaction. Relative rate tests revealed that the Dendranthema CHS genes significantly deviated from clocklike evolution at nonsynonymous sites. Maximum likelihood analysis showed that the nonsynonymous-synonymous (omega = d(N)/d(S)) rate ratio for the lineage ancestral to SF2 was much higher than for other lineages, with some sites having a ratio well above one. Positive selective pressure appears to have driven the divergence of SF2 from SF1 and SF3.  相似文献   
77.
Zhang  Hao  Wang  Jin-Yan  Chen  Yi-Juan  Siemann  Evan  Ji  Xiang-Yun  Jiang  Jie-Xian  Wan  Nian-Feng 《BioControl》2022,67(1):1-13
BioControl - The effects of plant volatiles on parasitoids are important with regards to the tri-trophic interactions among host plants, insect herbivores, and their natural enemies. However, the...  相似文献   
78.

Background

The meiotic program initiation pathway genes (CYP26B1, NANOS1 and STRA8) have been proposed to play key roles in spermatogenesis.

Objective

To elucidate the exact role of the genetic variants of the meiosis initiation genes in spermatogenesis, we genotyped the potential functional genetic variants of CYP26B1, NANOS1 and STRA8 genes, and evaluated their effects on spermatogenesis in our study population.

Design, Setting, and Participants

In this study, all subjects were volunteers from the affiliated hospitals of Nanjing Medical University between March 2004 and July 2009 (NJMU Infertile Study). Total 719 idiopathic infertile cases were recruited and divided into three groups according to WHO semen parameters: 201 azoospermia patients (no sperm in the ejaculate even after centrifugation), 155 oligozoospermia patients (sperm counts <20×106/ml) and 363 infertility/normozoospermia subjects (sperm counts >20×106/ml). The control group consisted of 383 subjects with normal semen parameters, all of which had fathered at least one child without assisted reproductive technologies.

Measurements

Eight single nucleotide polymorphisms (SNPs) in CYP26B1, NANOS1 and STRA8 genes were determined by TaqMan allelic discrimination assay in 719 idiopathic infertile men and 383 healthy controls.

Results and Limitations

The genetic variant rs10269148 of STRA8 gene showed higher risk of spermatogenic impairment in the groups of abnormospermia (including azoospermia subgroup and oligozoospermia subgroup) and azoospermia than the controls with odds ratios and 95% confidence intervals of 2.52 (1.29–4.94) and 2.92 (1.41–6.06), respectively (P = 0.006, 0.002 respective). Notably, larger sample size studies and in vivo or in vitro functional studies are needed to substantiate the biological roles of these variants.

Conclusions

Our results provided epidemiological evidence supporting the involvement of genetic polymorphisms of the meiotic program initiation genes in modifying the risk of azoospermia and oligozoospermia in a Han-Chinese population.  相似文献   
79.
Rice LTRPK1, which encodes a member of the casein kinase I family, has been reported to be involved in root development, hormone response, and metabolic processes. Here we further show that LTRPK1 participates in stress resistance by regulating cytoskeleton rearrangement and formation of cold tolerance and adaptation. Semiquantitative RT-PCR analysis revealed enhanced expression of LTRPK1 in plants subject to low-temperature stress at 4 °C, suggesting a role in low-temperature-related cell responses and signal transduction pathways. Further analysis of LTRPK1-deficient transgenic plants showed that under low-temperature treatment, the growth rate of transgenic plant primary roots, which is commonly used as an indicator for cold stress response abilities, was less inhibited than that of control plants. Moreover, damage to the plasma membrane of root cells in LTRPK1-deficient plants was greater than that of controls as measured by relative electrical conductivity (REC). The malondialdehyde (MDA) content of LTRPK1-deficient plants also increased over that of the control, indicating increased plasma membrane permeability. Further immunofluorescence localization observations indicated that microtubules of transgenic plants subject to low temperature disassembled more rapidly, whereas the control plant microtubules in most cells of the root elongation zone kept their normal habitus, which suggested that LTRPK1-deficient plants had reduced capacity to resist low-temperature stress through regulation of microtubule assembly. These results demonstrate involvement of LTRPK1 in low-temperature stress and provide new insight for rice breeding and germplasm innovation to improve crop cold tolerance.  相似文献   
80.
Fang DH  Fan CH  Ji Q  Qi BX  Li J  Wang L 《Molecular biology reports》2012,39(6):6801-6809
Paraoxonase is an HDL-associated enzyme that plays a preventive role against oxidative stress, which is thought to contribute to cancer development. PON1 activity varies widely among individuals, which is in part related to two common nonsynonymous polymorphisms in the PON1 gene (Q192R and L55M). The polymorphisms in PON1 have been implicated in cancer risk. However, results from the studies to date have been conflicting. To clarify the association, a meta-analysis was performed for 7,073 cases and 9,520 controls from 25 published case–control studies. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. Significant associations between PON1-L55M but not Q192R polymorphism and total cancer were observed from all the comparisons. In stratified analyses, PON1-55M allele was a risk factor for breast cancer. Similarly, increased risk was observed for prostate cancer (OR = 1.18, 95% CI: 1.01–1.36, P heterogeneity = 0.260) and Caucasian population (OR = 1.18, 95% CI: 1.02–1.38, P heterogeneity = 0.1) of the LM genotype, compared with the LL genotype. For PON1-Q192R polymorphism, PON1-192R allele was a decreased risk factor for cancer in the Asian group (RR vs QQ: OR = 0.61, 95% CI: 0.38–0.98, P heterogeneity = 0.268; QR vs QQ: OR = 0.71, 95% CI: 0.52–0.96, P heterogeneity = 0.130; RR + QR vs QQ: OR = 0.71, 95% CI: 0.53–0.95, P heterogeneity = 0.135). Although some modest bias could not be eliminated, this meta-analysis suggests that the PON1-55M allele is a risk factor for the development of cancer, in particular for breast cancer. Future studies with larger sample sizes are warranted to further evaluate these associations.  相似文献   
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