Results 81 to 90 of about 429,052 (284)

Clinical Implication and the Hereditary Factors of NM23 in Hepatocellular Carcinoma Based on Bioinformatics Analysis and Genome-Wide Association Study. [PDF]

open access: yesJ Oncol, 2018
Yang C   +17 more
europepmc   +1 more source

Tumor Necrosis Factor-α −308G>A Allelic Variant Modulates Iron Accumulation in Patients with Hereditary Hemochromatosis [PDF]

open access: bronze, 2006
Pierre‐Alexandre Krayenbuehl   +8 more
openalex   +1 more source

Hyperosmotic stress induces PARP1‐mediated HPF1‐dependent mono(ADP‐ribosyl)ation

open access: yesFEBS Letters, EarlyView.
Sorbitol‐induced hyperosmotic stress rapidly induces reversible mono(ADP‐ribosyl)ation (MARylation) on PARP1 without the signs of genotoxic signaling. We show that PARP1 autoMARylation is HPF1 dependent and forms hydroxylamine‐resistant O‐glycosidic linkages.
Anna Georgina Kopasz   +11 more
wiley   +1 more source

Nephropathy of type II diabetes: Evidence for hereditary factors?

open access: bronze, 1997
Krzysztof Strojek   +8 more
openalex   +1 more source

Factors associated with rapid improvement in visual acuity in patients with Leber's hereditary optic neuropathy after gene therapy [PDF]

open access: bronze, 2020
Hongli Liu   +8 more
openalex   +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

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

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