Results 111 to 120 of about 7,097 (288)

Modulation of Lung Adenocarcinoma by Phosphorylated FOXN3‐Mediated Transcriptional Inactivation of p53

open access: yesAdvanced Science, EarlyView.
In non‐tumorous lung tissues, FOXN3 promotes the transcriptional activation of p53 by facilitating its recruitment to target promoters, thereby suppressing lung tumorigenesis through activation of the p53 signaling pathway. Conversely, in lung adenocarcinoma tissues, hyperphosphorylated FOXN3 dissociates from the promoters of p53‐responsive genes and ...
Jinjin Yu   +16 more
wiley   +1 more source

cDNA Isolation and Gene Expression of the Maize Annexins p33 and p35 [PDF]

open access: yes, 1996
The isolation, cloning, and sequencing of two full-length cDNAs corresponding to the root tip forms of the maize (Zea mays L. cv Clipper) annexins p33 and p35 are described.
A. J. Greenland   +2 more
core   +1 more source

Artificial Host‐Guest Recognition Directs Glycometabolically Engineered Macrophages to Tumors

open access: yesAdvanced Science, EarlyView.
Glycoengineered supramolecular macrophages (GSAR‐M) are developed using glycometabolic labeling for bioorthogonal host‐guest tumor targeting. This engineering approach unexpectedly enhances macrophage migration, phagocytosis, and pseudopodia formation. Consequently, GSAR‐M demonstrate robust tumor‐targeting specificity, effectively arrest tumor growth,
Zhiqing Yang   +8 more
wiley   +1 more source

Biochemical characterisation of parasite annexins

open access: yes, 2009
No Full ...
Hofmann, Andreas   +2 more
core  

TET1 Inhibition Promotes Therapeutic Sensitivity in TP53‐Mutant GBM by Influencing Genome Fragility and Altering TAMs Biology

open access: yesAdvanced Science, EarlyView.
In TP53mut GBM cells, reduced P53 function is associated with increased TET1 expression. Genetic or pharmacological inhibition of TET1 correlates with genome fragility, including DNA damage, cellular senescence, telomere shortening, and reactive oxygen species accumulation, which may contribute to increased efficacy of antitumor therapy.
Zhuonan Pu   +12 more
wiley   +1 more source

Microenvironment‐Responsive Nanomedicine Enables Vertical Modulation of Mitochondrial Pathological Networks in Myocardial Ischemia–Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
A mitochondria‐targeted, microenvironment‐responsive nanoplatform enables pH/ROS‐triggered co‐delivery of berberine and isoliensinine to orchestrate ROS scavenging, inflammation suppression, and apoptosis inhibition. This vertical modulation of mitochondrial pathological networks preserves mitochondrial function and effectively mitigates myocardial ...
Jue Wang   +11 more
wiley   +1 more source

CALB2 is a Mechanoresistance Gene in Metastatic Prostate Cancer

open access: yesAdvanced Science, EarlyView.
Prostate cancer cell lines of differing origins were cultured over many passages while being subjected to semi‐lethal levels of fluid shear stress, representing the harsh mechanical environment these cells are subjected to in the circulation during the process of distant metastasis.
Abigail R. Fabiano   +10 more
wiley   +1 more source

Localization and quantitation of cardiac annexins II, V, and VI in hypertensive guinea pigs

open access: yes, 1999
Annexins are characterized by Ca2+-dependent binding to phospholipids. Annexin II mainly participates in cell-cell adhesion and signal transduction, whereas annexins V and VI also seem to regulate intracellular calcium cycling.
Pascal Trouvé   +7 more
core   +1 more source

High‐Throughput Mechanical Rupture of Nuclear Envelope and the Intracellular Dynamics of Massive Wound Repair

open access: yesAdvanced Science, EarlyView.
A microfluidic device with monolithically integrated nanostructures enables high‐throughput wounding of the cell membrane and nuclear envelope. The spatial distribution of charged multivesicular body protein 4B (CHMP4B) within the cell is mapped before and after wounding, showing involvement in repair of both the cell membrane and nuclear envelope ...
Apresio K. Fajrial   +5 more
wiley   +1 more source

Ubiquitination of ACSL4 by Parkin Suppresses Ferroptosis and Rescues Glucocorticoid‐Induced Bone Loss

open access: yesAdvanced Science, EarlyView.
GCs reduce Parkin, leading to ACSL4 accumulation and PUFA‐phospholipid‐driven ferroptosis in BMSCs, which impairs osteogenesis and promotes adipogenesis, causing GIOP. Parkin restoration (via OE‐Parkin or Parkin‐LNP@DSS6) ubiquitinates and degrades ACSL4, inhibiting ferroptosis, rescuing bone formation, and rescues GIOP bone loss.
Li‐jiang Han   +16 more
wiley   +1 more source

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