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Associations between polymorphisms in the NICD domain of bovine NOTCH1 gene and growth traits in Chinese Qinchuan cattle

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Liu M., Zhang C., Lai X., Xue J., Lan X., Lei C., Jia Y., Chen H.
Journal of Applied Genetics
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2017
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tom 58
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nr 2
2

Upregulation of CCL3/MIP-1alpha regulated by MAPKs and NF-kappaB mediates microglial inflammatory response in LPS-induced brain injury

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Zhu X., Wei D., Chen O., Zhang Z., Xue J., Huang S., Zhu W., Wang Y.
Acta Neurobiologiae Experimentalis
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2016
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tom 76
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nr 4
Growing evidence suggests that macrophage inflammatory protein (MIP)‑1alpha (synonym CCL3) is upregulated in the neuroinflammatory processes initiated by some brain disorders, but its precise role and regulatory mechanism remain unclear. The present work aims to evaluate the role of CCL3/MIP‑1alpha in lipopolysaccharide (LPS)‑induced brain injury, and investigate whether the MAPKs and NF‑kappaB regulate CCL3/MIP‑1alpha expression. We firstly examined the patterns of CCL3/MIP‑1alpha expression and phosphorylation of MAPKs in the brains of rats 6, 24, and 72 h after LPS administration. Additionally, LPS‑treated rats were administered an anti‑MIP‑1alpha neutralizing antibody, and the microglial reaction and the expression of both cyclooxygenase‑2 and inducible nitric oxide synthase (iNOS) were analyzed. We finally evaluated the effect of an inhibitor of P38 MAPK, an inhibitor of ERK1/2, or an inhibitor of NF‑kappaB, on the levels of CCL3/MIP‑1alpha protein and numbers of microglia in the brain. In the observation period, LPS induced CCL3/MIP‑1alpha expression, which localized to OX‑42‑labeled microglia, leading to time‑dependent increases in the phosphorylation of P38 MAPK and ERK1/2. The expression pattern of induced CCL3/MIP‑1alpha was partly consistent with the phosphorylation of MAPKs (P38 MAPK, ERK1/2). Anti‑MIP‑1alpha attenuated microglial accumulation and the upregulation of cyclooxygenase‑2 and iNOS. The inhibition of P38 MAPK, ERK1/2, or NF‑kappaB signaling reduced the induced upregulation of CCL3/MIP‑1alpha and the microglial accumulation. Our data suggest that upregulated CCL3/MIP‑1alpha mediates the accumulation of microglia and the neuroinflammatory reaction, and its expression may be regulated by MAPKs and NF‑kappaB in LPS‑induced brain injury.
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Identification and expression of GA-related genes associated with in vitro micro-tubers formation in Pinellia ternata

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Xue T., Yue E., Chao E., Su Y., Zhang W., Zhu Y., Teng J., Xue J.
Acta Scientiarum Polonorum. Hortorum Cultus
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2018
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tom 17
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nr 6
Pinellia ternata is one of the most important herbs in traditional Chinese medicine. Recently, its yield is hard to meet the market demand, therefore the system of in vitro micro-tubers was developed for its propagation and endogenous GA was revealed probably function negatively during micro-tubers induction. However, the mechanism is still unknown. In this study, 70 mg/L chlormequat chloride (CCC) was successfully used to inhibit the endogenous GA content and promote the micro-tubers induction. Subsequently, suppression subtractive hybridization (SSH) was performed to identify GA-related genes associated with in vitro micro-tubers formation in P. ternata. The cDNAs of micro-tubers induced with and without CCC were used as the “tester”, and “driver”, respectively. SSH library sequencing yielded 300 expressed sequence tags (ESTs). Finally, 226 ESTs were retained after screening, 84 of which had no significant homology to any of previously identified genes and 39 of the remaining 142 ESTs represented singletons. Real-time quantitative RT-PCR analysis of the expression patterns showed that all 5 transcripts showed signal alteration during the process of in vitro micro-tubers formation. The sequences appeared to be highly homologous with 60S ribosomal protein, 26S ribosomal RNA gene, zinc transporter protein, 12kD storage protein and malate dehydrogenase, respectively. These results would facilitate the functional characterization of the GA-related genes associated with in vitro micro-tubers development and subsequent in vitro manipulation.
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