173 results on '"Yin, Jinlong"'
Search Results
152. Synthesis and optical properties of an azo metal chelate compound for optical recording medium
- Author
-
Wang, Shuangqing, primary, Shen, Shuyin, additional, Xu, Huijun, additional, Gu, Donghong, additional, Yin, Jinlong, additional, and Tang, Xiaodong, additional
- Published
- 1999
- Full Text
- View/download PDF
153. Comparison of two types of phthalocyanine thin films
- Author
-
Yin, Jinlong, primary, Gu, Donghong, additional, Tang, Fulong, additional, Tang, Xiaodong, additional, and Gan, Fuxi, additional
- Published
- 1998
- Full Text
- View/download PDF
154. A novel preparative route to a silicalite membrane
- Author
-
Zhang, Changshan, primary, Yin, Jinlong, additional, Xiang, Shouhe, additional, and Li, Hexuan, additional
- Published
- 1996
- Full Text
- View/download PDF
155. Preanodized Cu Surface for Selective CO2Electroreduction to C1or C2+Products
- Author
-
Liu, Chang, Gong, Jun, Li, Jinmeng, Yin, Jinlong, Li, Wenzheng, Gao, Zeyu, Xiao, Li, Wang, Gongwei, Lu, Juntao, and Zhuang, Lin
- Abstract
The electrochemical CO2reduction over Cu catalysts has shown great potential in producing a wide range of valuable chemicals, but it is still plagued by a poor controllability on product distribution. Herein, we demonstrate an effective regulation of CO2reduction paths through a preanodization treatment of Cu foil electrodes in different electrolytes. The Cu electrode exhibits a superior C1and C2+product selectivity after being preanodized in NaClO4(Cu-NaClO4) and Na2HPO4electrolyte (Cu-Na2HPO4), respectively. Combined with in situelectrochemical Raman, ATR-SEIRAS, and SEM characterizations, the preferential C1path is due to the deposition of many Cu nanocrystals with dominant Cu(111) facets on the Cu-NaClO4electrode. In contrast, the preferential C2+path over the Cu-Na2HPO4is attributed to formation of a unique Cu nanodendritic morphology, which strengthens the *CO intermediate adsorption and induces an environment of low local H2O/CO2stoichiometric ratio, thus facilitating C–C coupling for C2+production. Our findings may shed light on the rational control of the CO2reduction path through engineering of the Cu surface structure.
- Published
- 2022
- Full Text
- View/download PDF
156. The MAP3K1/c-JUN signaling axis regulates glioblastoma stem cell invasion and tumor progression.
- Author
-
Zhou, Shuchang, Niu, Rui, Sun, Han, Kim, Sung-Hak, Jin, Xiong, and Yin, Jinlong
- Subjects
- *
CANCER invasiveness , *STEM cells , *GLIOBLASTOMA multiforme , *GLIOMAS , *CORPUS callosum , *CANCER stem cells - Abstract
Glioblastoma (GBM) stem cells (GSCs) are responsible for GBM initiation, progression, infiltration, standard therapy resistance, and recurrence. However, the mechanisms underlying GSC invasion remain incompletely understood. Using public single-cell RNA-Seq data, we identified MAP3K1 as a master regulator of infiltrative GSCs through c-JUN signaling regulation. MAP3K1 knockdown significantly decreased GSC invasion capacity, proliferation, and stemness in vitro. Moreover, in an orthotopic xenograft model, knockdown of MAP3K1 prominently suppressed GSC infiltration along the corpus callosum and tumor progression and prolonged mouse survival. Mechanistically, MAP3K1 regulates GSC invasion through phosphorylation of downstream c-JUN at serine 63 and 73, as confirmed using the CPTAC phosphoproteome dataset. Furthermore, the c-JUN inhibitor JNK-IN-8 significantly decreased GSC invasion, proliferation, and stemness. Taken together, our study demonstrates that MAP3K1 regulates GSC invasion and tumor progression via activation of c-JUN signaling and indicates that the MAP3K1/c-JUN signaling axis is a therapeutic target for infiltrative GBM. • Identified MAP3K1 as a driver gene for glioma infiltration by scRNA-Seq analysis. • MAP3K1/c-JUN signaling axis correlates with poor prognosis of glioma patients. • MAP3K1/c-JUN signaling axis regulates glioblastoma stem cells invasion. • MAP3K1/c-JUN signaling axis is a potential infiltrative glioma therapeutic target. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
157. Blockade of EGFR signaling promotes glioma stem-like cell invasiveness by abolishing ID3-mediated inhibition of p27KIP1 and MMP3 expression
- Author
-
Jin, Xun, Jin, Xiong, Sohn, Young-Woo, Yin, Jinlong, Kim, Sung-Hak, Joshi, Kaushal, Nam, Do-Hyun, Nakano, Ichiro, and Kim, Hyunggee
- Subjects
- *
EPIDERMAL growth factor receptors , *CELLULAR signal transduction , *GLIOMAS , *CANCER stem cells , *CANCER invasiveness , *MATRIX metalloproteinases , *GENE expression , *PROMOTERS (Genetics) , *GENETICS - Abstract
Abstract: Aberrant epidermal growth factor receptor (EGFR) signaling is a typical oncogenic signature in glioblastoma. Here, we show that EGFR inhibition in primary glioma stem cells (GSCs) with oncogenic EGFRvIII and EGFRvIII-transduced glioma stem-like cells promotes invasion by decreasing ID3 levels. ID3 suppresses GSC invasiveness by inhibiting p27KIP1-RhoA-dependent migration and MMP3 expression. Xenograft and human glioblastoma specimens show that ID3 localizes within glioblastoma cores, whereas p27KIP1 and MMP3 are predominantly expressed in glioma cells in invasive fronts. Together, our findings show that EGFR inhibition induces GSC invasiveness by abolishing ID3-mediated inhibition of p27KIP1 and MMP3 expression. [Copyright &y& Elsevier]
- Published
- 2013
- Full Text
- View/download PDF
158. Cross-talk between PARN and EGFR-STAT3 Signaling Facilitates Self-Renewal and Proliferation of Glioblastoma Stem Cells.
- Author
-
Yin J, Seo Y, Rhim J, Jin X, Kim TH, Kim SS, Hong JH, Gwak HS, Yoo H, Park JB, and Kim JH
- Subjects
- Humans, Cell Line, Tumor, Neoplastic Stem Cells pathology, ErbB Receptors genetics, ErbB Receptors metabolism, Cell Proliferation, STAT3 Transcription Factor genetics, STAT3 Transcription Factor metabolism, Gene Expression Regulation, Neoplastic, Glioblastoma pathology, Brain Neoplasms pathology
- Abstract
Glioblastoma is the most common type of malignant primary brain tumor and displays highly aggressive and heterogeneous phenotypes. The transcription factor STAT3 has been reported to play a key role in glioblastoma malignancy. Thus, discovering targets and functional downstream networks regulated by STAT3 that govern glioblastoma pathogenesis may lead to improved treatment strategies. In this study, we identified that poly(A)-specific ribonuclease (PARN), a key modulator of RNA metabolism, activates EGFR-STAT3 signaling to support glioblastoma stem cells (GSC). Functional integrative analysis of STAT3 found PARN as the top-scoring transcriptional target involved in RNA processing in patients with glioblastoma, and PARN expression was strongly correlated with poor patient survival and elevated malignancy. PARN positively regulated self-renewal and proliferation of GSCs through its 3'-5' exoribonuclease activity. EGFR was identified as a clinically relevant target of PARN in GSCs. PARN positively modulated EGFR by negatively regulating the EGFR-targeting miRNA miR-7, and increased EGFR expression created a positive feedback loop to increase STAT3 activation. PARN depletion in GSCs reduced infiltration and prolonged survival in orthotopic brain tumor xenografts; similar results were observed using siRNA nanocapsule-mediated PARN targeting. Pharmacological targeting of STAT3 also confirmed PARN regulation by STAT3 signaling. In sum, these results suggest that a STAT3-PARN regulatory network plays a pivotal role in tumor progression and thus may represent a target for glioblastoma therapeutics., Significance: A positive feedback loop comprising PARN and EGFR-STAT3 signaling supports self-renewal and proliferation of glioblastoma stem cells to drive tumor progression and can be targeted in glioblastoma therapeutics., (©2023 American Association for Cancer Research.)
- Published
- 2023
- Full Text
- View/download PDF
159. Dual-Role of Polyelectrolyte-Tethered Benzimidazolium Cation in Promoting CO 2 /Pure Water Co-Electrolysis to Ethylene.
- Author
-
Xue L, Gao Z, Ning T, Li W, Li J, Yin J, Xiao L, Wang G, and Zhuang L
- Abstract
Electrochemical CO
2 reduction reaction (CO2 RR), as a promising route to realize negative carbon emissions, is known to be strongly affected by electrolyte cations (i.e., cation effect). In contrast to the widely-studied alkali cations in liquid electrolytes, the effect of organic cations grafted on alkaline polyelectrolytes (APE) remains unexplored, although APE has already become an essential component of CO2 electrolyzers. Herein, by studying the organic cation effect on CO2 RR, we find that benzimidazolium cation (Beim+ ) significantly outperforms other commonly-used nitrogenous cations (R4 N+ ) in promoting C2+ (mainly C2 H4 ) production over copper electrode. Cyclic voltammetry and in situ spectroscopy studies reveal that the Beim+ can synergistically boost the CO2 to *CO conversion and reduce the proton supply at the electrocatalytic interface, thus facilitating the *CO dimerization toward C2+ formation. By utilizing the homemade APE ionomer, we further realize efficient C2 H4 production at an industrial-scale current density of 331 mA cm-2 from CO2 /pure water co-electrolysis, thanks to the dual-role of Beim+ in synergistic catalysis and ionic conduction. This study provides a new avenue to boost CO2 RR through the structural design of polyelectrolytes., (© 2023 Wiley-VCH GmbH.)- Published
- 2023
- Full Text
- View/download PDF
160. R SC3 K of soybean cv. Kefeng No.1 confers resistance to soybean mosaic virus by interacting with the viral protein P3.
- Author
-
Jin T, Yin J, Wang T, Xue S, Li B, Zong T, Yang Y, Liu H, Liu M, Xu K, Wang L, Xing G, Zhi H, and Li K
- Subjects
- Viral Proteins, Ribonucleases, Plant Diseases genetics, Glycine max genetics, Potyvirus genetics
- Abstract
Soybean mosaic virus (SMV) is one of the most devastating viral pathogens of soybean (Glycine max (L.) Merr). In total, 22 Chinese SMV strains (SC1-SC22) have been classified based on the responses of 10 soybean cultivars to these pathogens. However, although several SMV-resistance loci in soybean have been identified, no gene conferring SMV resistance in the resistant soybean cultivar (cv.) Kefeng No.1 has been cloned and verified. Here, using F
2 -derived F3 (F2:3 ) and recombinant inbred line (RIL) populations from a cross between Kefeng No.1 and susceptible soybean cv. Nannong 1138-2, we localized the gene in Kefeng No.1 that mediated resistance to SMV-SC3 strain to a 90-kb interval on chromosome 2. To study the functions of candidate genes in this interval, we performed Bean pod mottle virus (BPMV)-induced gene silencing (VIGS). We identified a recombinant gene (which we named RSC3 K) harboring an internal deletion of a genomic DNA fragment partially flanking the LOC100526921 and LOC100812666 reference genes as the SMV-SC3 resistance gene. By shuffling genes between infectious SMV DNA clones based on the avirulent isolate SC3 and virulent isolate 1129, we determined that the viral protein P3 is the avirulence determinant mediating SMV-SC3 resistance on Kefeng No.1. P3 interacts with RNase proteins encoded by RSC3 K, LOC100526921, and LOC100812666. The recombinant RSC3 K conveys much higher anti-SMV activity than LOC100526921 and LOC100812666, although those two genes also encode proteins that inhibit SMV accumulation, as revealed by gene silencing in a susceptible cultivar and by overexpression in Nicotiana benthamiana. These findings demonstrate that RSC3 K mediates the resistance of Kefeng No.1 to SMV-SC3 and that SMV resistance of soybean is determined by the antiviral activity of RNase proteins., (© 2022 Institute of Botany, Chinese Academy of Sciences.)- Published
- 2023
- Full Text
- View/download PDF
161. Preanodized Cu Surface for Selective CO 2 Electroreduction to C 1 or C 2+ Products.
- Author
-
Liu C, Gong J, Li J, Yin J, Li W, Gao Z, Xiao L, Wang G, Lu J, and Zhuang L
- Abstract
The electrochemical CO
2 reduction over Cu catalysts has shown great potential in producing a wide range of valuable chemicals, but it is still plagued by a poor controllability on product distribution. Herein, we demonstrate an effective regulation of CO2 reduction paths through a preanodization treatment of Cu foil electrodes in different electrolytes. The Cu electrode exhibits a superior C1 and C2+ product selectivity after being preanodized in NaClO4 (Cu- NaClO4 ) and Na2 HPO4 electrolyte (Cu- Na2 HPO4 ), respectively. Combined with in situ electrochemical Raman, ATR-SEIRAS, and SEM characterizations, the preferential C1 path is due to the deposition of many Cu nanocrystals with dominant Cu(111) facets on the Cu- NaClO4 electrode. In contrast, the preferential C2+ path over the Cu- Na2 HPO4 is attributed to formation of a unique Cu nanodendritic morphology, which strengthens the *CO intermediate adsorption and induces an environment of low local H2 O/CO2 stoichiometric ratio, thus facilitating C-C coupling for C2+ production. Our findings may shed light on the rational control of the CO2 reduction path through engineering of the Cu surface structure.- Published
- 2022
- Full Text
- View/download PDF
162. Blood-brain barrier-penetrating single CRISPR-Cas9 nanocapsules for effective and safe glioblastoma gene therapy.
- Author
-
Zou Y, Sun X, Yang Q, Zheng M, Shimoni O, Ruan W, Wang Y, Zhang D, Yin J, Huang X, Tao W, Park JB, Liang XJ, Leong KW, and Shi B
- Subjects
- Animals, Blood-Brain Barrier, CRISPR-Cas Systems, Gene Editing, Genetic Therapy, Mice, RNA, Guide, CRISPR-Cas Systems genetics, Glioblastoma genetics, Glioblastoma therapy, Nanocapsules
- Abstract
We designed a unique nanocapsule for efficient single CRISPR-Cas9 capsuling, noninvasive brain delivery and tumor cell targeting, demonstrating an effective and safe strategy for glioblastoma gene therapy. Our CRISPR-Cas9 nanocapsules can be simply fabricated by encapsulating the single Cas9/sgRNA complex within a glutathione-sensitive polymer shell incorporating a dual-action ligand that facilitates BBB penetration, tumor cell targeting, and Cas9/sgRNA selective release. Our encapsulating nanocapsules evidenced promising glioblastoma tissue targeting that led to high PLK1 gene editing efficiency in a brain tumor (up to 38.1%) with negligible (less than 0.5%) off-target gene editing in high-risk tissues. Treatment with nanocapsules extended median survival time (68 days versus 24 days in nonfunctional sgRNA-treated mice). Our new CRISPR-Cas9 delivery system thus addresses various delivery challenges to demonstrate safe and tumor-specific delivery of gene editing Cas9 ribonucleoprotein for improved glioblastoma treatment that may potentially be therapeutically useful in other brain diseases.
- Published
- 2022
- Full Text
- View/download PDF
163. Discovery and characterization of differentially expressed soybean miRNAs and their targets during soybean mosaic virus infection unveils novel insight into Soybean-SMV interaction.
- Author
-
Li B, Karthikeyan A, Wang L, Yin J, Jin T, Liu H, Li K, Gai J, and Zhi H
- Subjects
- Plant Diseases genetics, Glycine max genetics, Glycine max metabolism, MicroRNAs genetics, MicroRNAs metabolism, Potyvirus genetics
- Abstract
Background: Soybean mosaic virus (SMV) is one of the most devastating pathogens of soybean. MicroRNAs (miRNAs) are a class of non-coding RNAs (21-24 nucleotides) which are endogenously produced by the plant host as part of a general gene expression regulatory mechanisms, but also play roles in regulating plant defense against pathogens. However, miRNA-mediated plant response to SMV in soybean is not as well documented., Result: In this study, we analyzed 18 miRNA libraries, including three biological replicates from two soybean lines (Resistant and susceptible lines to SMV strain SC3 selected from the near-isogenic lines of Qihuang No. 1 × Nannong1138-2) after virus infection at three different time intervals (0 dpi, 7 dpi and 14 dpi). A total of 1,092 miRNAs, including 608 known miRNAs and 484 novel miRNAs were detected. Differential expression analyses identified the miRNAs profile changes during soybean-SMV interaction. Then, miRNAs potential target genes were predicted via data mining, and functional annotation was done by Gene Ontology (GO) analysis. The expression patterns of several miRNAs were validated by quantitative real-time PCR. We also validated the miRNA-target gene interaction by agrobacterium-mediated transient expression in Nicotiana benthamiana., Conclusion: We have identified a large number of miRNAs and their target genes and also functional annotations. We found that multiple miRNAs were differentially expressed in the two lines and targeted a series of NBS-LRR resistance genes. It is worth mentioning that many of these genes exist in the previous fine-mapping interval of the resistance gene locus. Our study provides additional information on soybean miRNAs and an insight into the role of miRNAs during SMV-infection in soybean., (© 2022. The Author(s).)
- Published
- 2022
- Full Text
- View/download PDF
164. Polymeric nanoparticle mediated inhibition of miR-21 with enhanced miR-124 expression for combinatorial glioblastoma therapy.
- Author
-
Liu Y, Zheng M, Jiao M, Yan C, Xu S, Du Q, Morsch M, Yin J, and Shi B
- Subjects
- Cell Line, Tumor, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Brain Neoplasms drug therapy, Brain Neoplasms genetics, Glioblastoma drug therapy, Glioblastoma genetics, MicroRNAs genetics, Nanoparticles
- Abstract
Glioblastoma (GBM) is the most common and fatal form of malignant brain tumor. Despite intensive effort, there is still no effective GBM treatment. Therefore, novel and more effective GBM therapeutic approaches are highly desired. In this study, we combined polymeric nanotechnology with microRNA (miRNA) regulation technology to develop a targeted polymeric nanoparticle to co-deliver anti-miR-21 and miR-124 into the brain to effectively treat GBM. The polymeric nanoparticle decorated with Angiopep-2 peptide not only can encapsulate miRNA via triple-interaction (electrostatic, hydrogen bond and hydrophobic bonding) to protect miRNA against enzyme degradation in the blood, but also is capable of crossing blood brain barrier (BBB) and allowing targeted delivery of miRNAs to GBM tissue due to the dual-targeting function of Angiopep-2. Moreover, the co-delivered anti-miR-21 and miR-124 simultaneously regulated the mutant RAS/PI3K/PTEN/AKT signaling pathway in tumor cells, consequently achieving combinatorial GBM therapy. This combinatorial effect was confirmed by our results showing that these miRNA nanomedicines can effectively reduce tumor cell proliferation, migration and invasion as well as reducing tumor angiogenesis. Consequently, effective suppression of tumor growth and significantly improved medium survival time are observed when these miRNA nanomedicines were assessed in an orthotopic GBM xenograft model. This work indicated that our new polymeric nanoparticles successfully mediate inhibition of miR-21 and miR-124 supplementation to significantly reduce tumorigenesis, and may have strong potential in GBM therapy., (Copyright © 2021 Elsevier Ltd. All rights reserved.)
- Published
- 2021
- Full Text
- View/download PDF
165. Transcriptional regulatory networks of tumor-associated macrophages that drive malignancy in mesenchymal glioblastoma.
- Author
-
Sa JK, Chang N, Lee HW, Cho HJ, Ceccarelli M, Cerulo L, Yin J, Kim SS, Caruso FP, Lee M, Kim D, Oh YT, Lee Y, Her NG, Min B, Kim HJ, Jeong DE, Kim HM, Kim H, Chung S, Woo HG, Lee J, Kong DS, Seol HJ, Lee JI, Kim J, Park WY, Wang Q, Sulman EP, Heimberger AB, Lim M, Park JB, Iavarone A, Verhaak RGW, and Nam DH
- Subjects
- Animals, Carcinogenesis, Cell Line, Tumor, Disease Models, Animal, Gene Expression Regulation, Neoplastic, Glioblastoma metabolism, Glioblastoma pathology, Glioma genetics, Humans, Immunotherapy, Macrophages metabolism, Mice, Neurofibromin 1 genetics, Phenotype, Prognosis, Stem Cells, Transcriptome, Tumor Microenvironment, Gene Regulatory Networks, Glioblastoma genetics, Tumor-Associated Macrophages
- Abstract
Background: Glioblastoma (GBM) is a complex disease with extensive molecular and transcriptional heterogeneity. GBM can be subcategorized into four distinct subtypes; tumors that shift towards the mesenchymal phenotype upon recurrence are generally associated with treatment resistance, unfavorable prognosis, and the infiltration of pro-tumorigenic macrophages., Results: We explore the transcriptional regulatory networks of mesenchymal-associated tumor-associated macrophages (MA-TAMs), which drive the malignant phenotypic state of GBM, and identify macrophage receptor with collagenous structure (MARCO) as the most highly differentially expressed gene. MARCO
high TAMs induce a phenotypic shift towards mesenchymal cellular state of glioma stem cells, promoting both invasive and proliferative activities, as well as therapeutic resistance to irradiation. MARCOhigh TAMs also significantly accelerate tumor engraftment and growth in vivo. Moreover, both MA-TAM master regulators and their target genes are significantly correlated with poor clinical outcomes and are often associated with genomic aberrations in neurofibromin 1 (NF1) and phosphoinositide 3-kinases/mammalian target of rapamycin/Akt pathway (PI3K-mTOR-AKT)-related genes. We further demonstrate the origination of MA-TAMs from peripheral blood, as well as their potential association with tumor-induced polarization states and immunosuppressive environments., Conclusions: Collectively, our study characterizes the global transcriptional profile of TAMs driving mesenchymal GBM pathogenesis, providing potential therapeutic targets for improving the effectiveness of GBM immunotherapy.- Published
- 2020
- Full Text
- View/download PDF
166. A DnaJ protein that interacts with soybean mosaic virus coat protein serves as a key susceptibility factor for viral infection.
- Author
-
Zong T, Yin J, Jin T, Wang L, Luo M, Li K, and Zhi H
- Subjects
- Host Microbial Interactions, Protein Binding, Capsid Proteins metabolism, HSP40 Heat-Shock Proteins metabolism, Plant Diseases virology, Plant Proteins metabolism, Potyvirus physiology, Glycine max metabolism, Glycine max virology, Virus Diseases virology
- Abstract
Soybean mosaic virus (SMV)-disease is one of the most serious and widespread diseases in soybean (Glycine max). In the present study, a DnaJ protein in soybean designated GmCPIP (SMV coat protein-interacting protein) was screened by the QIS-Seq (quantitative interactor screening with next-generation sequencing) method, and the interaction between SMV CP and GmCPIP was confirmed by the yeast two-hybrid (Y2H) system and bimolecular fluorescence complementation (BiFC) assay. Subcellular localization analysis indicated that both proteins are localized in the cytoplasm, cytomembrane and nucleus. Quantitative real-time polymerase chain reaction (qRT-PCR) analysis showed that infection with SMV-SC4 temporarily increased the transcription of GmCPIP. Virus-induced gene silencing (VIGS) down-regulated the GmCPIP gene by 82%, and the accumulation of SMV was decreased by 88.6% in GmCPIP-silenced plants inoculated with SMV-SC4. The interaction of GmCPIP with SMV CP seems to contribute to SMV infection in soybean., (Copyright © 2020 Elsevier B.V. All rights reserved.)
- Published
- 2020
- Full Text
- View/download PDF
167. Discovery of the Agrobacterium growth inhibition sequence in virus and its application to recombinant clone screening.
- Author
-
Yin J, Liu H, Xiang W, Jin T, Guo D, Wang L, and Zhi H
- Abstract
Infectious clone vectors used widely in genetic research. While constructing soybean mosaic virus (SMV) clone vectors, we found that transformed Agrobacterium grew significantly different depending on the viral strains used. In particular, the clone vectors constructed with SMV SC15 significantly suppressed the growth of Agrobacterium. Recombinant and truncated virus vector experiments showed that the polymorphism of a P1 protein coding sequence of SC15 leads to the growth inhibition of Agrobacterium. But the lack of other protein encoding sequences, except for the sequence encoding coat protein, should reduce the ability of SC15 to suppress Agrobacterium growth. A vector (pCB301-attL-SC15P) compatible with the Gateway cloning system was constructed using this Agrobacterium inhibitory sequence. The results from the LR recombination reaction with pCB301-attL-SC15P and Agrobacterium transformation showed the valuable application potential of the Agrobacterium inhibitory sequence to serve as a negative screening factor for effective recombinant clone screening in Agrobacterium.
- Published
- 2019
- Full Text
- View/download PDF
168. Fine-mapping and identifying candidate genes conferring resistance to Soybean mosaic virus strain SC20 in soybean.
- Author
-
Karthikeyan A, Li K, Li C, Yin J, Li N, Yang Y, Song Y, Ren R, Zhi H, and Gai J
- Subjects
- Amino Acid Sequence, China, Chromosome Mapping, Genes, Dominant, Genetic Markers, Phenotype, Plant Diseases virology, Glycine max virology, Disease Resistance genetics, Genes, Plant, Plant Diseases genetics, Potyvirus, Glycine max genetics
- Abstract
Key Message: The Mendelian gene conferring resistance to Soybean mosaic virus Strain SC20 in soybean was fine-mapped onto a 79-kb segment on Chr.13 where two closely linked candidate genes were identified and qRT-PCR verified. Soybean mosaic virus (SMV) threatens the world soybean production, particularly in China. A country-wide SMV strain system composed of 22 strains was established in China, among which SC20 is a dominant strain in five provinces in Southern China. Resistance to SC20 was evaluated in parents, F
1 , F2 and the F2:7 RIL (recombinant inbred line) population derived from a cross between Qihuang-1 (resistant) and NN1138-2 (susceptible). The segregation ratio of resistant to susceptible in the populations suggested a single dominant gene involved in the resistance to SC20 in Qihuang-1. A "partial genome mapping strategy" was used to map the resistance gene on Chromosome 13. Linkage analysis between 178 RILs and genetic markers showed that the SC20-resistance gene located at 3.9 and 3.8 cM to the flanking markers BARCSOYSSR_13_1099 and BARCSOYSSR_13_1185 on Chromosome 13. Subsequently, a residual heterozygote segregating population with 346 individuals was developed by selfing four plants heterozygous at markers adjacent to the tentative SC20-resistance gene; then, the candidate region was delimited to a genomic interval of approximately 79 kb flanked by the new markers gm-ssr_13-14 and gm-indel_13-3. Among the seven annotated candidate genes in this region, two genes, Glyma.13G194700 and Glyma.13G195100, encoding Toll Interleukin Receptor-nucleotide-binding-leucine-rich repeat resistance proteins were identified as candidate resistance genes by quantitative real-time polymerase chain reaction and sequence analysis. The two closely linked genes work together to cause the phenotypic segregation as a single Mendelian gene. These results will facilitate marker-assisted selection, gene cloning and breeding for the resistance to SC20.- Published
- 2018
- Full Text
- View/download PDF
169. Inhibition of BMP signaling overcomes acquired resistance to cetuximab in oral squamous cell carcinomas.
- Author
-
Yin J, Jung JE, Choi SI, Kim SS, Oh YT, Kim TH, Choi E, Lee SJ, Kim H, Kim EO, Lee YS, Chang HJ, Park JY, Kim Y, Yun T, Heo K, Kim YJ, Kim H, Kim YH, Park JB, and Choi SW
- Subjects
- Animals, Bone Morphogenetic Protein Receptors, Type I antagonists & inhibitors, Bone Morphogenetic Protein Receptors, Type I metabolism, Bone Morphogenetic Proteins antagonists & inhibitors, Bone Morphogenetic Proteins metabolism, Carcinoma, Squamous Cell metabolism, Carcinoma, Squamous Cell pathology, Cell Line, Tumor, Cetuximab administration & dosage, ErbB Receptors metabolism, Humans, Mice, Nude, Mouth Neoplasms metabolism, Mouth Neoplasms pathology, Pyrazoles administration & dosage, Quinolines administration & dosage, Signal Transduction drug effects, Smad Proteins metabolism, Antineoplastic Combined Chemotherapy Protocols pharmacology, Carcinoma, Squamous Cell drug therapy, Drug Resistance, Neoplasm drug effects, Mouth Neoplasms drug therapy, Xenograft Model Antitumor Assays
- Abstract
Despite expressing high levels of the epidermal growth factor receptor (EGFR), a majority of oral squamous cell carcinoma (OSCC) patients show limited response to cetuximab and ultimately develop drug resistance. However, mechanism underlying cetuximab resistance in OSCC is not clearly understood. Here, using a mouse orthotopic xenograft model of OSCC, we show that bone morphogenic protein-7-phosphorylated Smad-1, -5, -8 (BMP7-p-Smad1/5/8) signaling contributes to cetuximab resistance. Tumor cells isolated from the recurrent cetuximab-resistant xenograft models exhibited low EGFR expression but extremely high levels of p-Smad1/5/8. Treatment with the bone morphogenic protein receptor type 1 (BMPRI) inhibitor, DMH1 significantly reduced cetuximab-resistant OSCC tumor growth, and combined treatment of DMH1 and cetuximab remarkably reduced relapsed tumor growth in vivo. Importantly, p-Smad1/5/8 level was elevated in cetuximab-resistant patients and this correlated with poor prognosis. Collectively, our results indicate that the BMP7-p-Smad1/5/8 signaling is a key pathway to acquired cetuximab resistance, and demonstrate that combination therapy of cetuximab and a BMP signaling inhibitor as potentially a new therapeutic strategy for overcoming acquired resistance to cetuximab in OSCC., (Copyright © 2017 Elsevier B.V. All rights reserved.)
- Published
- 2018
- Full Text
- View/download PDF
170. Fine-mapping and identification of a novel locus Rsc15 underlying soybean resistance to Soybean mosaic virus.
- Author
-
Rui R, Liu S, Karthikeyan A, Wang T, Niu H, Yin J, Yang Y, Wang L, Yang Q, Zhi H, and Li K
- Subjects
- Alleles, Chromosome Mapping, Genes, Dominant, Genes, Plant, Genotype, Microsatellite Repeats, Plant Diseases virology, Glycine max virology, Disease Resistance genetics, Plant Diseases genetics, Potyvirus, Glycine max genetics
- Abstract
Key Message: Rsc15, a novel locus underlying soybean resistance to SMV, was fine mapped to a 95-kb region on chromosome 6. The Rsc15- mediated resistance is likely attributed to the gene GmPEX14 , the relative expression of which was highly correlated with the accumulation of H
2 O2 along with the activities of POD and CAT during the early stages of SMV infection in RN-9. Soybean mosaic virus (SMV) causes severe yield losses and seed quality deterioration in soybean [Glycine max (L.) Merr.] worldwide. A series of single dominant SMV resistance genes have been identified on respective soybean chromosomes 2, 13 and 14, while one novel locus, Rsc15, underlying resistance to the virulent SMV strain SC15 from soybean cultivar RN-9 has been recently mapped to a 14.6-cM region on chromosome 6. However, candidate gene has not yet been identified within this region. In the present study, we aimed to fine map the Rsc15 region and identify candidate gene(s) for this invaluable locus. High-resolution fine-mapping revealed that the Rsc15 gene was located in a 95-kb genomic region which was flanked by the two simple sequence repeat (SSR) markers SSR_06_17 and BARCSOYSSR_06_0835. Allelic sequence comparison and expression profile analysis of candidate genes inferred that the gene Glyma.06g182600 (designated as GmPEX14) was the best candidate gene attributing for the resistance of Rsc15, and that genes encoding receptor-like kinase (RLK) (i.e., Glyma.06g175100 and Glyma.06g184400) and serine/threonine kinase (STK) (i.e., Glyma.06g182900 and Glyma.06g183500) were also potential candidates. High correlations were established between the relative expression level of GmPEX14 and the hydrogen peroxide (H2 O2 ) concentration and activities of catalase (CAT) and peroxidase (POD) during the early stages of SMV-SC15 infection in RN-9. The results of the present study will be useful in marker-assisted breeding for SMV resistance and will lead to further understanding of the molecular mechanisms of host resistance against SMV.- Published
- 2017
- Full Text
- View/download PDF
171. Enhancement of the Hydrogen Evolution Reaction from Ni-MoS 2 Hybrid Nanoclusters.
- Author
-
Escalera-López D, Niu Y, Yin J, Cooke K, Rees NV, and Palmer RE
- Abstract
This report focuses on a novel strategy for the preparation of transition metal-MoS
2 hybrid nanoclusters based on a one-step, dual-target magnetron sputtering, and gas condensation process demonstrated for Ni-MoS2 . Aberration-corrected STEM images coupled with EDX analysis confirms the presence of Ni and MoS2 in the hybrid nanoclusters (average diameter = 5.0 nm, Mo:S ratio = 1:1.8 ± 0.1). The Ni-MoS2 nanoclusters display a 100 mV shift in the hydrogen evolution reaction (HER) onset potential and an almost 3-fold increase in exchange current density compared with the undoped MoS2 nanoclusters, the latter effect in agreement with reported DFT calculations. This activity is only reached after air exposure of the Ni-MoS2 hybrid nanoclusters, suggested by XPS measurements to originate from a Ni dopant atoms oxidation state conversion from metallic to 2+ characteristic of the NiO species active to the HER. Anodic stripping voltammetry (ASV) experiments on the Ni-MoS2 hybrid nanoclusters confirm the presence of Ni-doped edge sites and reveal distinctive electrochemical features associated with both doped Mo-edge and doped S-edge sites which correlate with both their thermodynamic stability and relative abundance.- Published
- 2016
- Full Text
- View/download PDF
172. Tumoral RANKL activates astrocytes that promote glioma cell invasion through cytokine signaling.
- Author
-
Kim JK, Jin X, Sohn YW, Jin X, Jeon HY, Kim EJ, Ham SW, Jeon HM, Chang SY, Oh SY, Yin J, Kim SH, Park JB, Nakano I, and Kim H
- Subjects
- Animals, Brain Neoplasms mortality, Brain Neoplasms pathology, Cell Line, Tumor, Cell Movement, Glioblastoma mortality, Glioblastoma pathology, Humans, Kaplan-Meier Estimate, Mice, Mice, Inbred BALB C, Mice, Nude, NF-kappa B metabolism, Neoplasm Invasiveness, Neoplasm Transplantation, Signal Transduction, Tumor Microenvironment, Astrocytes physiology, Brain Neoplasms metabolism, Cytokines physiology, Glioblastoma metabolism, RANK Ligand physiology
- Abstract
The invasiveness of glioblastoma is a major cause of poor prognosis and relapse. However, the molecular mechanism controlling glioma cell invasion is poorly understood. Here, we report that receptor activator of nuclear factor kappa-B (NFκB) ligand (RANKL) promotes glioma cell invasion in vivo, but not in vitro. Unlike the invasiveness under in vitro culture conditions, in vivo xenograft studies revealed that LN229 cells expressing high endogenous RANKL generated more invasive tumors than U87MG cells expressing relatively low endogenous RANKL. Consistently, RANKL-overexpressing U87MG resulted in invasive tumors, whereas RANKL-depleted LN229 generated rarely invasive tumors. We found that the number of activated astrocytes was markedly increased in the periphery of RANKL-high invasive tumors. RANKL activated astrocytes through NFκB signaling and these astrocytes in turn secreted various factors which regulate glioma cell invasion. Among them, transforming growth factor β (TGF-β) signaling was markedly increased in glioblastoma specimens and xenograft tumors expressing high levels of RANKL. These results indicate that RANKL contributes to glioma invasion by modulating the peripheral microenvironment of the tumor, and that targeting RANKL signaling has important implications for the prevention of highly invasive glioblastoma., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
173. Blockade of EGFR signaling promotes glioma stem-like cell invasiveness by abolishing ID3-mediated inhibition of p27(KIP1) and MMP3 expression.
- Author
-
Jin X, Jin X, Sohn YW, Yin J, Kim SH, Joshi K, Nam DH, Nakano I, and Kim H
- Subjects
- Animals, Cell Line, Tumor, Cell Movement drug effects, Cell Movement genetics, ErbB Receptors genetics, ErbB Receptors metabolism, Glioma genetics, Humans, Inhibitor of Differentiation Proteins genetics, Mice, Neoplasm Proteins genetics, Quinazolines pharmacology, Quinazolines toxicity, Tyrphostins pharmacology, Tyrphostins toxicity, Cyclin-Dependent Kinase Inhibitor p27 metabolism, ErbB Receptors antagonists & inhibitors, Glioma metabolism, Inhibitor of Differentiation Proteins metabolism, Matrix Metalloproteinase 3 metabolism, Neoplasm Proteins metabolism, Neoplastic Stem Cells metabolism, Signal Transduction drug effects
- Abstract
Aberrant epidermal growth factor receptor (EGFR) signaling is a typical oncogenic signature in glioblastoma. Here, we show that EGFR inhibition in primary glioma stem cells (GSCs) with oncogenic EGFRvIII and EGFRvIII-transduced glioma stem-like cells promotes invasion by decreasing ID3 levels. ID3 suppresses GSC invasiveness by inhibiting p27(KIP1)-RhoA-dependent migration and MMP3 expression. Xenograft and human glioblastoma specimens show that ID3 localizes within glioblastoma cores, whereas p27(KIP1) and MMP3 are predominantly expressed in glioma cells in invasive fronts. Together, our findings show that EGFR inhibition induces GSC invasiveness by abolishing ID3-mediated inhibition of p27(KIP1) and MMP3 expression., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2013
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.