-
Mashup Score: 12Unraveling hallmark suitability for staging pre- and post-implantation stem cell models - 15 hour(s) ago
Onfray et al. report the comparison of hTSCs, hTELCs, and primed, extended, and naive hPSCs by transcriptomics, proteomics, DNAme quantification, X, and metabolic activity. TELCs have features of trophectoderms, while TSCs represent post-implantation trophoblasts. hEPSCs are clearly primed cells but display a higher metabolic and clonogenic potential than regular primed PSCs.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 11Modulation of GPR133 (ADGRD1) signaling by its intracellular interaction partner extended synaptotagmin 1 - 18 hour(s) ago
Stephan et al. use proximity biotinylation proteomics to identify an interaction between GPR133, an adhesion GPCR, and extended synaptotagmin 1 (ESYT1), a Ca2+-dependent mediator of ER-plasma membrane bridges. ESYT1-driven repression of GPR133 signaling is relieved by increases in cytosolic Ca2+. This interaction may be relevant to the pathogenesis of glioblastoma.
Source: www.cell.comCategories: General Medicine News, General Journals & SocietTweet
-
Mashup Score: 10Podocyte SIRPα reduction aggravates lupus nephritis via promoting T cell inflammatory responses - 19 hour(s) ago
Qian et al. show that SIRPα expression is downregulated in podocytes exposed to LN. The decrease of SIRPα stimulates podocyte antigen presentation through the SHP-1/p-Syk axis. In lupus-prone mice, podocyte-specific knockout of SIRPα aggravates T cell immune response and renal damage, while the Syk inhibitor GS-9973 effectively alleviates renal disease progression and T cell immune response.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 4TDP1 mutation causing SCAN1 neurodegenerative syndrome hampers the repair of transcriptional DNA double-strand breaks - 22 hour(s) ago
Geraud et al. generate human SCAN1 cells by CRISPR-Cas9 to study SCAN1 disease. SCAN1 cells accumulate transcriptional DSBs specifically in G1 phase due to enhanced DSB formation and defective repair. The presence of mutated TDP1, rather than loss of its activity, causes defective repair by hampering a TDP2-dependent backup pathway.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 66A unified mechanism for PARP inhibitor-induced PARP1 chromatin retention at DNA damage sites in living cells - 1 day(s) ago
Employing newly introduced measures of PARP1 dynamics and activity in vivo, Kanev et al. reveal that both catalytic inhibition and allosteric trapping by PARP inhibitors define the overall retention of PARP1 at damaged chromatin. The extent of PARP1 retention corresponds to a delay in downstream DNA repair events and PARPi cytotoxicity.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 98Metabolic regulation of single synaptic vesicle exo- and endocytosis in hippocampal synapses - 2 day(s) ago
Synaptic transmission is energetically costly. Myeong et al. demonstrate that hippocampal synapses can bypass glycolysis using oxidative fuels. Mitochondria, rather than glycolysis, control the spatiotemporal properties of vesicle release and ultrafast endocytosis. Mitochondrial localization in nerve terminals enhances vesicle release and reuptake, thus representing a form of synaptic plasticity.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 17
(Cell Reports 39, 110675; April 12, 2022)
Source: www.cell.comCategories: General Medicine News, General Journals & SocietTweet
-
Mashup Score: 61
The mechanism that initiates cardiac dysfunction during endotoxemia remains unknown. Tang et al. show that GSDMD-N triggers early mitochondrial pore and heart dysfunction directly via oxidized cardiolipin by complex II in cardiomyocytes. Such pores further incorporate into BAX and VDAC1 oligomers to exacerbate the apoptotic process in cardiomyocytes.
Source: www.cell.comCategories: General Medicine News, General Journals & SocietTweet
-
Mashup Score: 78Loss of POLE3-POLE4 unleashes replicative gap accumulation upon treatment with PARP inhibitors - 2 day(s) ago
Hill et al. show that the loss of the POLE3-POLE4 subunits of Polε induces replicative gap accumulation upon treatment with PARP inhibitors. Polε-dependent replicative gaps lead to BRCA1-independent sensitization to PARP inhibitors and bypass a common mechanism of resistance to these compounds, such as the loss of 53BP1.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
-
Mashup Score: 45A ZBP1 isoform blocks ZBP1-mediated cell death - 3 day(s) ago
The intrinsic mechanisms that dampen ZBP1 activation to fine-tune inflammatory responses are poorly understood. Cai et al. characterize a short isoform of ZBP1 (ZBP1-S) that acts as a suppressor via its Zα domains to counteract cell death mediated by full-length ZBP1, thus revealing an autogenic inhibition mechanism for regulating ZBP1 signaling.
Source: www.cell.comCategories: General Medicine News, General HCPsTweet
Unraveling hallmark suitability for staging pre- and post-implantation stem cell models https://t.co/Cy9HmlKCbL