Results 61 to 70 of about 2,483,935 (295)

Bacterial porin disrupts mitochondrial membrane potential and sensitizes host cells to apoptosis [PDF]

open access: yes, 2009
The bacterial PorB porin, an ATP-binding beta-barrel protein of pathogenic Neisseria gonorrhoeae, triggers host cell apoptosis by an unknown mechanism. PorB is targeted to and imported by host cell mitochondria, causing the breakdown of the mitochondrial
Kepp, Oliver   +45 more
core   +2 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

Neurodegenerative stress related mitochondrial proteostasis [PDF]

open access: yes, 2015
1.1 Background: Mitochondria are the main site of energy production in most cells. Furthermore, they are involved in a multitude of other essential cellular processes, such as regulating the cellular calcium pool, lipid metabolism and programmed cell ...
Fang, Lei
core   +1 more source

Microbiome−host proteostasis crosstalk—An emerging perspective on mechanisms and interventions toward healthy longevity

open access: yesFEBS Letters, EarlyView.
Proteostasis and the gut microbiota play a key role in shaping host physiology. Microbiota‐derived metabolites, vitamins, and RNA modulate host proteostasis. Findings from model systems, including C. elegans, indicate microbes can either stabilize or disrupt host proteostasis.
Abhishek Anil Dubey, Maria Ermolaeva
wiley   +1 more source

The mitochondrial receptor complex [PDF]

open access: yes, 1993
The receptor complex in the mitochondrial outer membrane, which consists of at least seven different proteins, is responsible for the recognition and translocation of cytosolically synthesized preproteins.
Klei, Ida J. van der; id_orcid   +12 more
core   +2 more sources

Structural insights and therapeutic targets in Acinetobacter baumannii capsule biosynthesis

open access: yesFEBS Letters, EarlyView.
Hypervirulent KL49 A. baumannii's capsular polysaccharide contains the nonulosonic acid 8‐epi‐Leg5,7Ac2, synthesized by epimerization via ElaA, ElaB, and ElaC. Crystal structures of ElaA, ElaB, and ElaC reveal their role in CMP‐Leg5,7Ac2 synthesis and regioselective C8 epimerization.
Woo Cheol Lee   +7 more
wiley   +1 more source

A nuclear-based quality control pathway for non-imported mitochondrial proteins

open access: yeseLife, 2021
Mitochondrial import deficiency causes cellular toxicity due to the accumulation of non-imported mitochondrial precursor proteins, termed mitoprotein-induced stress.
Viplendra PS Shakya   +5 more
doaj   +1 more source

Protein translocation across mitochondrial membranes [PDF]

open access: yes, 1992
Protein translocation across biological membranes is of fundamental importance for the biogenesis of organelles and in protein secretion. We will give an overview of the recent achievements in the understanding of protein translocation across ...
Walter Neupert   +3 more
core   +1 more source

Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential

open access: yesFEBS Letters, EarlyView.
Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta   +3 more
wiley   +1 more source

Mitochondrial Quality Control and Cellular Proteostasis: Two Sides of the Same Coin

open access: yesFrontiers in Physiology, 2020
Mitochondrial dysfunction is a hallmark of cardiac pathophysiology. Defects in mitochondrial performance disrupt contractile function, overwhelm myocytes with reactive oxygen species (ROS), and transform these cellular powerhouses into pro-death ...
Justin M. Quiles, Åsa B. Gustafsson
doaj   +1 more source

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