Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis +3 more
wiley +1 more source
Cytoplasmic and Nuclear Estradiol Receptor in the Corpus Luteum of the Pseudopregnant Rabbit
SummaryEstradiol binding activity has been measured in the rabbit corpus luteum on Days 2, 4, and 6 of pseudopregnancy. The results show that receptor activity is significantly greater on Day 4 than on Day 2 with continued increases on Day 6. In addition, the estradiol receptor activity is translocated into the nucleus within 30 min of injection of 100
openaire +2 more sources
Nuclear Translocation of the p75 Neurotrophin Receptor Cytoplasmic Domain in Response to Neurotrophin Binding [PDF]
The intracellular domain of the p75 neurotrophin receptor (p75ICD) can be released by γ-secretase in response to the previous activation of α-secretase by phorbol esters. However, ligand-dependent release of p75ICDhas yet to be described. We show here that nerve growth factor can induce the release of p75ICDand facilitate its translocation to the ...
openaire +3 more sources
RoboMic is an automated confocal microscopy pipeline for high‐throughput functional imaging in living cells. Demonstrated with fluorescence recovery after photobleaching (FRAP), it integrates AI‐driven nuclear segmentation, ROI selection, bleaching, and analysis.
Selçuk Yavuz +6 more
wiley +1 more source
Importin 7 and Nup358 promote nuclear import of the protein component of human telomerase.
In actively dividing eukaryotic cells, chromosome ends (telomeres) are subject to progressive shortening, unless they are maintained by the action of telomerase, a dedicated enzyme that adds DNA sequence repeats to chromosomal 3'end.
Cornelia Frohnert +4 more
doaj +1 more source
Nuclear β-arrestin1 is a critical cofactor of hypoxia-inducible factor-1α signaling in endothelin-1-induced ovarian tumor progression [PDF]
Hypoxia-inducible factor-1α (HIF-1α) mediates the response to hypoxia or other stimuli, such as growth factors, including endothelin-1 (ET-1), to promote malignant progression in numerous tumors.
Bagnato, Anna +6 more
core +1 more source
Mouse pre‐implantation development involves a transition from totipotency to pluripotency. Integrating transcriptomics, epigenetic profiling, low‐input proteomics and functional assays, we show that eight‐cell embryos retain residual totipotency features, whereas cytoskeletal remodeling regulated by the ubiquitin‐proteasome system drives progression ...
Wanqiong Li +8 more
wiley +1 more source
Noncanonical IFN Signaling, Steroids, and STATs: A Probable Role of V-ATPase
A small group of only seven transcription factors known as STATs (signal transducer and activator of transcription) are considered to be canonical determinants of specific gene activation for a plethora of ligand/receptor systems. The activation of STATs
Howard M. Johnson +2 more
doaj +1 more source
BMI‐1 modulation and trafficking during M phase in diffuse intrinsic pontine glioma
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
Transcriptional reprogramming via signaling domains of CD2, CD28, and 4-1BB
Summary: Costimulatory signals provided to T cells during antigen encounter have a decisive role in the outcome of immune responses. Here, we used chimeric receptors harboring the extracellular domain of mouse inducible T cell costimulator (mICOS) to ...
Annika De Sousa Linhares +3 more
doaj +1 more source

