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Showing 1–18 of 18 results
Advanced filters: Author: Junyuan Gao Clear advanced filters

  • Yongfeng Liu, Xianjin Xu, Junyuan Gao et al. perform in silico screening targeting compounds that resemble both KCNQ1 and PIP2 structures and identify CP1 as a compound that could restore KCNQ1 currents after PIP2 depletion. Like PIP2, this compound can mediate VSD-pore coupling of the channel, albeit via a different mechanism from PIP2.

    • Yongfeng Liu
    • Xianjin Xu
    • Jianmin Cui
    ResearchOpen Access
    Communications Biology
    Volume: 3, P: 1-12

  • An organic regulator that can tune the crystallization sequence of active layer components has been described, achieving a certified efficiency of over 20% in single-junction organic solar cells, demonstrating remarkable tolerance for active layer thickness of 100–400 nm.

    • Haiyang Chen
    • Yuting Huang
    • Yongfang Li
    Research
    Nature Materials
    Volume: 24, P: 444-453

  • Qu et al. report a self-assembled material with π-expanded conjugation to form hydrophilic ordered bilayer as hole selective layer for inverted perovskite solar cells. The enhanced interfacial charge extraction and transport enable certified efficiency of 26.39% and 25.21% for 7.15 mm2 - and 99.12 mm2 -devices, respectively.

    • Geping Qu
    • Letian Zhang
    • Zong-Xiang Xu
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-12

  • Comprehensive analyses of 178 lung squamous cell carcinomas by The Cancer Genome Atlas project show that the tumour type is characterized by complex genomic alterations, with statistically recurrent mutations in 11 genes, including TP53 in nearly all samples; a potential therapeutic target is identified in most of the samples studied.

    • Peter S. Hammerman
    • Michael S. Lawrence
    • Matthew Meyerson
    ResearchOpen Access
    Nature
    Volume: 489, P: 519-525

  • An integrative genomic analysis of several hundred endometrial carcinomas shows that a minority of tumour samples carry copy number alterations or TP53 mutations and many contain key cancer-related gene mutations, such as those involved in canonical pathways and chromatin remodelling; a reclassification of endometrial tumours into four distinct types is proposed, which may have an effect on patient treatment regimes.

    • Douglas A. Levine
    • Gad Getz
    • Douglas A. Levine
    ResearchOpen Access
    Nature
    Volume: 497, P: 67-73

  • The Cancer Genome Atlas Research Network reports an integrative analysis of more than 400 samples of clear cell renal cell carcinoma based on genomic, DNA methylation, RNA and proteomic characterisation; frequent mutations were identified in the PI(3)K/AKT pathway, suggesting this pathway might be a potential therapeutic target, among the findings is also a demonstration of metabolic remodelling which correlates with tumour stage and severity.

    • Chad J. Creighton
    • Margaret Morgan
    • Heidi J. Sofia.
    ResearchOpen Access
    Nature
    Volume: 499, P: 43-49

  • The Cancer Genome Atlas presents an integrative genome-wide analysis of genetic alterations in 279 head and neck squamous cell carcinomas (HNSCCs), which are classified by human papillomavirus (HPV) status; alterations in EGFR, FGFR, PIK3CA and cyclin-dependent kinases are shown to represent candidate targets for therapeutic intervention in most HNSCCs.

    • Michael S. Lawrence
    • Carrie Sougnez
    • Wendell G. Yarbrough
    ResearchOpen Access
    Nature
    Volume: 517, P: 576-582

  • This paper reports integrative molecular analyses of urothelial bladder carcinoma at the DNA, RNA, and protein levels performed as part of The Cancer Genome Atlas project; recurrent mutations were found in 32 genes, including those involved in cell-cycle regulation, chromatin regulation and kinase signalling pathways; chromatin regulatory genes were more frequently mutated in urothelial carcinoma than in any other common cancer studied so far.

    • John N. Weinstein
    • Rehan Akbani
    • Greg Eley
    ResearchOpen Access
    Nature
    Volume: 507, P: 315-322

  • This paper describes molecular subtypes of cervical cancers, including squamous cell carcinoma and adenocarcinoma clusters defined by HPV status and molecular features, and distinct molecular pathways that are activated in cervical carcinomas caused by different somatic alterations and HPV types.

    • Robert D. Burk
    • Zigui Chen
    • David Mutch
    ResearchOpen Access
    Nature
    Volume: 543, P: 378-384

  • An integrated transcriptome, genome, methylome and proteome analysis of over 200 lung adenocarcinomas reveals high rates of somatic mutations, 18 statistically significantly mutated genes including RIT1 and MGA, splicing changes, and alterations in MAPK and PI(3)K pathway activity.

    • Eric A. Collisson
    • Joshua D. Campbell
    • Ming-Sound Tsao
    ResearchOpen Access
    Nature
    Volume: 511, P: 543-550

  • The Cancer Genome Atlas consortium reports on their genome-wide characterization of somatic alterations in colorectal cancer; in addition to revealing a remarkably consistent pattern of genomic alteration, with 24 genes being significantly mutated, the study identifies new targets for therapeutic intervention and suggests an important role for MYC-directed transcriptional activation and repression.

    • Donna M. Muzny
    • Matthew N. Bainbridge
    • Elizabeth Thomson.
    ResearchOpen Access
    Nature
    Volume: 487, P: 330-337

  • The Cancer Genome Atlas Network describe their multifaceted analyses of primary breast cancers, shedding light on breast cancer heterogeneity; although only three genes (TP53, PIK3CA and GATA3) are mutated at a frequency greater than 10% across all breast cancers, numerous subtype-associated and novel mutations were identified.

    • Daniel C. Koboldt
    • Robert S. Fulton
    • Jacqueline D. Palchik
    ResearchOpen Access
    Nature
    Volume: 490, P: 61-70

  • Current clinical practice is organized according to tissue or organ of origin of tumors. Now, The Cancer Genome Atlas (TCGA) Research Network has started to identify genomic and other molecular commonalities among a dozen different types of cancer. Emerging similarities and contrasts will form the basis for targeted therapies of the future and for repurposing existing therapies by molecular rather than histological similarities of the diseases.

    • Kyle Chang
    • Chad J Creighton
    • Joshua M Stuart
    Comments & OpinionOpen Access
    Nature Genetics
    Volume: 45, P: 1113-1120