Results 131 to 140 of about 260,635 (281)

AARS1‐Mediated H3K27 Lactylation Rewires Glycolysis to Sustain Aggressive and Recurrent Bladder Cancer

open access: yesAdvanced Science, EarlyView.
AARS1 drives PI3K–AKT–mTOR‐dependent glycolysis in bladder cancer, promoting lactate accumulation, increased lactylation, H3K27la enrichment at the HK2 promoter, and HK2 transcription. HK2 reinforces glycolysis, sustaining a metabolic–epigenetic program associated with tumor progression, recurrence, and metastasis.
Qin Yuan   +13 more
wiley   +1 more source

YTHDC1 Orchestrates Glucose and Glutamate Rewiring to Overcome Lethal Metabolic Stress in Triple‐Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
Lai et al. find that m6A reader YTHDC1 is specifically overexpressed in triple‐negative breast cancer (TNBC) and orchestrates glucose and glutamine metabolism in an m6A‐dependent manner to confer robust adaptability to lethal metabolic stress. Leveraging YTHDC1 knockdown‐induced metabolic vulnerability, an ATF4 mRNA‐targeted nanotherapy is developed to
Zheng‐Hao Lai   +12 more
wiley   +1 more source

Efficient in vitro transduction of naive murine B cells with lentiviral vectors

open access: yes, 2004
The aim of this study was to determine the impact of lentiviral transduction on primary murine B cells. Studying B cell activities in vivo or using them for tolerance induction requires that the cells remain unaltered in their biological behavior except ...
Beyer, Winfried   +7 more
core  

Deubiquitination of Vangl by USP6 and USP32 Regulates Planar Cell Polarity Signaling

open access: yesAdvanced Science, EarlyView.
Compartment‐specific deubiquitination controls Vangl dosage and planar cell polarity signaling. USP6 and USP32 regulate distinct subcellular pools of Vangl by removing distinct ubiquitin modifications from Vangl proteins. This regulatory mechanism safeguards PCP‐dependent embryonic morphogenesis, while aberrant USP32‐dependent stabilization of VANGL ...
Fangzi Zha   +13 more
wiley   +1 more source

The TUBA1B–G3BP2 Axis Sustains p65 Transcriptional Activity to Promote Hepatocellular Carcinoma Progression

open access: yesAdvanced Science, EarlyView.
TUBA1B is consistently upregulated in hepatocellular carcinoma and sustains malignant progression by stabilizing G3BP2. By restraining TRIM25‐associated K48‐linked ubiquitination, TUBA1B preserves the G3BP2–IκBα complex and basal NF‐κB/p65 activity. Concurrent TUBA1B/G3BP2 upregulation identifies an aggressive HCC subgroup with enhanced p65 activation ...
Fen Lin   +10 more
wiley   +1 more source

Designing and Constructing the Lentiviral Vector Coding miRNA-499a and Transduction of Human Mesenchymal Stem Cells

open access: yesJournal of Mazandaran University of Medical Sciences, 2018
Background and purpose: Lentiviral vectors (LVs) are suitable candidates for gene delivery to cells with stable and high-level of transgene expression in target cells.
Vajiheh Neshati   +5 more
doaj  

Lentiviral gene transfer into peripheral blood–derived CD34+ NOD/SCID-repopulating cells

open access: yes, 2002
This study reports a lentiviral gene transfer protocol for efficient transduction of adult human peripheral blood (PB)–derived CD34+ NOD/SCID-repopulating cells (SRCs) using vesicular stomatitis virus–G protein (VSV-G)–pseudotyped lentiviruses encoding ...
Matthias Eder   +6 more
core   +1 more source

DLST Succinylation‐Mediated Mitochondrial Metabolic Remodeling and Cuproptosis Resistance Promote Malignant Progression of Lung Adenocarcinoma

open access: yesAdvanced Science, EarlyView.
The DLST K409 succinylation mediated by CPT1A promotes OXPHOS and redox homeostasis through regulating enzyme activity, thereby promoting the malignant progression of LUAD. Notably, the succinylation of DLST can enhance the cuproptosis resistance by inhibiting its lipoylation.
Xuanxuan Li   +9 more
wiley   +1 more source

Epigenetic Reactivation of TNFRSF19 Suppresses Mitophagy and Sensitizes Triple‐Negative Breast Cancer to Doxorubicin

open access: yesAdvanced Science, EarlyView.
TNFRSF19 is an epigenetically silenced regulator of mitophagy in triple‐negative breast cancer. TNFRSF19 deficiency activates the TGFBR1–SMAD3–PINK1 axis to promote mitophagy and confer doxorubicin resistance, whereas decitabine‐mediated restoration of TNFRSF19 suppresses mitophagy and enhances doxorubicin sensitivity, revealing a targetable epigenetic–
Shiyang Liu   +7 more
wiley   +1 more source

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