Results 151 to 160 of about 1,477,881 (298)

BMI‐1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma

open access: yesFEBS Open Bio, EarlyView.
The schematic illustrates BMI‐1 phosphorylation during M phase, which triggers its translocation from the nucleus to the cytoplasm. In cycling cells, BMI‐1 functions within the PRC1 complex to mediate H2A K119 monoubiquitination. Following PTC596‐induced M phase arrest, phosphorylated BMI‐1 dissociates from PRC1 and is exported to the cytoplasm via its
Banlanjo Umaru   +6 more
wiley   +1 more source

Nuclear pore links Fob1‐dependent rDNA damage relocation to lifespan control

open access: yesFEBS Open Bio, EarlyView.
Damaged rDNA accumulates at a specific perinuclear interface that couples nucleolar escape with nuclear envelope association. Nuclear pores at this site help inhibit Fob1‐induced rDNA instability. This spatial organization of damage handling supports a functional link between nuclear architecture, rDNA stability, and replicative lifespan in yeast.
Yamato Okada   +5 more
wiley   +1 more source

Dihydroorotate dehydrogenase (DHODH) regulates trophoblast syncytialization through organelle stress–induced cellular senescence

open access: yesFEBS Open Bio, EarlyView.
The inhibition of mitochondrial dihydroorotate dehydrogenase (DHODH) impairs syncytialization and induces cellular senescence via mitochondrial and endoplasmic reticulum stress in human trophoblast stem cells, elevating sFlt1/PlGF levels, a hallmark of placental dysfunction in hypertensive disorders of pregnancy.
Kanoko Yoshida   +6 more
wiley   +1 more source

Decoding SR protein regulation: kinases, phosphatases, and therapeutic targeting strategies. [PDF]

open access: yesCell Oncol (Dordr)
Liu N   +3 more
europepmc   +1 more source

PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines

open access: yesFEBS Open Bio, EarlyView.
Talazoparib is the most potent inducer of senescence among different PARP1 inhibitors in human NSCLC cells. In the absence of PARP, no senescence phenotype was observed, demonstrating that PARP1 is necessary for the induction of senescence by this inhibitor.
Camille Huart   +7 more
wiley   +1 more source

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