Results 231 to 240 of about 108,982 (307)

TP53BP2 Promotes Placental Autophagy and Preeclampsia via G9a and DNMT1 Cooperatively Modulating E2F1

open access: yesAdvanced Science, EarlyView.
G9a, and DNA Methyltransferase1 (DNMT1) cooperatively modulates E2F1 on the promoter of tumor suppressor p53‐binding protein 2 (TP53BP2) increased autophagy in preeclampsia. TP53BP2 promotes autophagy in trophoblasts through DNA methylation and H3K9me2‐mediated transcriptional regulation.
Nan Jiang   +12 more
wiley   +1 more source

CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

open access: yesAdvanced Science, EarlyView.
This study identifies CRISPLD2 as a key protector against IVDD. By regulating ferroptosis through the CRISPLD2–miR‐548I–IL17A axis, CRISPLD2 maintains NPCs homeostasis and reduces oxidative stress. Restoring CRISPLD2 expression effectively alleviates disc degeneration and highlights a promising therapeutic strategy for discogenic low back pain ...
Yangyang Shi   +11 more
wiley   +1 more source

SETDB2 Mitigates Podocyte Dysfunction in Diabetic Kidney Disease Through Epigenetic Silencing of SMAD3

open access: yesAdvanced Science, EarlyView.
SETDB2 epigenetically represses Smad3 transcription by increasing H3K9me3 enrichment at its promoter, thereby mitigating podocyte dysfunction in DKD. The transcription factor TCF21 binds directly to the Setdb2 promoter and enhances its expression in podocytes. Abstract Podocyte dysfunction represents both an early pathological hallmark and a key driver
Lanfang Li   +14 more
wiley   +1 more source

OCTN2 Activates a Non‐Canonical Carnitine Metabolic Pathway to Promote MASH‐HCC Progression and Immunotherapy Resistance

open access: yesAdvanced Science, EarlyView.
In non‐MASH‐HCC, L‐carnitine promotes tumor progression primarily through its classical role in enhancing fatty acid oxidation (FAO). However, in MASH‐HCC, where FAO is markedly suppressed, L‐carnitine shifts from this canonical function to serve instead as an intracellular acetyl group buffer.
Chuqi Xia   +11 more
wiley   +1 more source

Depletion of the RNA‐Editing Enzyme ADAR1 Invigorates the Antitumor Immunity of NK Cells

open access: yesAdvanced Science, EarlyView.
ADAR1 is upregulated in NK cells from melanoma patients, impairing their function. Its loss enhances NK cell tumor infiltration and cytotoxicity in vitro and in vivo. Mechanistically, ADAR1 deficiency destabilizes CD38 mRNA to reduce its expression, thereby increasing NK cell mobility and killing, which nominates it as a therapeutic target for NK cell ...
Shuhan Chen   +11 more
wiley   +1 more source

Induction and Repression of the Histidine-degrading Enzymes in Aerobacter aerogenes

open access: yesJournal of Biological Chemistry, 1965
B, Magasanik   +3 more
openaire   +2 more sources

EIF5A Couples Translational Control With Transcriptional Reprogramming Through Chromocenter Reorganization During Spermiogenesis

open access: yesAdvanced Science, EarlyView.
The translation factor Eukaryotic translation initiation factor 5A (eIF5A) is essential for male fertility in mice. It supports the translation of proteins crucial for heterochromatin organization and acrosome formation. eIF5A deficiency disrupts chromocenter integrity, increases chromatin accessibility, and causes transcriptional dysregulation ...
Yuling Cai   +15 more
wiley   +1 more source

Gabpα‐Pparγ Complex Determines Glycolytic Capacity and Lactic Acid Homeostasis in Brown Fat

open access: yesAdvanced Science, EarlyView.
This study identifies the Gabpα–Pparγ complex as a key transcriptional regulator that couples glycolysis to lactate‐driven thermogenesis in brown adipose tissue by directly activating Eno1 transcription. ‌Competitive disruption of this interaction impairs lactate metabolism and thermogenic capacity.
Zhihan Wang   +22 more
wiley   +1 more source

Review 1 - Nature (Busby) [PDF]

open access: yes, 2009
Scarlato, Vincenzo
core  

Integrin β3 Orchestrates Hepatic Steatosis via a Novel CD36‐Dependent Lipid Uptake Complex

open access: yesAdvanced Science, EarlyView.
In MASH, ITGB3 recruits LYN and drives its ubiquitin‐proteasomal degradation via phosphorylation. This relieves DHHC5 inhibition, enabling ITGB3/DHHC5/CD36 complex assembly to enhance CD36 palmitoylation and fatty acid uptake, thereby exacerbating disease. Targeting ITGB3 blocks this pathogenic axis and ameliorates MASH.
Ying Zhang   +13 more
wiley   +1 more source

Home - About - Disclaimer - Privacy