Results 151 to 160 of about 24,694 (278)

Structural characterization of the D290V mutation site in hnRNPA2 low-complexity-domain polymers. [PDF]

open access: yes, 2018
Human genetic studies have given evidence of familial, disease-causing mutations in the analogous amino acid residue shared by three related RNA binding proteins causative of three neurological diseases. Alteration of aspartic acid residue 290 of hnRNPA2
Kato, Masato   +5 more
core  

MiR‐375 in CAFs‐Derived EVs Promotes HCC Progression via Regulating RASA1 and May Potentially Serve as a Biomarker for HCC

open access: yesCancer Science, EarlyView.
CAFs could transfer EVs miR‐375 into endothelial cells with a low level of RASA1 and further promote EC angiogenesis. Plasma EVs miR‐375 have the potential values as a novel diagnostic and prognostic biomarker for HCC. ABSTRACT Cancer‐associated fibroblasts (CAFs) in the tumor microenvironment play an important role in cancer initiation and progression
Wei Qin   +6 more
wiley   +1 more source

MTAP Deficiency as a Metabolic Vulnerability in Cancer: Implications for Synthetic Lethal Therapy

open access: yesCancer Science, EarlyView.
MTAP deletion creates a therapeutically actionable metabolic vulnerability through MTA accumulation and PRMT5 dependency. This review summarizes the biochemical basis of MTAP‐directed synthetic lethality, emerging PRMT5/MAT2A inhibitors, clinicogenomic features of MTAP‐deleted tumors, and future strategies for precision oncology.
Hiroaki Ikushima, Hidenori Kage
wiley   +1 more source

Multiplexed Transcriptomics for Screening Drug Combinations and Defining the Mechanism of Action of HCC Therapeutics at Single‐Cell Resolution

open access: yesCell Proliferation, EarlyView.
We designed a framework for screening clinical drug combinations with anti‐hepatocellular carcinoma (HCC) activity, comprising four parts: primary screening, single‐cell screening, functional validation, and mechanism research. High‐throughput single‐cell screening identifies HY (HHT and YM155) as a potent anti‐HCC drug combination, validated by in ...
Mengmeng Jiang   +12 more
wiley   +1 more source

Proteostasis of organelles in aging and disease

open access: yesThe FEBS Journal, EarlyView.
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi   +5 more
wiley   +1 more source

Genetic dissection reveals distinct contributions of the eS31 N‐terminal domain to translational accuracy in Saccharomyces cerevisiae

open access: yesThe FEBS Journal, EarlyView.
The eukaryote‐specific N‐terminal domain (NTD) of eS31 uses two distinct strategies to maintain translation fidelity. During elongation, a positively charged “hotspot” fine‐tunes the selection of incoming aa‐tRNA. During termination, the entire NTD acts as a structural scaffold to ensure the correct positioning of the release factor eRF1.
Qingxuan Gao   +3 more
wiley   +1 more source

Unraveling in vitro phase separation and aggregation properties of the structured region of FMRP and the impact of Fragile X syndrome‐linked mutations

open access: yesThe FEBS Journal, EarlyView.
Fragile X messenger ribonucleoprotein 1 (FMRP) is a multidomain RNA‐binding protein associated with Fragile X Syndrome (FXS). We found that its N‐terminal structured region has an intrinsic propensity to undergo liquid–liquid phase separation and fibril formation. FXS‐associated mutations perturb protein stability and aggregation propensity, suggesting
Flavia Catalano   +10 more
wiley   +1 more source

Australian clinical practice guideline: diagnosis and treatment of idiopathic multicentric Castleman disease

open access: yesInternal Medicine Journal, EarlyView.
Abstract Idiopathic multicentric Castleman disease (iMCD) is a rare condition. The pathogenesis is incompletely understood; however, interleukin‐6 (IL‐6) is a major mediator. The clinical presentation is heterogeneous, from mild constitutional symptoms to severe multi‐organ failure.
Dipti Talaulikar   +16 more
wiley   +1 more source

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