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Articles by F Chen
Total Records ( 5 ) for F Chen
  H Tang , F Chen , Q Tan , S Tan , L Liu and F. Zhang

Polycomb repressive complex 2 (PRC2), which mediates trimethylation of lysine 27 on histone H3 (K27me3), plays an important role in many types of stem cell differentiation. Here, we try to reveal how PRC2, PRC2-mediated repressive histone marker H3K27me3, and active histone marker histone H4 acetylation (acH4) regulate the CD11b transcription during all-trans retinoic acid (ATRA)-induced HL-60 leukemia cell differentiation. By using quantitative real-time polymerase chain reaction (qPCR) and western blot analysis, we found that the mRNA and protein expression levels of two members of PRC2 were decreased during ATRA-induced HL-60 differentiation, respectively. When treated with ATRA for 72 h, the EZH2 and SUZ12 mRNA levels were decreased to 35% and 38% of the control group, respectively. At the same time, the granulocytic mature surface marker CD11b expression was increased significantly at mRNA level detected by qPCR and protein level detected by flow cytometry. By using chromatin immunoprecipitation assay, we compared the local changes in SUZ12 binding and PRC2-mediated H3K27me3 at the promoter of CD11b during ATRA-induced HL-60 differentiation. Both the levels of SUZ12 binding and PRC2-mediated H3K27me3 at the promoter of CD11b were decreased for 4.1 and 3.8 folds, respectively. And we also found the increase in the acH4 level up to 4 folds after 72 h of ATRA treatment. These results suggested that the histone modification including PRC2-mediated repressive histone marker H3K27me3 and active histone marker acH4 may involve in CD11b transcription during HL-60 leukemia cells reprogramming to terminal differentiation.

  C. y Liu , M. C Wu , F Chen , M Ter Minassian , K Asomaning , R Zhai , Z Wang , L Su , R. S Heist , M. H Kulke , X Lin , G Liu and D. C. Christiani

The incidence of esophageal adenocarcinoma (EA) has been increasing rapidly, particularly among white males, over the past few decades in the USA. However, the etiology of EA and the striking male predominance is not fully explained by known risk factors. To identify susceptible genes for EA risk, we conducted a pathway-based candidate gene association study on 335 Caucasian EA cases and 319 Caucasian controls. A total of 1330 single-nucleotide polymorphisms (SNPs) selected from 354 genes were analyzed using an Illumina GoldenGate assay. The genotyped common SNPs include missense and exonic SNPs, SNPs within untranslated regions and 2 kb 5' of the gene, and tagSNPs for genes with little functional information available. Logistic regression adjusted for potential confounders was used to assess the genetic effect of each SNP on EA risk. We also tested gene–gender interactions using the likelihood ratio tests. We found that the genetic variants in the apoptosis pathway were significantly associated with EA risk after correcting for multiple comparisons. SNPs of rs3127075 in Caspase-7 (CASP7) and rs4661636 in Caspase-9 (CASP9) genes that play a critical role in apoptosis were found to be associated with an increased risk of EA. A protective effect of SNP rs572483 in the progesterone receptor (PGR) gene was observed among women carrying the variant G allele [adjusted odds ratio (OR) = 0.19; 95% confidence interval (CI) = 0.08–0.46] but was not observed among men (adjusted OR = 1.38; 95% CI = 0.95–2.00). In conclusion, this study suggests that the genetic variants of CASP7 and CASP9 in the apoptosis pathway may be important predictive markers for EA susceptibility and that PGR in the sex hormone signaling pathway may be associated with the gender differences in EA risk.

  O Wurtzel , R Sapra , F Chen , Y Zhu , B. A Simmons and R. Sorek

Organisms of the third domain of life, the Archaea, share molecular characteristics both with Bacteria and Eukarya. These organisms attract scientific attention as research models for regulation and evolution of processes such as transcription, translation, and RNA processing. We have reconstructed the primary transcriptome of Sulfolobus solfataricus P2, one of the most widely studied model archaeal organisms. Analysis of 625 million bases of sequenced cDNAs yielded a single-base-pair resolution map of transcription start sites and operon structures for more than 1000 transcriptional units. The analysis led to the discovery of 310 expressed noncoding RNAs, with an extensive expression of overlapping cis-antisense transcripts to a level unprecedented in any bacteria or archaea but resembling that of eukaryotes. As opposed to bacterial transcripts, most Sulfolobus transcripts completely lack 5'-UTR sequences, suggesting that mRNA/ncRNA interactions differ between Bacteria and Archaea. The data also reveal internal hotspots for transcript cleavage linked to RNA degradation and predict sequence motifs that promote RNA destabilization. This study highlights transcriptome sequencing as a key tool for understanding the mechanisms and extent of RNA-based regulation in Bacteria and Archaea.

  F Chen , M. J Gao , Y. S Miao , Y. X Yuan , M. Y Wang , Q Li , B. Z Mao , L. W Jiang and Z. H. He

The rice pattern recognition receptor (PRR) XA21 confers race-specific resistance in leaf infection by bacterial blight Xathomonas oryzae pv. oryzae (Xoo), and was shown to be primarily localized to the endoplasmic reticulum (ER) when expressed with its native promoter or overexpressed in the protoplast. However, whether the protein is still ER-localization in the intact cell when overexpressed remains to be identified. Here, we showed that XA21, its kinase-dead mutant XA21PK736EP, and the triple autophosphorylation mutant XA21PS686A/T688A/S699A GFP fusions were primarily localized to the plasma membrane (PM) when overexpressed in the intact transgenic rice cell, and also localized to the ER in the transgenic protoplast. The transgenic plants constitutively expressing the wild-type XA21 or its GFP fusion displayed race-specific resistance to Xoo at the adult and seedling stages. XA21 and XA21PK736EP could be internalized probably via the SCAMP-positive early endosomal compartment in the protoplast, suggesting that XA21 might be endocytosed to initiate resistance responses during pathogen infection. We also established a root infection system and demonstrated that XA21 also mediated race-specific resistance responses to Xoo in the root. Our current study provides an insight into the nature of the XA21-mediated resistance and a practical approach using the root cell system to further dissect the cellular signaling of the PRR during the rice–Xoo interaction.

  R Pardossi Piquard , S. P Yang , S Kanemoto , Y Gu , F Chen , C Bohm , J Sevalle , T Li , P. C Wong , F Checler , G Schmitt Ulms , P St. George Hyslop and P. E. Fraser

Complexes involved in the /-secretase-regulated intramembranous proteolysis of substrates such as the amyloid-β precursor protein are composed primarily of presenilin (PS1 or PS2), nicastrin, anterior pharynx defective-1 (APH1), and PEN2. The presenilin aspartyl residues form the catalytic site, and similar potentially functional polar transmembrane residues in APH1 have been identified. Substitution of charged (E84A, R87A) or polar (Q83A) residues in TM3 had no effect on complex assembly or activity. In contrast, changes to either of two highly conserved histidines (H171A, H197A) located in TM5 and TM6 negatively affected PS1 cleavage and altered binding to other secretase components, resulting in decreased amyloid generating activity. Charge replacement with His-to-Lys substitutions rescued nicastrin maturation and PS1 endoproteolysis leading to assembly of the formation of structurally normal but proteolytically inactive -secretase complexes. Substitution with a negatively charged side chain (His-to-Asp) or altering the structural location of the histidines also disrupted -secretase binding and abolished functionality of APH1. These results suggest that the conserved transmembrane histidine residues contribute to APH1 function and can affect presenilin catalytic activity.

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