Results 121 to 130 of about 646,683 (270)
SIRT4 positively regulates autophagy via ULK1, but independently of HDAC6 and OPA1
FEBS Open Bio, EarlyView.Cells expressing SIRT4 (H161Y), a catalytically inactive mutant of the sirtuin SIRT4, fail to upregulate LC3B‐II and exhibit a reduced autophagic flux under stress conditions. Interestingly, SIRT4(H161Y) promotes phosphorylation of ULK1 at S638 and S758 that are associated with inhibition of autophagy initiation.
Isabell Lehmkuhl +13 more
wiley +1 more source
FEBS Open Bio, EarlyView.Clinical analysis reveals significant dysregulation of FGFRL1 in esophageal cancer (EC) patients. RNAi‐coupled next‐generation sequencing (NGS) and in vitro study reveal FGFRL1‐mediated EC progression via EMT, PI3K/Akt, and Notch pathways. Functional assays confirm its role in tumor growth, migration, and invasion.
Aprajita Srivastava +3 more
wiley +1 more source
Unraveling the Role of TP53 in Colorectal Cancer Therapy: From Wild-Type Regulation to Mutant
Frontiers in Bioscience-LandmarkThe p53, a pivotal tumor suppressor, regulates various cellular responses, including DNA repair and apoptosis. Normally, p53 levels are low due to murine double minute clone 2 (MDM2) mediated polyubiquitination.
Wenshu Li +6 more
doaj +1 more source
Targeting oncogenic mutant p53 for cancer therapy
Frontiers in Oncology, 2015 Among genetic alterations in human cancers, mutations in the tumor suppressor p53 gene are the most common, occurring in over 50% of human cancers. The majority of p53 mutations are missense mutations and result in the accumulation of dysfunctional p53 ...
Tomoo eIwakuma, Alejandro eParrales
doaj +1 more source
The role of lipid metabolism in neuronal senescence
FEBS Open Bio, EarlyView.Disrupted lipid metabolism, through alterations in lipid species or lipid droplet accumulation, can drive neuronal senescence. However, lipid dyshomeostasis can also occur alongside neuronal senescence, further amplifying tissue damage. Delineating how lipid‐induced senescence emerges in neurons and glial cells, and how it contributes to ageing and ...
Dikaia Tsagkari +2 more
wiley +1 more source
BMC Cell Biology, 2001 Background The p53 protein is activated by genotoxic stress, oncogene expression and during senescence, p53 transcriptionally activates genes involved in growth arrest and apoptosis.
Price Brendan D, Turenne Gaetan A
doaj +1 more source
FEBS Open Bio, EarlyView.A tri‐culture of iPSC‐derived neurons, astrocytes, and microglia treated with ferroptosis inducers as an Induced ferroptosis model was characterized by scRNA‐seq, cell survival, and cytokine release assays. This analysis revealed diverse microglial transcriptomic changes, indicating that the system captures key aspects of the complex cellular ...
Hongmei Lisa Li +6 more
wiley +1 more source
FEBS 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
Mutant p53: multiple mechanisms define biologic activity in cancer
Frontiers in Oncology, 2015 The functional importance of p53 as a tumor suppressor gene is evident through its pervasiveness in cancer biology. The p53 gene is the most commonly altered gene in human cancer; however, not all genetic alterations are biologically equivalent.
Michael Paul Kim +3 more
doaj +1 more source
PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines
FEBS 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