Yan Zhang
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Pubmed
Journal: Nature genetics
February/21/2013
Abstract

Watermelon, Citrullus lanatus, is an important cucurbit crop grown throughout the world. Here we report a high-quality draft genome sequence of the east Asia watermelon cultivar 97103 (2n = 2× = 22) containing 23,440 predicted protein-coding genes. Comparative genomics analysis provided an evolutionary scenario for the origin of the 11 watermelon chromosomes derived from a 7-chromosome paleohexaploid eudicot ancestor. Resequencing of 20 watermelon accessions representing three different C. lanatus subspecies produced numerous haplotypes and identified the extent of genetic diversity and population structure of watermelon germplasm. Genomic regions that were preferentially selected during domestication were identified. Many disease-resistance genes were also found to be lost during domestication. In addition, integrative genomic and transcriptomic analyses yielded important insights into aspects of phloem-based vascular signaling in common between watermelon and cucumber and identified genes crucial to valuable fruit-quality traits, including sugar accumulation and citrulline metabolism.

Pubmed
Journal: FEBS letters
July/23/2007
Abstract

Fusion controls mitochondrial morphology and is important for normal mitochondrial function, including roles in respiration, development, and apoptosis. Key components of the mitochondrial fusion machinery have been identified, allowing an initial dissection of its molecular mechanism. Outer and inner membrane fusion events are coordinately coupled but are mechanistically distinct. Mitofusins are mitochondrial GTPases that likely mediate outer membrane fusion. The dynamin-related protein OPA1/Mgm1p is required for inner membrane fusion and maintenance of normal cristae structure. We highlight recent findings that have advanced our understanding of the mechanism, function, and regulation of mitochondrial fusion.

Pubmed
Journal: Journal of virology
April/23/2012
Abstract

Duck tembusu virus (DTMUV) is an emerging agent that causes a severe disease in ducks. We report herein the first complete genome sequences of duck tembusu virus strains YY5, ZJ-407, and GH-2, isolated from Shaoxing ducks, breeder ducks, and geese, respectively, in China. The genomes of YY5, ZJ-407, and GH-2 are all 10,990 nucleotides (nt) in length and encode a putative polyprotein of 3,426 amino acids. It is flanked by a 5' and a 3' noncoding region (NCR) of 94 and 618 nt, respectively. Knowledge of the whole sequence of DTMUV will be useful for further studies of the mechanisms of virus replication and pathogenesis.

Pubmed
Journal: Biochemistry
June/15/2003
Abstract

Abietadiene synthase from grand fir catalyzes two sequential, mechanistically distinct cyclizations, of geranylgeranyl diphosphate and of copalyl diphosphate, in the formation of a mixture of abietadiene isomers as the committed step of diterpenoid resin acid biosynthesis. Each reaction is independently conducted at a separate active site residing in what were considered to be structurally distinct domains typical of terpene cyclases. Despite the presence of an unusual 250-residue N-terminal insertional element, a tandem pair of charged residues distal to the insertion was shown to form a functional part of the C-terminal active site. Because abietadiene synthase resembles the ancestral plant terpene cyclase, this observation suggests an early evolutionary origin of catalytically important positively charged residues at the N-terminus of enzymes of this general class. A series of N- and C-terminal truncations of this enzyme were constructed and characterized, both alone and as mixtures of adjacent polypeptide pairs, to assess the proposed domain architecture, the function of the insertional element, and the role of presumptive interdomain contacts. These studies indicated a requirement for the insertional element in functional folding and allowed definition of the minimum primary structure of N- and C-terminal active site peptides. Most importantly, the results showed that, although the two active sites of abietadiene synthase are catalytically independent, substantial contact between the two regions is essential for the functional competence of this enzyme. Thus, the two cyclization sites of abietadiene synthase cannot be dissected into catalytically distinct domains, and, therefore, abietadiene synthase is unlikely to have arisen by fusion of two previously independent genes.

Pubmed
Journal: Cell
May/19/2010
Abstract

Actively dividing cells perform robust and accurate DNA replication during fluctuating nutrient availability, yet factors that prevent disruption of replication remain largely unknown. Here we report that DksA, a nutrient-responsive transcription factor, ensures replication completion in Escherichia coli by removing transcription roadblocks. In the absence of DksA, replication is rapidly arrested upon amino acid starvation. This arrest requires active transcription and is alleviated by RNA polymerase mutants that compensate for DksA activity. This replication arrest occurs independently of exogenous DNA damage, yet it induces the DNA-damage response and recruits the main recombination protein RecA. This function of DksA is independent of its transcription initiation activity but requires its less-studied transcription elongation activity. Finally, GreA/B elongation factors also prevent replication arrest during nutrient stress. We conclude that transcription elongation factors alleviate fundamental conflicts between replication and transcription, thereby protecting replication fork progression and DNA integrity.

Pubmed
Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology
July/20/2010
Abstract

Granulin epithelin precursor (GEP) has been implicated in development, tissue regeneration, tumorigenesis, and inflammation. Herein we report that GEP stimulates chondrocyte differentiation from mesenchymal stem cells in vitro and endochondral ossification ex vivo, and GEP-knockdown mice display skeleton defects. Similar to bone morphogenic protein (BMP) 2, application of the recombinant GEP accelerates rabbit cartilage repair in vivo. GEP is a key downstream molecule of BMP2, and it is required for BMP2-mediated chondrocyte differentiation. We also show that GEP activates chondrocyte differentiation through Erk1/2 signaling and that JunB transcription factor is one of key downstream molecules of GEP in chondrocyte differentiation. Collectively, these findings reveal a novel critical role of GEP growth factor in chondrocyte differentiation and the molecular events both in vivo and in vitro.

Pubmed
Journal: Dalton transactions (Cambridge, England : 2003)
July/7/2016
Abstract

Two series of lanthanide dinuclear complexes with the general formulae, [Ln(n-PNO)(Bza)3(H2O)] {Bza = benzoic acid; n = 3, n-PNO = 3-picoline N-oxide, Dy(1) and Er(2); and n = 4, n-PNO = 4-picoline N-oxide, Nd(3), Eu(4), Gd(5), Tb(6), Dy(7), Er(8) and Y(9)} have been successfully synthesized by the hydrothermal method. Single-crystal X-ray diffraction experiments illustrate that the two series of compounds possess similar carboxylic ligand-bridged dinuclear structure and coordination geometry around the lanthanide ions despite the different methyl-substituent positions on the neutral ligand. Comparative studies of the Dy analogues in the static-field measurements reveal only a little difference with a small butterfly-shaped opening for complex 1 and a close hysteresis loop for 7 at 2.0 K. However, systematic investigations of the alternating-current (ac) measurements indicate that the different substituent positions of the picoline N-oxide ligand have a significant effect on the magnetic relaxation dynamics. A more substantial suppression of the quantum tunnelling of magnetization (QTM) effect and pronounced slow magnetic relaxation were observed in complex 7 as compared to 1 under both zero and a 1 kOe static field.

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Pubmed
Journal: Psychiatry and clinical neurosciences
October/12/2009
Abstract

OBJECTIVE

Repeated exposure to heroin, a typical opiate, causes neuronal adaptation and may result in anatomical changes in specific brain regions, particularly the frontal and limbic cortices. The volume changes of gray matter (GM) of these brain regions, however, have not been identified in heroin addiction.

METHODS

Using structural magnetic resonance imaging and an optimized voxel-based morphometry approach, the GM volume difference between 15 Chinese heroin-dependent and 15 healthy subjects was tested.

RESULTS

Compared to healthy subjects, the heroin-dependent subjects had reduced GM volume in the right prefrontal cortex, left supplementary motor cortex and bilateral cingulate cortices.

CONCLUSIONS

Frontal and cingulate atrophy may be involved in the neuropathology of heroin dependence.

Pubmed
Journal: PloS one
April/1/2012
Abstract

BACKGROUND

Large-scale outbreaks of hand, foot, and mouth disease (HFMD) occurred repeatedly in the Central Plain of China (Shandong, Anhui, and Henan provinces) from 2007 until now. These epidemics have increased in size and severity each year and are a major public health concern in mainland China.

RESULTS

Phylogenetic analysis was performed and a Bayesian Markov chain Monte Carlo tree was constructed based on the complete VP1 sequences of HEV71 isolates. These analyses showed that the HFMD epidemic in the Central Plain of China was caused by at least 5 chains of HEV71 transmission and that the virus continued to circulate and evolve over the winter seasons between outbreaks. Between 1998 and 2010, there were 2 stages of HEV71 circulation in mainland China, with a shift from evolutionary branch C4b to C4a in 2003-2004. The evolution rate of C4a HEV71 was 4.99×10(-3) substitutions per site per year, faster than the mean of all HEV71 genotypes. The most recent common ancestor estimates for the Chinese clusters dated to October 1994 and November 1993 for the C4a and C4b evolutionary branches, respectively. Compared with all C4a HEV71 strains, a nucleotide substitution in all C4b HEV71 genome (A to C reversion at nt2503 in the VP1 coding region, which caused amino acid substitution of VP1-10: Gln to His) had reverted.

CONCLUSIONS

The data suggest that C4a HEV71 strains introduced into the Central Plain of China are responsible for the recent outbreaks. The relationships among HEV71 isolates determined from the combined sequence and epidemiological data reveal the underlying seasonal dynamics of HEV71 circulation. At least 5 HEV71 lineages circulated in the Central Plain of China from 2007 to 2009, and the Shandong and Anhui lineages were found to have passed through a genetic bottleneck during the low-transmission winter season.

Pubmed
Journal: Journal of hepatology
February/24/2016
Abstract

OBJECTIVE

Hepatic ischemia/reperfusion (I/R) injury is characterized by anoxic cell injury and the generation of inflammatory mediators, leading to hepatic parenchymal cell death. The activation of interferon regulatory factors (IRFs) has been implicated in hepatic I/R injury, but the role of IRF9 in this progression is unclear.

METHODS

We investigated the function and molecular mechanisms of IRF9 in transgene and knockout mice subjected to warm I/R of the liver. Isolated hepatocytes from IRF9 transgene and knockout mice were subjected to hypoxia/reoxygenation (H/R) injury to determine the in vitro effects of IRF9.

RESULTS

The injuries were augmented in IRF9-overexpressing mice that were subjected to warm I/R of the liver. In contrast, a deficiency in IRF9 markedly reduced the necrotic area, serum alanine amino transferase/aspartate amino transferase (ALT/AST), immune cell infiltration, inflammatory cytokine levels, and hepatocyte apoptosis after liver I/R. Sirtuin (SIRT) 1 levels were significantly higher and the acetylation of p53 was decreased in the IRF9 knockout mice. Notably, IRF9 suppressed the activity of the SIRT1 promoter luciferase reporter and deacetylase activity. Liver injuries were significantly more severe in the IRF9/SIRT1 double knockout (DKO) mice in the I/R model, eliminating the protective effects observed in the IRF9 knockout mice.

CONCLUSIONS

IRF9 has a novel function of inducing hepatocyte apoptosis after I/R injury by decreasing SIRT1 expression and increasing acetyl-p53 levels. Targeting IRF9 may be a potential strategy for ameliorating ischemic liver injury after liver surgery.

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