Results 81 to 90 of about 222,748 (293)

SNX8 enables lysosome reformation and reverses lysosomal storage disorder

Nature Communications
Lysosomal Storage Disorders (LSDs), which share common phenotypes, including enlarged lysosomes and defective lysosomal storage, are caused by mutations in lysosome-related genes.
Xinran Li, Cong Xiang, Shilei Zhu, Jiansheng Guo, Chang Liu, Ailian Wang, Jin Cao, Yan Lu, Dante Neculai, Pinglong Xu, Xin-Hua Feng   +10 more
doaj   +1 more source

Mycobacterium tuberculosis resides in lysosome-poor monocyte-derived lung cells during chronic infection.

PLoS Pathogens
Mycobacterium tuberculosis (Mtb) infects lung myeloid cells, but the specific Mtb-permissive cells and host mechanisms supporting Mtb persistence during chronic infection are incompletely characterized.
Weihao Zheng, I-Chang Chang, Jason Limberis, Jonathan M Budzik, Beth Shoshana Zha, Zachary Howard, Lucas Chen, Joel D Ernst   +7 more
doaj   +1 more source

The mTOR–lysosome axis at the centre of ageing

FEBS Open Bio, 2022
Age‐related diseases represent some of the largest unmet clinical needs of our time. While treatment of specific disease‐related signs has had some success (for example, the effect of statin drugs on slowing progression of atherosclerosis), slowing ...
Julian M. Carosi, Célia Fourrier, Julien Bensalem, Timothy J. Sargeant   +3 more
doaj   +1 more source

Rab14 regulates the maturation of macrophage phagosomes containing the fungal pathogen Candida albicans and the outcome of the host-pathogen interaction [PDF]

, 2015
Date of Acceptance: 02/02/2015 Copyright © 2015, American Society for Microbiology.
Bain, Judith M, Erwig, Lars-Peter, Gow, Neil A R, Lyall, Natalie, Okai, Blessing   +4 more
core   +2 more sources

The role of lipid metabolism in neuronal senescence

FEBS Open Bio, EarlyView.
Disrupted lipid metabolism, through alterations in lipid species or lipid droplet accumulation, can drive neuronal senescence. However, lipid dyshomeostasis can also occur alongside neuronal senescence, further amplifying tissue damage. Delineating how lipid‐induced senescence emerges in neurons and glial cells, and how it contributes to ageing and ...
Dikaia Tsagkari, Eleftheria Panagiotidou, Nektarios Tavernarakis   +2 more
wiley   +1 more source

Age- and stress-associated C. elegans granulins impair lysosomal function and induce a compensatory HLH-30/TFEB transcriptional response. [PDF]

, 2019
The progressive failure of protein homeostasis is a hallmark of aging and a common feature in neurodegenerative disease. As the enzymes executing the final stages of autophagy, lysosomal proteases are key contributors to the maintenance of protein ...
Ashrafi, Kaveh, Butler, Victoria J, Caballero, Benjamin, Coppola, Giovanni, Corrales, Christian I, Cortopassi, Wilian A, Cuervo, Ana Maria, Gao, Fuying, Jacobson, Matthew P, Kao, Aimee W, Vohra, Mihir   +10 more
core   +1 more source

Large‐scale bidirectional arrayed genetic screens identify OXR1 and EMC4 as modifiers of αSynuclein aggregation

FEBS Open Bio, EarlyView.
Activation of the mitochondrial protein OXR1 increases pSyn129 αSynuclein aggregation by lowering ATP levels and altering mitochondrial membrane potential, particularly in response to MSA‐derived fibrils. In contrast, ablation of the ER protein EMC4 enhances autophagic flux and lysosomal clearance, broadly reducing α‐synuclein aggregates.
Sandesh Neupane, Lea Nikolić, Lorenzo Maraio, Thomas Goiran, Nathan Karpilovsky, Stefano Sellitto, Vangelis Bouris, Jiang‐An Yin, Ronald Melki, Edward A Fon, Adriano Aguzzi, Elena De Cecco   +11 more
wiley   +1 more source

Protein trafficking through the endosomal system prepares intracellular parasites for a home invasion [PDF]

, 2013
Toxoplasma (toxoplasmosis) and Plasmodium (malaria) use unique secretory organelles for migration, cell invasion, manipulation of host cell functions, and cell egress. In particular, the apical secretory micronemes and rhoptries of apicomplexan parasites
A Fomovska, AE Topolska, B Lige, B Shen, BF Kafsack, BJ Luft, C Lord, CA Hunter, Chetan E. Chitnis, Christian Slomianny, CY He, D Richard, DL Alexander, F Parussini, H El Hajj, HC Hoppe, HC Hoppe, I Mellman, J Schrevel, JB Dacks, JC Boothroyd, JE Rothman, JF Dubremetz, JM Harper, K Kremer, K Miranda, KA Joiner, KA Joiner, KM Hager, L Pelletier, L Sheiner, LH Bannister, LH Bannister, LM Kats, M Elias, M Tufet-Bayona, M Yang, Markus Meissner, ME Francia, MH Ngo, MH Ngo, MK Shaw, MS Breinich, MS Marks, NA Counihan, PJ Bradley, PJ Sloves, S Mogelsvang, SD Brydges, Stanislas Tomavo, VB Carruthers, Vern B. Carruthers, WM Henne, X Que, Z Dou   +54 more
core   +2 more sources

Intercompartmental communication in senescence

FEBS Open Bio, EarlyView.
Senescent cells experience structural changes in the plasma membrane, endoplasmic reticulum, mitochondria, lysosomes, nucleus, and cytoskeleton. These alterations disrupt crosstalk among cellular compartments, impairing vesicular trafficking, contact sites, and molecular flow.
Krystyna Mazan‐Mamczarz, Eleanor J. Wind, Jixiang Leng, Myriam Gorospe   +3 more
wiley   +1 more source

Characterization of avirulent mutant Legionella pneumophila that survive but do not multiply within human monocytes. [PDF]

, 1987
Legionella pneumophila, the causative agent of Legionnaires' disease, is a Gram-negative bacterium and a facultative intracellular parasite that multiplies in human monocytes and alveolar macrophages. In this paper, mutants of L.
Horwitz, MA
core