Results 81 to 90 of about 2,739,032 (319)

Valosin‐containing protein counteracts ATP‐driven dissolution of FUS condensates through its ATPase activity in vitro

open access: yesFEBS Letters, EarlyView.
Biomolecular condensates formed by fused in sarcoma (FUS) are dissolved by high ATP concentrations yet persist in cells. Using a reconstituted system, we demonstrate that valosin‐containing protein (VCP), an AAA+ ATPase, counteracts ATP‐driven dissolution of FUS condensates through its D2 ATPase activity.
Hitomi Kimura   +2 more
wiley   +1 more source

Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders

open access: yesFEBS Letters, EarlyView.
Mitochondrial remodeling shapes neural and glial lineage progression by matching metabolic supply with demand. Elevated OXPHOS supports differentiation and myelin formation, while myelin compaction lowers mitochondrial dependence, revealing mitochondria as key drivers of developmental energy adaptation.
Sahitya Ranjan Biswas   +3 more
wiley   +1 more source

Iron metabolism and incidence of metabolic syndrome [PDF]

open access: yesNutrition, Metabolism and Cardiovascular Diseases, 2015
Whether iron metabolism affects metabolic syndrome (METS) is debated. We assessed the association between several markers of iron metabolism and incidence of METS.Data from 3271 participants (1870 women, 51.3 ± 10.4 years), free of METS at baseline and followed for 5.5 years.
Kilani, N.   +3 more
openaire   +4 more sources

An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane

open access: yesFEBS Letters, EarlyView.
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa   +3 more
wiley   +1 more source

Plasma protein metabolism: regulation of synthesis, distribution, and degradation

open access: yes, 1970
xxiv+560hlm ...
PLASMA PROTEIN METABOLISM   +2 more
core  

Lipid Metabolism in Inflammation and Immune Function

open access: yes, 2022
Lipid metabolism plays an essential role in modulating inflammation within the context of acute and chronic diseases [...
Catherine J. Andersen
core   +1 more source

pH‐mediated activation of the lysosomal arginine sensor SLC38A9

open access: yesFEBS Letters, EarlyView.
Cells monitor nutrient levels via the lysosomal transporter SLC38A9 to activate the mechanistic target of rapamycin complex 1 (mTORC1). This study reveals that SLC38A9 function is regulated by pH. We identified histidine 544 as a critical pH sensor that undergoes conformational changes to control amino acid efflux from lysosomes; therefore, it ...
Xuelang Mu, Ampon Sae Her, Tamir Gonen
wiley   +1 more source

Parasitic Behavior of Leukemic Cells in Systemic Host Metabolism

open access: yes, 2018
© 2018 Elsevier Inc. Metabolic reprogramming is a hallmark of cancer cell metabolism. Recently, in Cancer Cell, Ye and colleagues (2018) reported that leukemic cells have the capacity to modulate glucose metabolism in multiple organs of their host ...
Mak, Tak Wah   +2 more
core   +1 more source

Oncology Therapeutics Targeting the Metabolism of Amino Acids

open access: yes, 2020
Amino acid metabolism promotes cancer cell proliferation and survival by supporting building block synthesis, producing reducing agents to mitigate oxidative stress, and generating immunosuppressive metabolites for immune evasion.
Nefertiti Muhammad   +2 more
core   +1 more source

Mapping the Metabolic Niche of Citrate Metabolism and SLC13A5

open access: yes, 2023
The small molecule citrate is a key molecule that is synthesized de novo and involved in diverse biochemical pathways influencing cell metabolism and function. Citrate is highly abundant in the circulation, and cells take up extracellular citrate via the
Hanna Friederike Willenbockel   +2 more
core   +1 more source

Home - About - Disclaimer - Privacy