Results 61 to 70 of about 1,533,855 (292)

ACSS2 involved in acetyl‐CoA synthesis regulates skeletal muscle function

open access: yesFEBS Letters, EarlyView.
The enzyme acyl‐coenzyme A synthetase short‐chain family member‐2 (ACSS2) catalyzes the conversion of acetate to acetyl‐CoA, but its function in skeletal muscle is unclear. We studied ACSS2 deficiency in mouse and fly models. Skeletal muscle from the mouse model showed atrophic fibers, excess lipid, and depleted NADH.
Mekala Gunasekaran   +6 more
wiley   +1 more source

A working model for cytoplasmic assembly of H/ACA snoRNPs

open access: yesFEBS Letters, EarlyView.
Dyskerin is the component of nuclear H/ACA ribonucleoproteins (RNPs) endowed with pseudouridine synthase catalytic activity. Two isoforms of human dyskerin have been characterized: the abundant Iso1, mainly nuclear, and the shorter Iso3, mainly cytoplasmic but occasionally imported into nuclei.
Alberto Angrisani, Maria Furia
wiley   +1 more source

Mechanistic basis for inhibition of the extended‐spectrum β‐lactamase GES‐1 by enmetazobactam and tazobactam

open access: yesFEBS Letters, EarlyView.
Antimicrobial resistance (AMR) is of huge importance, resulting in over 1 million deaths each year. Here, we describe how a new drug, enmetazobactam, designed to help fight resistant bacterial diseases, inhibits a key enzyme (GES‐1) responsible for AMR. Our data show it is a more potent inhibitor than the related tazobactam, with high‐level computation
Michael Beer   +10 more
wiley   +1 more source

The Prevalence of Smoking in Middle-Aged Patients with Metabolic Syndrome in Comparison with Healthy People, Isfahan City, Iran, 2018

open access: yesمجله دانشکده پزشکی اصفهان, 2019
Background: Metabolic syndrome is a physiologic and biochemical disorder. Due to the possible important role of smoking in metabolic syndrome, we aimed to assess this role.
Anahita Babak   +3 more
doaj   +1 more source

C9orf72 ALS‐causing mutations lead to mislocalization and aggregation of nucleoporin Nup107 into stress granules

open access: yesFEBS Letters, EarlyView.
Mutations in the C9orf72 gene represent the most common genetic cause of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease. Using patient‐derived neurons and C. elegans models, we find that the nucleoporin Nup107 is dysregulated in C9orf72‐associated ALS. Conversely, reducing Nup107 levels mitigates disease‐related changes.
Saygın Bilican   +7 more
wiley   +1 more source

Novel and unscrutinized immune entities of the zebrafish gut

open access: yesFEBS Letters, EarlyView.
Understudied cells of the zebrafish immune system include bona fide immune cells and epithelial (‐derived) cells with immune functions. Research focusing on zebrafish cells which demonstrate similarities to mammalian immune cell counterparts may help us understand the pathologies in which they are implicated. Currently available and advanced tools make
Audrey Inge Schytz Andersen‐Civil   +5 more
wiley   +1 more source

Falconry in the Middle Ages [PDF]

open access: yesScientific American, 1910
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openaire   +2 more sources

From lactation to malignancy: A comparison between healthy and cancerous breast gland at single‐cell resolution reveals new issues for tumorigenesis

open access: yesFEBS Letters, EarlyView.
Single‐cell RNA sequencing reveals an opposite role of SLPI in basal tumors based on metastatic spread, along with shared activation of specific regulons in cancer cells and mature luminal lactocytes, as well as downregulation of MALAT1 and NEAT1 in the latter.
Pietro Ancona   +4 more
wiley   +1 more source

Imeglimin attenuates liver fibrosis by inhibiting vesicular ATP release from hepatic stellate cells

open access: yesFEBS Letters, EarlyView.
Imeglimin, at clinically relevant concentrations, inhibits vesicular ATP accumulation and release from hepatic stellate cells, thereby attenuating purinergic signaling and reducing fibrogenic activation. This mechanism reveals a newly identified antifibrotic action of imeglimin beyond glycemic control.
Seiji Nomura   +8 more
wiley   +1 more source

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