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Marco Gatti et al.
Cell reports, 32(5), 107985-107985 (2020-08-07)
PARP inhibitors (PARPi) cause synthetic lethality in BRCA-deficient tumors. Whether specific vulnerabilities to PARPi exist beyond BRCA mutations and related defects in homology-directed repair (HDR) is not well understood. Here, we identify the ubiquitin E3 ligase TRIP12 as negative regulator
Hayden T Pacl et al.
Nature communications, 14(1), 5472-5472 (2023-09-07)
Mycobacterium tuberculosis (Mtb) disrupts glycolytic flux in infected myeloid cells through an unclear mechanism. Flux through the glycolytic pathway in myeloid cells is inextricably linked to the availability of NAD+, which is maintained by NAD+ salvage and lactate metabolism. Using
Wencui Wan et al.
Journal of inflammation research, 14, 3129-3143 (2021-07-22)
Retinal pigment epithelium (RPE) cellular senescence is an important process in degenerative retinal disorders. Grape seed proanthocyanidin extract (GSPE) alleviates senescence-related degenerative disorders; however, the potential effects of GSPE intake on RPE cellular senescence through regulating NAMPT/SIRT1/NLRP3 pathway remain unclear.
Hala Elnakat Thomas et al.
Cell reports, 24(9), 2404-2417 (2018-08-30)
Cells adapt to nutrient and energy deprivation by inducing autophagy, which is regulated by the mammalian target of rapamycin (mTOR) and AMP-activated protein kinases (AMPKs). We found that cell metabolism significantly influences the ability to induce autophagy, with mitochondrial complex
Yejun Zou et al.
Developmental cell, 53(2), 240-252 (2020-03-21)
Understanding of NAD+ metabolism provides many critical insights into health and diseases, yet highly sensitive and specific detection of NAD+ metabolism in live cells and in vivo remains difficult. Here, we present ratiometric, highly responsive genetically encoded fluorescent indicators, FiNad, for
Michael M Murata et al.
Molecular biology of the cell, 30(20), 2584-2597 (2019-08-08)
DNA damage signaling is critical for the maintenance of genome integrity and cell fate decision. Poly(ADP-ribose) polymerase 1 (PARP1) is a DNA damage sensor rapidly activated in a damage dose- and complexity-dependent manner playing a critical role in the initial
Marianne Agerholm et al.
American journal of physiology. Endocrinology and metabolism, 314(4), E377-E395 (2017-12-07)
Nicotinamide adenine dinucleotide (NAD+) can be synthesized by nicotinamide phosphoribosyltransferase (NAMPT). We aimed to determine the role of NAMPT in maintaining NAD+ levels, mitochondrial function, and metabolic homeostasis in skeletal muscle cells. We generated stable Nampt knockdown (sh Nampt KD)
Edgar Sánchez-Ramírez et al.
The Journal of cell biology, 221(12) (2022-10-06)
Adipocytes are the main cell type in adipose tissue, which is a critical regulator of metabolism, highly specialized in storing energy as fat. Adipocytes differentiate from multipotent mesenchymal stromal cells (hMSCs) through adipogenesis, a tightly controlled differentiation process involving close
Zhongju Tan et al.
Annals of clinical and translational neurology, 7(5), 742-756 (2020-04-18)
FK866 is an inhibitor of nicotinamide phosphoribosyltransferase (NAMPT), which exhibits neuroprotective effects in ischemic brain injury. However, in traumatic brain injury (TBI), the role and mechanism of FK866 remain unclear. The present research was aimed to investigate whether FK866 could
Congxin Sun et al.
Cell reports, 42(5), 112372-112372 (2023-04-22)
Autophagy is a homeostatic process critical for cellular survival, and its malfunction is implicated in human diseases including neurodegeneration. Loss of autophagy contributes to cytotoxicity and tissue degeneration, but the mechanistic understanding of this phenomenon remains elusive. Here, we generated
FK866 compromises mitochondrial metabolism and adaptive stress responses in cultured cardiomyocytes
Oyarzun AP, et al.
Biochemical Pharmacology, 98(1), 92-101 (2015)
Min-Kyoo Shin et al.
Cell, 184(10), 2715-2732 (2021-04-15)
Traumatic brain injury (TBI) is the largest non-genetic, non-aging related risk factor for Alzheimer's disease (AD). We report here that TBI induces tau acetylation (ac-tau) at sites acetylated also in human AD brain. This is mediated by S-nitrosylated-GAPDH, which simultaneously
Xie Li et al.
Cell metabolism, 35(1), 200-211 (2022-10-30)
Despite its central importance in cellular metabolism, many details remain to be determined regarding subcellular lactate metabolism and its regulation in physiology and disease, as there is sensitive spatiotemporal resolution of lactate distribution, and dynamics remains a technical challenge. Here
Chye Ling Tan et al.
The Journal of investigative dermatology, 139(8), 1638-1647 (2019-02-19)
Nicotinamide (NAM) is the main precursor of nicotinamide adenine dinucleotide (NAD+), a coenzyme essential for DNA repair, glycolysis, and oxidative phosphorylation. NAM has anti-aging activity on human skin, but the underlying mechanisms of action are unclear. Using 3-dimensional organotypic skin models
Huitao Liu et al.
Theranostics, 11(9), 4187-4206 (2021-03-24)
Axonal degeneration is a common pathological feature in many acute and chronic neurological diseases such as spinal cord injury (SCI). SARM1 (sterile alpha and TIR motif-containing 1), the fifth TLR (Toll-like receptor) adaptor, has diverse functions in the immune and
Nicotinamide riboside, a form of vitamin B3, protects against excitotoxicity-induced axonal degeneration
Chen CX, et al.
Neuroscience, 356, 193-206 (2017)
Nikolaos K Ziogas et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 38(16), 4031-4047 (2018-03-24)
Traumatic axonal injury (TAI) is a common neuropathology in traumatic brain injury and is featured by primary injury to axons. Here, we generated TAI with impact acceleration of the head in male Thy1-eYFP-H transgenic mice in which specific populations of
Eleonora Ciarlo et al.
Nutrients, 14(13) (2022-07-10)
Through evolution, eukaryote organisms have developed the ability to use different molecules as independent precursors to generate nicotinamide adenine dinucleotide (NAD+), an essential molecule for life. However, whether these different precursors act in an additive or complementary manner is not
Metabolic modulation of CtBP dimeric status impacts the repression of DNA damage repair genes and the platinum sensitivity of ovarian cancer.
Li, et al.
International Journal of Biological Sciences, 19, 2081-2096 (2023)
J Patrick Murphy et al.
Cell reports, 24(9), 2381-2391 (2018-08-30)
NAD+ is a key metabolic redox cofactor that is regenerated from nicotinamide through the NAD+ salvage pathway. Here, we find that inhibiting the NAD+ salvage pathway depletes serine biosynthesis from glucose by impeding the NAD+-dependent protein, 3-phosphoglycerate dehydrogenase (PHGDH). Importantly, we
Liana R Stein et al.
The EMBO journal, 33(12), 1321-1340 (2014-05-09)
Neural stem/progenitor cell (NSPC) proliferation and self-renewal, as well as insult-induced differentiation, decrease markedly with age. The molecular mechanisms responsible for these declines remain unclear. Here, we show that levels of NAD(+) and nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in
Marius Walter et al.
bioRxiv : the preprint server for biology (2022-01-13)
SARS-CoV-2 non-structural protein Nsp14 is a highly conserved enzyme necessary for viral replication. Nsp14 forms a stable complex with non-structural protein Nsp10 and exhibits exoribonuclease and N7-methyltransferase activities. Protein-interactome studies identified human sirtuin 5 (SIRT5) as a putative binding partner
Natasja Franceschini et al.
International journal of molecular sciences, 22(12) (2021-07-03)
For osteosarcoma (OS), the most common primary malignant bone tumor, overall survival has hardly improved over the last four decades. Especially for metastatic OS, novel therapeutic targets are urgently needed. A hallmark of cancer is aberrant metabolism, which justifies targeting
Yuexian Cui et al.
Neurobiology of disease, 134, 104672-104672 (2019-11-11)
Ischemic white matter injuries underlie cognitive decline in the elderly and vascular dementia. Ischemia in the subcortical white matter is caused by chronic reduction of blood flow due to narrowing of small arterioles. However, it remains unclear how chronic ischemia
Takuto Nishida et al.
Cell death discovery, 8(1), 195-195 (2022-04-13)
Oxidative stress is a state in which the accumulation of reactive oxygen species exceeds the capacity of cellular antioxidant systems. Both apoptosis and necrosis are observed under oxidative stress, and we have reported that these two forms of cell death
Mathieu Membrez et al.
Nature metabolism, 6(3), 433-447 (2024-03-20)
Mitochondrial dysfunction and low nicotinamide adenine dinucleotide (NAD+) levels are hallmarks of skeletal muscle ageing and sarcopenia1-3, but it is unclear whether these defects result from local changes or can be mediated by systemic or dietary cues. Here we report
Phosphatidylserine is a marker for axonal debris engulfment but its exposure can be decoupled from degeneration
Shacham-Silverberg V, et al.
Cell Death & Disease, 9(11), 1116-1116 (2018)
Lalrawngbawli Annie et al.
The Journal of steroid biochemistry and molecular biology, 204, 105763-105763 (2020-09-29)
Pubertal ovarian function might be dependent on the factors present in the pre-pubertal stages. Visfatin regulates ovarian steroidogenesis in adult. To date, no study has investigated the role of visfatin either in pre-pubertal or pubertal mice ovary. Thus, we investigated
Daniela Buonvicino et al.
Cell chemical biology, 25(4), 471-482 (2018-02-27)
Interest in the modulation of nicotinamide adenine dinucleotide (NAD) metabolome is gaining great momentum because of its therapeutic potential in different human disorders. Suppression of nicotinamide salvage by nicotinamide phosphoribosyl transferase (NAMPT) inhibitors, however, gave inconclusive results in neoplastic patients because
Federica Gaudino et al.
Antioxidants & redox signaling, 31(15), 1150-1165 (2019-08-29)
Aim: Nicotinamide adenine dinucleotide (NAD+) plays central roles in a wide array of normal and pathological conditions. Inhibition of
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