Search PubMed⌕ Search

Biomedical subjects

Yupeng Wang

Publications and source records attributed to Yupeng Wang.

10 recordsLinked to original sources

Diverse evolutionary rates and gene duplication patterns among families of functional olfactory receptor genes in humans.

In humans, odors are detected by ~400 functional olfactory receptor (OR) genes. The superfamily of functional OR genes can be further divided into tens of families. In large part, the OR genes have experienced extensive tandem duplications, which have led to gene gains and losses. However, whether different OR gene families have experienced distinct modes of gene duplication has yet to be reported. We conducted comparative genomic and evolutionary analyses for human functional OR genes. Based on analysis of human-mouse 1-1 orthologs, we found that human functional OR genes show higher-than-average evolutionary rates, and there are significant differences among families of functional OR genes. Via comparison with seven vertebrate outgroups, families of human functional OR genes show different extents of gene synteny conservation. Although the superfamily of human functional OR genes is enriched in tandem and proximal duplications, there are particular families which are enriched in segmental duplications. These findings suggest that human functional OR genes may be governed by different evolutionary mechanisms and that large-scale gene duplications have contributed to the early evolution of human functional OR genes.

Humans↗

Brain-derived neurotrophic factor activates ERK5 in cortical neurons via a Rap1-MEKK2 signaling cascade.

The extracellular signal-regulated kinase 5 (ERK5) is activated in neurons of the central nervous system by neurotrophins including brain-derived neurotrophic factor (BDNF). Although MEK5 is known to mediate BDNF stimulation of ERK5 in central nervous system neurons, other upstream signaling components have not been identified. Here, we report that BDNF induces a sustained activation of ERK5 in rat cortical neurons and activates Rap1, a small GTPase, as well as MEKK2, a MEK5 kinase. Our data indicate that activation of Rap1 or MEKK2 is sufficient to stimulate ERK5, whereas inhibition of either Rap1 or MEKK2 attenuates BDNF activation of ERK5. Furthermore, BDNF stimulation of MEKK2 is regulated by Rap1. Our evidence also indicates that Ras and MEKK3, a MEK5 kinase in non-neuronal cells, do not play a significant role in BDNF activation of ERK5. This study identifies Rap1 and MEKK2 as critical upstream signaling molecules mediating BDNF stimulation of ERK5 in central nervous system neurons.

Animals↗

Extracellular signal-regulated kinase (ERK) 5 is necessary and sufficient to specify cortical neuronal fate.

Multipotent cortical progenitor cells differentiate into neurons and glial cells during development; however, mechanisms governing the specification of progenitors to a neuronal fate are not well understood. Although both extrinsic and intrinsic factors regulate this process, little is known about kinase signaling mechanisms that direct neuronal fate. Here, we report that extracellular signal-regulated kinase (ERK) 5 is expressed and active in proliferating cortical progenitors. Lentiviral gene delivery of a dominant negative ERK5 or dominant negative MAP kinase kinase 5 reduced the number of neurons generated from rat cortical progenitor cells in culture, whereas constitutive activation of ERK5 increased the production of neurons. Furthermore, when cortical progenitor cells were treated with ciliary neurotrophic factor, which induces precocious glial differentiation, ERK5 activation still promoted neuronal fate while suppressing glial differentiation. Our data also indicate that ERK5 does not directly regulate proliferation or apoptosis of cultured cortical progenitors. We conclude that ERK5 is necessary and sufficient to stimulate the generation of neurons from cortical progenitors. These results suggest a previously uncharacterized function for ERK5 signaling during brain development and raise the interesting possibility that extrinsic factors may instruct cortical progenitors to become neurons by activating the ERK5 pathway.

Animals↗

Quantum size effects on the perpendicular upper critical field in ultrathin lead films.

We report the thickness-dependent (in terms of atomic layers) oscillation behavior of the perpendicular upper critical field Hc2perpendicular in the ultrathin lead films at the reduced temperature (t = T/Tc). Distinct oscillations of the normal-state resistivity as a function of film thickness have also been observed. Compared with the Tc oscillation, the Hc2perpendicular shows a considerable large oscillation amplitude and a pi phase shift. The oscillatory mean free path caused by the quantum size effect plays a role in Hc2perpendicular oscillation.

Journal Article↗

[Cu and Zn pollution and soil enzyme activities in sewage irrigation area near smeltery].

This paper studied the Cu and Zn status in soil and rice plant as well as the soil enzyme activities in the sewage irrigation area near a smeltery. The results showed that the soils near the smeltery were polluted. The soil total and extractable Cu contents at the distance of 100 m were 182.45 and 81.91 mg x kg(-1), respectively, 9.3 and 34 times higher than the control. The Cu concentration in different parts of rice was in order of root > leaf and stem > grain, while the Zn concentration was in order of leaf and stem > root > grain. Zn was more mobile than Cu which was likely to accumulate in rice root. It was considered that root could act as a barrier which retarded the upwards transport of Cu and protected the above ground parts of rice from toxication. The Cu contents of rice stem and leaf had a significant correlation with soil Cu contents in the sewage irrigation area. Among the three test enzymes, urease was the most sensitive one to Cu, and its activity had a significant correlation with soil Cu content. Therefore, it is feasible to use soil urease activity as an indicator of soil Cu pollution in sewage irrigation area near the smeltery.

Copper↗

[Effects of Alternaria azukiae on physiological metabolism and active oxygen-eliminating enzyme activities of Trifolium repens].

A pot experiment was installed to study the effects of Alternaria azukiae inoculation on the cell membrane permeability, pigment and MDA contents, and activities of SOD, POD and CAT of Trifolium repens. The results showed that A. azukiae infection made T. repens leaf tissue increase its cell membrane permeability, electric conductivity, over-oxidation and MDA content, but decrease its pigment content. The electric conductivity and MDA content were positively related with infection time, whereas the pigment content was negatively related with it. Due to the stimulation by A. azukiae, the over-oxidation of cell membrane was intensified, which resulted in a large amount of active oxygen accumulated and beyond the defense ability, the active oxygen metabolism system was destroyed, and the balance of protective enzyme system was broken. After 12 days of A. azukiae inoculation, the activities of SOD and CAT decreased by 55.2% and 37.8%, respectively, while the POD activity increased by 1.6 times.

Alternaria↗

Do intradot electron-electron interactions induce dephasing?

We investigate the degree of coherence of electronic transport through a quantum dot (QD) in the presence of an intradot electron-electron interaction. By using an open multiterminal Aharonov-Bohm (AB) setup, we find that the intradot interaction does not induce any dephasing effect and the electron transport through the QD is fully coherent. We also observe that the asymmetric amplitude of the AB oscillation in the conductance through the two-terminal AB setup originates from the interplay between the confined structure and the electron-electron interaction. Thus, one cannot associate a dephasing process with this asymmetric amplitude, as has been done in previous studies.

Journal Article↗

Rotenone-induced apoptosis is mediated by p38 and JNK MAP kinases in human dopaminergic SH-SY5Y cells.

Rotenone is a naturally derived pesticide that has recently been shown to evoke the behavioral and pathological symptoms of Parkinson's disease in animal models. Though rotenone is known to be an inhibitor of the mitochondrial complex I electron transport chain, little is known about downstream pathways leading to its toxicity. We used human dopaminergic SH-SY5Y cells to study mechanisms of rotenone-induced neuronal cell death. Our results suggest that rotenone, at nanomolar concentrations, induces apoptosis in SH-SY5Y cells that is caspase-dependent. Furthermore, rotenone treatment induces phosphorylation of c-Jun, the c-Jun N-terminal protein kinase (JNK), and the p38 mitogen activated protein (MAP) kinase, indicative of activation of the p38 and JNK pathways. Importantly, expression of dominant interfering constructs of the JNK or p38 pathways attenuated rotenone-induced apoptosis. These data suggest that rotenone induces apoptosis in the dopaminergic SH-SY5Y cells that requires activation of the JNK and p38 MAP kinases and caspases. These studies provide insights concerning the molecular mechanisms of rotenone-induced apoptosis in neuronal cells.

Apoptosis↗

ERK5 activation of MEF2-mediated gene expression plays a critical role in BDNF-promoted survival of developing but not mature cortical neurons.

Extracellular signal-regulated kinase 5 (ERK5) is a member of the mitogen-activated protein kinase family whose biological function in the CNS has not been defined. In contrast to ERK1 and ERK2, which are activated by neurotrophins (NTs), cAMP, and neuronal activity in cortical neurons, ERK5 is activated only by NTs. Here, we report that ERK5 expression is high in the brain during early embryonic development but declines as the brain matures to almost undetectable levels by postnatal day (P) 49. Interestingly, expression of a dominant-negative ERK5 blocked brain-derived neurotrophic factor protection against trophic withdrawal in primary cortical neurons cultured from embryonic day (E) 17 but not P0. Furthermore, expression of a dominant-negative ERK5 induced apoptosis in E17 but not P0 cortical neurons maintained in the presence of serum. We also present evidence that ERK5 protection of E17 cortical neurons may be mediated through myocyte enhancer factor 2-induced gene expression. These data suggest that ERK5 activation of myocyte enhancer factor 2-induced gene expression may play an important and novel role in the development of the CNS by mediating NT-promoted survival of embryonic neurons.

Animals↗

Spin-dependent transport through an interacting quantum dot.

We study the nonequilibrium spin transport through a quantum dot coupled to the magnetic electrodes. A formula for the spin-dependent current is obtained and is applied to discuss the linear conductance and magnetoresistance in the interacting regime. We show that the Kondo resonance and the correlation-induced spin splitting of the dot levels may be systematically controlled by internal magnetization in the electrodes. As a result, when the electrodes are in parallel magnetic configuration, the linear conductance is characterized by two spin-resolved peaks. Furthermore, the presence of the spin-flip process in the dot splits the Kondo resonance into three peaks.

Journal Article↗